CN212491164U - Cerebral apoplexy treatment equipment - Google Patents

Abstract

The utility model relates to a treatment facility of cerebral apoplexy, including luminous mechanism, luminous mechanism includes: the light source unit is used for emitting 40Hz white light, the switch unit is connected with the light source unit, and the switch unit is also used for being connected with a power supply; the driving unit is connected with the switch unit and used for controlling the switch unit to be switched on or switched off. The therapeutic equipment emits white light of 40Hz through the light-emitting mechanism to irradiate the affected part, can improve the exploration behavior of the cerebral apoplexy patient, improve the anxiety mood, repair the damage of spatial cognition and the damage of synaptic plasticity of the hippocampal CA1 area, and inhibit the degeneration or death of neuron cells in the hippocampal CA1 area, so as to improve the nerve function of the cerebral apoplexy patient and achieve the effect of treating the cerebral apoplexy.

Description

Cerebral apoplexy treatment equipment

Technical Field

The utility model relates to the technical field of biology, in particular to cerebral apoplexy treatment equipment.

Background

Cerebral apoplexy is also called cerebral apoplexy or cerebrovascular accident, and is a group of diseases with cerebral ischemia and hemorrhagic injury symptoms as main clinical manifestations. Cerebral apoplexy is one of three diseases which endanger human life and health. Cerebral apoplexy is characterized by high three highs, namely high morbidity, high mortality and high disability rate. Of the survivors of cerebral stroke, approximately 75% leave sequelae, 40% with severe disability. Therefore, there is a great need to obtain a therapeutic device for the treatment of cerebral stroke.

SUMMERY OF THE UTILITY MODEL

Based on this, there is a need for a cerebral stroke treatment device.

A cerebral stroke treatment device comprising a light emitting mechanism, the light emitting mechanism comprising:

a light source unit for emitting white light of 40 Hz;

the switch unit is connected with the light source unit and is also used for being connected with a power supply; and

and the driving unit is connected with the switch unit and is used for controlling the switch-on or switch-off of the switch unit.

The therapeutic equipment emits white light of 40Hz through the light-emitting mechanism to irradiate the affected part, can improve the exploration behavior of the cerebral apoplexy patient, improve the anxiety mood, repair the damage of spatial cognition and the damage of synaptic plasticity of the hippocampal CA1 area, and inhibit the degeneration or death of neuron cells in the hippocampal CA1 area, so as to improve the nerve function of the cerebral apoplexy patient and achieve the effect of treating the cerebral apoplexy.

In one embodiment, the light source unit includes a plurality of light emitting diodes, and the plurality of light emitting diodes are connected in series.

In one embodiment, the therapeutic apparatus further comprises a signal source connected to the driving unit to provide a control signal to the driving unit, so that the driving unit controls the switch unit to be turned on or off according to the control signal.

In one embodiment, the signal source is a frequency-modulated signal generator.

In one embodiment, the light-emitting mechanism further comprises a first protection unit, and the first protection unit is used for connecting the signal source and the driving unit.

In one embodiment, the light emitting mechanism further includes a current limiting unit located between and connecting the light source unit and the switch unit.

In one embodiment, the light emitting mechanism further comprises a voltage stabilizing unit, and the voltage stabilizing unit is connected with the driving circuit.

In one embodiment, the light emitting mechanism further includes a second protection unit connected to the voltage stabilizing unit and connected to the switch unit.

In one embodiment, the second protection unit includes at least one of reverse connection protection and overcurrent protection.

In one embodiment, the light emitting mechanism is a plurality of light emitting mechanisms, and the plurality of light emitting mechanisms are connected in parallel.

Drawings

In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings used in the description of the embodiments or the prior art will be briefly described below, it is obvious that the drawings in the following description are only some embodiments of the present invention, and for those skilled in the art, other drawings of the embodiments can be obtained according to the drawings without creative efforts.

FIG. 1 is a schematic diagram of a therapeutic apparatus according to one embodiment;

FIG. 2 is a schematic diagram of the construction of the signal source, a power source and a light source unit in the treatment apparatus shown in FIG. 1;

FIG. 3 is a statistical graph of the total movement distance of four groups of mice in example 3;

FIG. 4 is a statistical graph of the percentage of time four groups of mice in example 3 stayed in the central zone;

FIG. 5 is a statistical graph showing the moving distances in the central region of four groups of mice in example 3;

FIG. 6 is a statistical graph of escape latencies for four groups of mice in example 3;

FIG. 7 is a statistical graph showing the residence time of four groups of mice in example 3 in the target quadrant (quadrant where the platform is located);

FIG. 8 is a statistical graph of the average distance of each point in the path to the target platform for four groups of mice in example 3;

FIG. 9 is a schematic representation of the waveforms before and after intense direct stimulation of four groups of mice fEPSPs in example 4;

FIG. 10 is the slope change of fEPSP before and after the tonic stimulation on day 3 of the light treatment of the four groups of mice in example 4;

FIG. 11 is the slope change of fEPSP before and after the tonic stimulation on day 7 of the light treatment of the four groups of mice in example 4;

FIG. 12 is the slope change of fEPSP before and after the tonic stimulation on day 14 of the light treatment of the four groups of mice in example 4;

FIG. 13 is a graph of the percent increase in slope of fEPSPs recorded for the last 15 minutes of an hour following the tonic stimulation in four groups of mice in example 4;

FIG. 14 is a fluorescent microscope photograph showing degeneration and death of neuronal cells in the CA1 region of the hippocampus of 2VO group and 2VO + LED group mice in example 5;

FIG. 15 is a graph showing the degeneration and death of neuronal cells in the CA1 region of the hippocampus of four groups of mice in example 5.

Detailed Description

In order to facilitate understanding of the present invention, the present invention will be described more fully hereinafter with reference to the accompanying drawings. Preferred embodiments of the present invention are shown in the drawings. The invention may, however, be embodied in many different forms and should not be construed as limited to the embodiments set forth herein. Rather, these embodiments are provided so that this disclosure will be thorough and complete.

Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. The terminology used in the description of the invention herein is for the purpose of describing particular embodiments only and is not intended to be limiting of the invention.

Cerebral apoplexy is mainly divided into hemorrhagic stroke and ischemic stroke, and the ischemic stroke is the most common. Ischemic cerebral apoplexy is mainly caused by ischemia and hypoxia in corresponding cerebral area due to the blockage of intracranial artery by thrombus, thus leading to a series of changes of brain such as excitotoxicity, depolarization in the peripheral area of infarction focus, inflammation and delayed nerve cell death in penumbra area, and further leading to the damage of brain function. Patients with cerebral stroke develop epileptiform activity (epileptiform discharges) after several hours of stroke, which is believed to be one of the causes of neurological dysfunction. Research shows that the death risk of a patient with epileptiform activity symptoms after cerebral apoplexy is remarkably increased by two times, and the death rate of an early epileptic patient is obviously higher than that of a patient without epileptic seizure. Periodic epileptiform discharges are also a major cause of stroke. Therefore, repairing neuronal damage and promoting recovery of neural function are issues that need to be addressed for post-stroke rehabilitation.

Research on the field potential of the CA1 region of rat brain shows that 2VO (bilateral common carotid artery occlusion model) rat has reduced energy of low-frequency gamma wave (30 Hz-50 Hz), and the damage of the gamma wave is closely related to the damage of synaptic plasticity. Also, it was found that light stimulation at 40Hz increased the low frequency gamma wave energy of the corresponding brain region. Experiments prove that the white light irradiation treatment at 40Hz can improve the exploration behavior of a patient with cerebral apoplexy, improve anxiety, repair damage of spatial cognition and damage of synaptic plasticity in a hippocampal CA1 area, and inhibit degeneration or death of neuron cells in a hippocampal CA1 area, so that the nerve function of the patient with cerebral apoplexy can be improved, and the effect of treating cerebral apoplexy is achieved.

As shown in fig. 1, one embodiment of a therapeutic device 10 can be used to treat a cerebral stroke. Specifically, the treatment device 10 includes a light emitting mechanism 100. The light emitting mechanism 100 is used to emit white light at 40Hz, and the white light at 40Hz is used to treat cerebral stroke.

Referring to fig. 2, the light emitting mechanism 100 includes a light source unit 110, a switch unit 120, and a driving unit 130. The switching unit 120 is connected to the light source unit 110. The switching unit 120 is also used to connect with the power supply 300. The driving unit 130 is connected to the switching unit 120. The driving unit 130 is used to control the switching unit 120 to be turned on or off.

The light source unit 110 can emit white light of 40 Hz. Further, the light source unit 110 includes a plurality of light emitting diodes (not shown). The plurality of light emitting diodes are connected in series. Further, the color temperature of each light emitting diode was 6000K. The power, voltage rating and current rating of each led can be selected as desired, and can be, for example, 3W, 3V, 1A.

The switch unit 120 is turned on to turn on the light source unit 110 and the power supply 300, so as to control the light source unit 110 to emit light. The switching unit 120 is turned off to disconnect the light source unit 110 from the power supply 300 to control the light source unit 110 to be turned off. Further, the switching unit 120 is a MOSFET switch. The MOSFET switch refers to a metal oxide semiconductor field effect transistor and is a voltage control device.

In one embodiment, the light emitting mechanism 100 further includes a current limiting unit 140. The current limiting unit 140 connects the light source unit 110 and the switching unit 120. The current limiting unit 140 serves to provide a current limiting resistance to ensure that the current passing through the light source unit 110 is within a rated range. Further, the current limiting unit 140 includes a plurality of current limiting resistors, and the plurality of resistors are connected in series or in parallel.

The driving unit 130 is used to control the flicker frequency of the light source unit 110. Further, the driving unit 130 can control the switching unit 120 to be turned on or off according to the control signal of the signal source 200 to control the led flashing frequency.

Further, the treatment device 10 also includes a signal source 200. The signal source 200 is connected to the driving unit 130 to provide a control signal to the driving unit 130. Specifically, the signal source 200 supplies a first voltage to the driving unit 130, and the driving unit 130 controls the switching unit 120 to be conductive according to the first voltage. The signal source 200 supplies a second voltage to the driving unit 130, and the driving unit 130 controls the switching unit 120 to be turned off according to the second voltage. The driving unit 130 controls the blinking frequency of the light source unit 110 according to the switching frequency of the first voltage and the second voltage, so that the treatment device 10 emits white light of 40 Hz. More specifically, the signal source 200 is a frequency-modulated signal generator. In one specific example, the signal source 200 is a PWM pulse width adjustable signal generator.

It should be noted that the first voltage may be set as a high level signal and the second voltage may be set as a low level signal according to actual conditions; the first voltage can be set to be a low level signal and the second voltage can be set to be a high level signal according to actual conditions.

Further, the light emitting mechanism 100 further includes a first protection unit 150 a. The first protection unit 150a is used to connect the signal source 200 and the driving unit 130. The first protection unit 150a controls the control signal output from the signal source 200 within a threshold range.

The driving unit 130 can also pass through an optical isolator device to realize photoelectric conversion of the control signal. Specifically, the driving unit 130 can convert the control signal in an electrical signal-optical signal-electrical signal manner through the optical isolator device, so as to completely isolate the control loop from the working loop of the light source unit 110, thereby avoiding the influence of the harmonic generated when the light emitting diode works on the control loop. The control loop is capable of controlling the flicker frequency and the average intensity of the light emitted by the light source unit 110.

In one embodiment, the light emitting mechanism 100 further includes a voltage stabilizing unit 160. The voltage stabilization unit 160 is connected to the driving circuit. The voltage stabilizing unit 160 can control the voltage output from the power supply 300 within the threshold range of the driving unit. Further, the light emitting mechanism 100 further includes a second protection unit 150 b. The second protection unit 150b is connected to the voltage regulation unit 160 and the switch unit 120. The second protection unit 150b includes at least one of reverse connection protection and overcurrent protection. Still further, the therapeutic apparatus 10 includes a power source 300. The power supply 300 is connected to the second protection unit 150b to supply power to the second protection unit 150 b.

In one embodiment, the light emitting mechanism 100 is plural. The plurality of light emitting mechanisms 100 are connected in parallel. Each light emitting means 100 is connected to a signal source 200. Further, the power supply 300 is plural. The plurality of power supplies 300 are connected to the plurality of light emitting mechanisms 100, respectively. In the illustrated embodiment, the light emitting mechanism 100 is six. The number of power supplies 300 is six.

The operation of the treatment apparatus 10 of the above embodiment is as follows:

the signal source 200 outputs a first voltage, the first protection unit 150a controls the first voltage within a threshold range, and the driving unit 130 controls the switching unit 120 to be turned on according to the first voltage, so that the connection between the light source unit 110 and the power source 300 is turned on to make the light emitting diode emit light.

The signal source 200 outputs a second voltage, the first protection unit 150a controls the second voltage within a threshold range, and the driving unit 130 controls the switching unit 120 to be turned off according to the second voltage, so that the connection between the light source unit 110 and the power supply 300 is disconnected and the light emitting diode is turned off.

The power supply 300 supplies power to the driving circuit through the second protection unit 150b and the voltage stabilizing unit 160, and the second protection unit 150b and the voltage stabilizing unit 160 control the current and the voltage output by the power supply 300 to protect the normal operation of the driving circuit; when the switch unit 120 is turned on, the power supply 300, the second protection unit 150b, the light source unit 110 and the switch unit 120 form a loop, and the second protection unit 150b controls the current output by the power supply 300 to protect the light source unit 110 from normal operation.

The therapeutic apparatus 10 of the above embodiment emits white light of 40Hz through the light emitting mechanism 100 to irradiate the affected part, so as to enhance the exploration behavior of the stroke patient, improve the anxiety, repair the damage of spatial cognition and the damage of synaptic plasticity in the hippocampal CA1 region, and inhibit the degeneration or death of neuron cells in the hippocampal CA1 region, so as to improve the nerve function of the stroke patient, thereby achieving the effect of treating the stroke.

The following are specific examples.

In the following examples, all animal experiments were approved by the southern university of science and technology laboratory animal ethics committee.

Example 1

Construction of bilateral-vascular occlusion model (2 VO) mouse

1. Laboratory animal

SPF-grade male C57BL/6 mice (hereinafter referred to as C57BL/6 mice) were provided from the center of Experimental animals in Guangdong province, weighing 30. + -.1 g, and aged 11. + -.1 weeks. The C57BL/6 mice were housed in the Experimental animals center SPF barrier System of southern science and technology university, Shenzhen. Every 4-5 mice are placed in a mouse cage to be raised, and the mice live in a 12h light and shade period, if no special experiment requires the mice to eat freely.

2. 2VO mouse construction process

C57BL/6 mice were fasted for 12h prior to surgery. Anesthesia of C57BL/6 mice was induced with 2.5% by volume isoflurane gas, and the anesthesia of C57BL/6 mice during surgery was maintained with 1.5% by volume isoflurane gas. The anesthetized C57BL/6 mouse is fixed on a heat preservation plate in a supine position, and the temperature of the C57BL/6 mouse in the operation is maintained to be 37 +/-0.5 ℃. The hair in the neck center of the C57BL/6 mouse was removed with depilatory cream, and the skin in the neck center of the C57BL/6 mouse was twice sterilized with iodophor and 75% by volume of alcohol, respectively. A longitudinal incision was made along the center of the neck of C57BL/6 mice, approximately 1cm long, exposing the left and right Common Carotid Artery (CCA), respectively, taking care not to injure the vagus nerve and puncture the blood vessels. A virtual knot (namely a knot which does not block blood flow) is respectively tied on the left and right CCAs by using No. 6 braided wires, the mass percentage content of isoflurane is improved to 5 percent, so that the blood pressure of a mouse is reduced, when a blood pressure monitor shows that the blood pressure of the mouse is reduced to 50mmHg, the virtual knot on the left and right CCAs is immediately pulled tightly to block the blood flow, the ligature is loosened after 5min of blocking, the concentration of isoflurane is adjusted to 0, and the wound is cleaned and sutured. After the operation, the mice are kept warm for 1h in an ICU cage (Intensive Care Unit), the body temperature of the mice is maintained to 37 +/-0.5 ℃, and then the mice are transferred to a breeding room for normal breeding to obtain 2VO mice. The 2VO mouse is an experimental animal model for stroke, and mainly damages neurons in the CA1 region of the hippocampus cerebri and synaptic plasticity, which causes the decline of learning and memory functions of animals.

Example 2

Experiments on light therapy of mice

1. Experiment grouping

The experiment is divided into four groups, wherein the four groups are respectively named as a false operation group (namely a Sham group), a model group (namely a 2VO group), a false operation illumination group (namely a Sham + LED group) and a model illumination group (namely a 2VO + LED group). Each group had 8 mice tested.

Wherein, the experimental mice of the model group and the model illumination group are 2VO mice. The experimental mice of the sham operation group and the sham operation illumination group are sham operation mice, and the composition process is as follows: c57BL/6 mice were fasted for 12h prior to surgery. Anesthesia of C57BL/6 mice was induced with 2.5% by volume isoflurane gas, and the anesthesia of C57BL/6 mice during surgery was maintained with 1.5% by volume isoflurane gas. The anesthetized C57BL/6 mouse is fixed on a heat preservation plate in a supine position, and the temperature of the C57BL/6 mouse in the operation is maintained to be 37 +/-0.5 ℃. The hair in the neck center of the C57BL/6 mouse was removed with depilatory cream, and the skin in the neck center of the C57BL/6 mouse was twice sterilized with iodophor and 75% by volume of alcohol, respectively. A longitudinal incision is made along the center of the neck of a C57BL/6 mouse, the incision is about 1cm long, the left and right Common Carotid Arteries (CCA) are respectively exposed, the vagus nerve is not damaged and the blood vessels are not punctured, the mouse is kept warm in an ICU cage (Intensive Care Unit) for 1h after the operation, the body temperature of the mouse is maintained to 37 +/-0.5 ℃, and then the mouse is transferred to a breeding room for normal breeding to obtain a sham operated mouse.

2. The experimental process comprises the following steps:

the treatment equipment of figures 1-2 was used to perform phototherapy on each mouse in both the sham-operated and model light groups. The specific light treatment process is as follows: each mouse is subjected to first 40Hz LED illumination treatment for 1h after model construction surgery, and the first illumination is completed within 3h after the model construction surgery. After the first irradiation treatment, 40Hz LED irradiation treatment is given every 12h, and the irradiation time is 1 h. Each mouse was irradiated over its entire body with each light. Changes in neurological function were measured separately for each mouse. Each mouse in the sham-operated group and the model group was not given light treatment and was only normally bred as a control.

Example 3

Cognitive behavioral function test-water maze and open field experiment

1. Open field experiment

The open field experiment is mainly used for detecting the autonomous behavior of the mouse in a new and different environment and exploring behavior and tensity. Four experimental groups were performed according to the procedure of example 2, and each mouse in the sham-operated and model light groups was light-treated. Open field experiments were performed 6 days after the mice received light treatment. And the sham operation group and the model group were used as controls.

Open field experiments consisted of a 40cm x 40cm blue uncovered box and a data acquisition system. The open field is virtually divided into a peripheral and a central region, the size of the central region being 15cm by 15 cm. The mouse is gently placed in the center of the open field, the mouse freely moves for 10min, the motion track of the mouse is collected through a camera and a computer system right above the open field, and data analysis is automatically completed through Smart V3.0 and Panlab software. After each mouse finishes the experiment, alcohol with the volume percentage of 75% is used for disinfecting and wiping the open field, so that the influence on the activity of the next mouse is avoided. The parameters of the main analysis of the experiment include: total Distance traveled (i.e., Total Distance), Distance traveled in the center area (i.e., Time in center), and percentage of Time spent in the center area (i.e., Distance in center). The total movement distance was used to examine spontaneous exploratory behavior of the mice. The moving distance and the percentage of stay time in the central area are used for judging the behaviors of anxiety and the like of the mice. The experimental results are shown in FIGS. 3 to 5. Fig. 3 is a statistical graph of the total movement distance of four groups of mice. Figure 4 is a statistical graph of the percentage of time four groups of mice stayed in the central zone. Fig. 5 is a statistical graph of the distance traveled in the central zone by four groups of mice.

As can be seen from figure 3, the total distance that the 2VO group mice were free to move 10min in the open field was significantly reduced compared to the Sham group (Sham vs.2vo, P <0.05), indicating that the spontaneous exploratory activity of the 2VO group mice was significantly reduced. The total distance of movement of the mice in the 2VO + LED group was significantly increased compared to the mice in the 2VO group (2VO vs.2vo + LED, P <0.05), indicating that the spontaneous exploratory behavior of the mice was improved after 40Hz LED illumination.

As can be seen from FIGS. 4-5, the center distance of movement and percentage of residence time (Sham Vs.2VO, P <0.05) in the open field were significantly less for the 2VO group mice than for the Sham group, indicating that the mice exhibited some anxiety behavior 6 days after bilateral common carotid artery ligation. Compared with the mice in the 2VO group, the percentage of the residence time (2VO Vs.2VO + LED, P <0.01) and the moving distance (2VO Vs.2VO + LED, P <0.05) of the mice in the 2VO + LED group in the open field center after being irradiated for 6 days are obviously increased, which shows that the anxiety of the mice can be effectively relieved by 40Hz LED irradiation.

Water maze test

The Morris water maze test is primarily used to examine the spatial cognitive function of mice. Four experimental groups were performed according to the procedure of example 2, and each mouse in the sham-operated and model light groups was light-treated. The water maze test began on day 8 and ended on day 13 when mice received light treatment, during which the mice received 40Hz light treatment with LED lamps every 12 h. And the sham operation group and the model group were used as controls.

The water maze system consists of a blue circular water pool and a set of data acquisition system, wherein the diameter of the water pool is 120cm, 2/3 of clear and sterile water is contained, markers with different shapes and colors are attached to the periphery of the water pool for mouse reference, the water maze is virtually divided into four quadrants, and a platform with the diameter of 14cm is arranged in the center of one quadrant and is below 1.5cm of the water surface. The signal acquisition system comprises a camera and a computer system in the middle of a water maze, and data analysis is automatically completed by Smart V3.0 and Panlab software. Performing positioning navigation training for 5 days from 8 th to 12 th days of light treatment of the mouse, and respectively putting the mouse into the water maze from four different quadrants in different orders every afternoon, wherein the training time is 60s every time and 15min intervals; if the mouse finds the platform within 60s, the mouse is put back into the mouse cage for rest, otherwise, the experimenter guides the mouse to stay on the platform for 20s, and therefore learning and memory of the mouse on the position of the platform are enhanced. At this stage, the time from water entry to platform finding of each group of mice was recorded, and the average of four training sessions was calculated as the performance of the mice on the same day, namely the Escape latency (Escape latency), to evaluate the spatial learning ability of the mice. On day 13, the platform was removed and the mouse was left to explore freely in the water maze for 60s, and the average distance from each point in the target quadrant (quadrant where the platform is located) and its path to the current platform (Mean distance to target) was recorded to assess the spatial reference memory of the mouse. The results are shown in FIGS. 6 to 8. Figure 6 is a statistical plot of escape latencies for four groups of mice. Fig. 7 is a statistical graph of the residence time of four groups of mice in the target quadrant (quadrant in which the platform is located). Figure 8 is a statistical plot of the average distance of each point in the path to the target platform for four groups of mice.

As can be seen from fig. 6, in the localized sailing test stage of the water maze test, the time required for four groups of mice to find the platform after five days of training is gradually shortened, which indicates that each group of mice finally learns to find the position of the platform. The time required for the 2VO mice to find the platform is remarkably prolonged from the second day compared with the Sham mice (day 2: P <0.05, day 3: P <0.05, day 4: P <0.05, day 5: P <0.001), which indicates that the spatial learning ability of the 2VO mice is obviously weaker than that of the Sham group, and the mice show certain spatial learning ability damage. Compared with 2VO mice, the time for finding the platform after the 2VO + LED mice are irradiated by 40Hz LED light is obviously shortened from the 3 rd day (the 3 rd day: P is less than 0.05, the 4 th day: P is less than 0.05, and the 5 th day: P is less than 0.001), which shows that the 40Hz LED light can effectively improve the spatial learning ability damage of the 2VO model mice.

From fig. 7-8, the residence time of 2VO group mice is significantly less than that of the Sham operation group (Sham vs.2VO, P <0.05), while the residence time of 2VO + LED group mice is significantly greater than that of 2VO group (2VO + LED vs.2vo, P <0.05), but there is no significant difference in average distance from the track point of the swimming path of the four groups of mice to the platform, which indicates that the spatial reference memory capacity of the 2VO model mice can be improved to some extent by 40Hz LED illumination.

Example 4

Measurement of synaptic plasticity-long term potentiation (LTP, a phenomenon of long term potentiation recognized as a biological basis at the cellular level of learning and memory activity as one manifestation of synaptic plasticity)

1. Four experimental groups were performed according to the procedure of example 2, and each mouse in the sham-operated and model light groups was light-treated. Synaptic plasticity was measured in each mouse 3 days, 7 days, and 14 days after the light treatment. And the sham operation group and the model group were used as controls.

2. The specific detection process is as follows:

(1) after anesthetizing each group of mice with ether, the mice are quickly broken head on ice to take out the brain, immediately placed in artificial cerebrospinal fluid at 0-4 ℃, mixed gas of 95% (v/v, volume percentage content) O2 and 5% (v/v, volume percentage content) CO2 is introduced for saturation treatment, and a vibration microtome (VT 1000S, Leica) is used for cutting a coronal plane at a hippocampal brain region to obtain a hippocampal brain slice with the thickness of 400 mu m. The artificial cerebrospinal fluid comprises 120mM NaCl, 2.5mM KCl, 1.2mM NaH2PO4, 2.0mM CaCl2, 2.0mM MgSO4, 26mM NaHCO3 and 10mM glucose.

(2) Placing the hippocampal brain slices in artificial cerebrospinal fluid at 34 ℃ and incubating for 0.5h, incubating at room temperature (25 +/-1 ℃) for 2h-8h, and continuously introducing mixed gas (including O2 with the volume fraction of 95% and CO2 with the volume fraction of 5%) during the incubation. The incubated hippocampal brain slices are completely immersed in a constant-temperature perfusion tank (32-34 ℃) by a nylon net, and artificial cerebrospinal fluid is continuously introduced at the flow rate of 3mL/min, and meanwhile, mixed gas (comprising O2 with the volume fraction of 95% and CO2 with the volume fraction of 5%) is continuously introduced. The same artificial cerebrospinal fluid was injected into a glass microelectrode, and the electrode was placed under a dissecting microscope in the radiation layer of the CA1 region of the hippocampus, while the Schaffer collators side branch of pyramidal cells of CA3 region were stimulated with bipolar stimulating electrodes to induce group peak potentials (fEPSP). Firstly, a single pulse which is stimulated to be gradually strengthened (pulse wave width is 0.15ms and delta is 0.5mV) once every 30 seconds is used for recording an IO curve (namely a stimulation response curve), the intensity corresponding to about 50% of the maximum response of the group peak potential caused by stimulation is selected for recording a base line value, the time is 30min, and one pulse is recorded every 30 seconds. Following this tonic stimulation (100Hz, 10s duration), the intensity was consistent with that of the baseline values recorded, and the group peak potential response was recorded for more than one hour, one every 30 s. Wherein, the group peak potential amplitude is increased by 20% after the application of the tonic stimulation and lasts for more than 30min, and then the long-term enhancement is judged to occur. The measurement results are shown in FIGS. 9 to 13. Fig. 9 is a graphical representation of waveforms before and after tonic stimulation of fEPSP for four groups of mice, with "baseline" in fig. 9, i.e., baseline, and "LTP" long-term potentiation. Fig. 10 is a graph of the fpsps slope change (where the basal fpsps slopes are averaged and normalized) for four groups of mice before and after the tonic stimulation on day 3 of light group mice; fig. 11 is a graph of the slope of fEPSP for four groups of mice before and after the tonic stimulation on day 7 of light treatment in the light group of mice; fig. 12 is a graph of the slope change of fEPSP before and after the tonic stimulation on day 14 of light group mice; in FIGS. 10-12, "Fepsp slope" is the fEPSP slope and "HFS" is the tonic stimulation. Figure 13 is a graph of the percent slope increase (i.e., LTP) recorded for the last 15 minutes of four groups of mice after tonic stimulation in fEPSP.

As can be seen from fig. 9 to 13, the long-term potentiation was hardly induced in the CA1 region in the mice 3, 7 and 14 days after ligation of the bilateral common carotid arteries (2VO group (3 days) ═ 103.47 ± 4.01%, 2VO group (7 days) ═ 104.42 ± 3.81%, 2VO group (14 days) ═ 103.48 ± 2.85%, and Sham group ═ 122.327 ± 3.31%), which is consistent with the results of behavioral performance in the water maze. After 40Hz LED illumination is given, LTP of mice in the 2VO + LED group is significantly increased compared to LTP at the time point corresponding to mice in the 2VO group (3day) 110.769 ± 4.51%, P <0.05, 7 days 116.351 ± 5.81%, P <0.01, 14 days 116.384 ± 4.81%, and P <0.01), which indicates that synaptic plasticity of mice in the 2VO + LED group is significantly improved, and further indicates that 40Hz LED illumination treatment can repair synaptic plasticity injury caused by bilateral common carotid artery ligation to a certain extent.

Example 5

Determination of neuronal degeneration or death in the CA1 region of the hippocampus of mice

1. Four experimental groups were performed according to the procedure of example 2, and each mouse in the sham-operated and model light groups was light-treated. Synaptic plasticity was measured in each mouse 3 days, 7 days, and 14 days after the light treatment. And the sham operation group and the model group were used as controls.

2. The specific detection process is as follows:

after perfusing 1X PBS (phosphate buffered saline) and 4% paraformaldehyde aqueous solution (namely 4% PFA aqueous solution) by heart, taking brains from each group of mice, fixing the brains by 4% PFA aqueous solution for 24 hours, and then performing gradient dehydration by using 10% sucrose aqueous solution and 30% sucrose aqueous solution. The dehydrated rat brain was sliced into 25 μm brain slices with a cryomicrotome (LEICA CM1950) for Fluoro Jade B (Certificate of analysis, 3043567) staining. The glass slide is plated with 2 mass percent of gelatin to prevent the occurrence of the slide falling phenomenon. During slicing, slices were first placed in 0.1M PB solution (i.e., phosphate buffer) and then floated onto the slide from the coronal plane to the hippocampal brain region. Drying in the air, and baking at 50 deg.C for 40 min. And then dyeing operation is carried out according to the instruction of Fluoro Jade B, namely, the potassium permanganate solution with the mass percentage of 0.06 percent is incubated for 15min after being soaked in 100 percent alcohol for 5min, then being soaked in 70 percent alcohol for 2min, and then being soaked in ddH2O (namely double distilled water) for 2min, and the potassium permanganate solution is placed on a shaking table to be gently shaken in the process. And then, dripping 0.001 mass percent of Fluoro Jade B dye on the glass slide after soaking for 2min by mass percent, and dyeing for 20 min. The mass percentage content is that the slices are thoroughly aired after being soaked and washed for 2min, and then the neutral resin is used for sealing the slices after being soaked in dimethylbenzene for 2 min. Neuronal cell degeneration and death in the hippocampal CA1 region were measured using a fluorescence microscope in four groups of mice. The results are shown in FIGS. 14 to 15. FIG. 14 is a fluorescent microscope photograph showing degeneration and death of neuronal cells in the CA1 region of the hippocampus of mice in the 2VO group and the 2VO + LED group. FIG. 15 is a graph showing the degeneration and death of neuronal cells in CA1 region of hippocampus of four groups of mice, and "F-J positive cell in CA 1" in FIG. 15 shows the degenerated and dead neuronal cells.

As can be seen from FIGS. 14 to 15, the mice in the 2VO group exhibited a large number of degenerated and dead cells in the hippocampal CA1 region 3 days and 7 days after bilateral common carotid artery ligation, as compared to the Sham group. Compared with the 2VO group, after the 2VO + LED group mice are irradiated by 40Hz LED, the number of degenerated and dead cells in the CA1 region of the hippocampus is obviously reduced (the 3 rd day: P is less than 0.01, and the 7 th day: P is less than 0.01), which shows that the phenomenon of the neural necrosis in the CA1 region of the 2VO model mice can be obviously improved by 40Hz LED irradiation.

In summary, the therapeutic apparatus 10 of the above embodiment emits white light of 40Hz through the light emitting mechanism 100 to irradiate the affected part, so as to improve the exploration behavior of the stroke patient, improve the anxiety, repair the damage of spatial cognition and the damage of synaptic plasticity in the hippocampal CA1 region, and inhibit the degeneration or death of neuronal cells in the hippocampal CA1 region, so as to improve the neurological function of the stroke patient, thereby achieving the effect of treating the stroke.

The technical features of the embodiments described above may be arbitrarily combined, and for the sake of brevity, all possible combinations of the technical features in the embodiments described above are not described, but should be considered as being within the scope of the present specification as long as there is no contradiction between the combinations of the technical features.

The above-mentioned embodiments only represent some embodiments of the present invention, and the description thereof is specific and detailed, but not to be construed as limiting the scope of the present invention. It should be noted that, for those skilled in the art, without departing from the spirit of the present invention, several variations and modifications can be made, which are within the scope of the present invention. Therefore, the protection scope of the present invention should be subject to the appended claims.

Claims (10)

1. A cerebral stroke treatment device, characterized in that it comprises a light emitting means comprising:

a light source unit for emitting white light of 40 Hz;

the switch unit is connected with the light source unit and is also used for being connected with a power supply; and

and the driving unit is connected with the switch unit and is used for controlling the switch-on or switch-off of the switch unit.

2. The apparatus for treating cerebral stroke according to claim 1, wherein the light source unit includes a plurality of light emitting diodes, the plurality of light emitting diodes being connected in series.

3. The apparatus for treating cerebral apoplexy according to claim 1, further comprising a signal source connected to the driving unit to provide a control signal to the driving unit to make the driving unit control the switching unit to be turned on or off according to the control signal.

4. The stroke therapy device of claim 3, wherein said signal source is a frequency modulated signal generator.

5. The apparatus for treating cerebral apoplexy according to claim 3 or 4, wherein the light emitting mechanism further comprises a first protection unit for connecting the signal source and the driving unit.

6. The apparatus for treating cerebral stroke according to claim 1, wherein the light emitting mechanism further includes a current limiting unit which is located between and connects the light source unit and the switch unit.

7. The apparatus for treating cerebral apoplexy according to claim 1, wherein the light emitting mechanism further comprises a voltage stabilizing unit, and the voltage stabilizing unit is connected to the driving circuit.

8. The apparatus for treating cerebral apoplexy according to claim 7, wherein the light emitting mechanism further comprises a second protection unit connected to the voltage stabilizing unit and to the switch unit.

9. The apparatus for treating cerebral stroke according to claim 8, wherein the second protection unit includes at least one of reverse connection protection and overcurrent protection.

10. The device for treating cerebral apoplexy according to any one of claims 1 to 4 and 6 to 9, wherein the number of the light emitting means is plural, and plural light emitting means are connected in parallel.

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