CN115998780A - Probiotic composition capable of improving cognitive level of Alzheimer disease and application thereof - Google Patents
Probiotic composition capable of improving cognitive level of Alzheimer disease and application thereof Download PDFInfo
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- 208000024827 Alzheimer disease Diseases 0.000 title claims abstract description 26
- 239000006041 probiotic Substances 0.000 title claims abstract description 18
- 235000018291 probiotics Nutrition 0.000 title claims abstract description 18
- 239000000203 mixture Substances 0.000 title claims abstract description 17
- 230000000529 probiotic effect Effects 0.000 title claims abstract description 16
- 230000001149 cognitive effect Effects 0.000 title claims abstract description 9
- VYPSYNLAJGMNEJ-UHFFFAOYSA-N Silicium dioxide Chemical compound O=[Si]=O VYPSYNLAJGMNEJ-UHFFFAOYSA-N 0.000 claims abstract description 12
- 241000901050 Bifidobacterium animalis subsp. lactis Species 0.000 claims abstract description 6
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- Y—GENERAL TAGGING OF NEW TECHNOLOGICAL DEVELOPMENTS; GENERAL TAGGING OF CROSS-SECTIONAL TECHNOLOGIES SPANNING OVER SEVERAL SECTIONS OF THE IPC; TECHNICAL SUBJECTS COVERED BY FORMER USPC CROSS-REFERENCE ART COLLECTIONS [XRACs] AND DIGESTS
- Y02—TECHNOLOGIES OR APPLICATIONS FOR MITIGATION OR ADAPTATION AGAINST CLIMATE CHANGE
- Y02A—TECHNOLOGIES FOR ADAPTATION TO CLIMATE CHANGE
- Y02A50/00—TECHNOLOGIES FOR ADAPTATION TO CLIMATE CHANGE in human health protection, e.g. against extreme weather
- Y02A50/30—Against vector-borne diseases, e.g. mosquito-borne, fly-borne, tick-borne or waterborne diseases whose impact is exacerbated by climate change
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- Medicines Containing Material From Animals Or Micro-Organisms (AREA)
Abstract
The invention discloses a probiotic composition capable of improving cognitive level of Alzheimer's disease and application thereof. The composition comprises: 25-30 parts of maltitol, 20-25 parts of resistant dextrin, 5-8 parts of bifidobacterium lactis, 5-8 parts of lactobacillus plantarum, 1-2 parts of lactobacillus acidophilus, 1-2 parts of lactobacillus casei, 1-2 parts of lactobacillus rhamnosus, 1-2 parts of lactobacillus paracasei, 1-2 parts of bifidobacterium breve, 1-2 parts of lactobacillus reuteri, 1-2 parts of streptococcus thermophilus, 2-5 parts of isomaltooligosaccharide, 2-5 parts of fructooligosaccharide, 2-5 parts of galactooligosaccharide, 2-5 parts of stachyose, 2-5 parts of inulin, 18-23 parts of silicon dioxide and 10-15 parts of wall-broken ganoderma lucidum spore powder.
Description
Technical Field
The invention relates to a traditional Chinese medicine composition and application thereof, in particular to a probiotic composition capable of improving cognitive level of Alzheimer disease and application thereof.
Background
Alzheimer's Disease (AD) is a very common senile neurodegenerative disease and is the most leading cause of dementia in humans, and no effective therapeutic measures exist at present.
Environmental and genetic factors play a role in the development of AD. Previous studies have shown that mitochondrial dysfunction, insulin resistance and cerebral hypoperfusion may mediate, drive and even trigger pathological molecular cascades in AD, ultimately promoting aβ deposition, tau protein (Tau protein) hyperphosphorylation, synaptic degeneration and neuronal dysfunction. However, these do not fully explain the etiology and underlying pathophysiological mechanisms of AD. Recent studies have shown that the pathogenesis of AD may be related to the intestinal flora. Intestinal flora can promote AD generation and development by promoting Abeta deposition, inducing neuroinflammation, destroying permeability of blood brain barrier, regulating neurotransmitter, etc.
Microbiota is an ecological community symbiotic with human body and plays an important regulatory role in human health and diseases. Intestinal microorganisms constitute the vast majority of human microorganisms, mainly consisting of bacteria, most of which are anaerobic, and in addition fungi, viruses, protozoa, and monocyte organisms. The number, type, etc. of intestinal flora is in a dynamic balance to maintain the homeostasis of the host immune system. However, the existence of many factors such as poor eating habits, application of antibacterial drugs, and life pressure may break the dynamic balance, impair the activity of intestinal flora, and cause gastrointestinal diseases. In addition, these diseases are not limited to the gastrointestinal tract, but intestinal dysbacteriosis is also associated with cardiovascular diseases, type 2 diabetes, renal failure, and the like. Some essential vitamins and important substances involved in central nervous system development and immunomodulation are produced by the intestinal microbiota. In addition to the destruction of the stability of the intestinal environment, disorders of intestinal microorganisms can also affect the occurrence of behavioral, learning, memory, neurological disorders, etc. Human intestinal microbiota is considered to be the second brain, possibly one of the causes of AD and other neurodegenerative diseases
Research shows that a large amount of ingested probiotics and prebiotics can improve the neurocognitive ability and reduce the risk of AD. After feeding fructooligosaccharides to AD animals by Pistonto et al, a decrease in the number of neuronal apoptosis in the brain, a decrease in Tau protein phosphorylation and a down-regulation of Aβ42 expression were found.
Disclosure of Invention
The invention aims to: the object of the present invention is to provide probiotic compositions and coatings for improving cognitive levels in Alzheimer's disease.
The technical scheme is as follows: the probiotic composition capable of improving the cognitive level of the Alzheimer disease comprises the following raw materials in parts by weight: 25-30 parts of maltitol, 20-25 parts of resistant dextrin, 5-8 parts of bifidobacterium lactis, 5-8 parts of lactobacillus plantarum, 1-2 parts of lactobacillus acidophilus, 1-2 parts of lactobacillus casei, 1-2 parts of lactobacillus rhamnosus, 1-2 parts of lactobacillus paracasei, 1-2 parts of bifidobacterium breve, 1-2 parts of lactobacillus reuteri, 1-2 parts of streptococcus thermophilus, 2-5 parts of isomaltooligosaccharide, 2-5 parts of fructooligosaccharide, 2-5 parts of galactooligosaccharide, 2-5 parts of stachyose, 2-5 parts of inulin, 18-23 parts of silicon dioxide and 10-15 parts of wall-broken ganoderma lucidum spore powder.
Preferably, the maltitol is 25 parts, the resistant dextrin is 20 parts, the bifidobacterium lactis is 5 parts, the lactobacillus plantarum is 5 parts, the lactobacillus acidophilus is 1 part, the lactobacillus casei is 1 part, the lactobacillus rhamnosus is 1 part, the lactobacillus paracasei is 1 part, the bifidobacterium breve is 1 part, the lactobacillus reuteri is 1 part, the streptococcus thermophilus is 1 part, the isomaltooligosaccharide is 2 parts, the fructooligosaccharide is 2 parts, the galactooligosaccharide is 2 parts, the stachyose is 2 parts, the inulin is 2 parts, the silicon dioxide is 18 parts, and the wall-broken ganoderma lucidum spore powder is 10 parts.
The application of the probiotic composition in preparing medicines for treating Alzheimer disease.
The beneficial effects are that: compared with the prior art, the invention has the following advantages: at present, no effective treatment measures are available for the Alzheimer disease, most of the medicines are western medicines, the toxic and side effects are large after long-term administration, the adverse effects are small after long-term administration of the probiotic composition, and the probiotic composition can directly regulate intestinal colony formation or indirectly regulate intestinal flora metabolites, play the roles of resisting neuroinflammation, maintaining blood brain barrier and the like, so that the cognitive level of the Alzheimer disease is improved.
Detailed Description
Preparation of probiotic composition: mixing the following raw materials in proportion, and preparing by a conventional method.
Among 100g, 25g of maltitol, 20g of resistant dextrin, 5g of bifidobacterium lactis, 5g of lactobacillus plantarum, 1g of lactobacillus acidophilus, 1g of lactobacillus casei, 1g of lactobacillus rhamnosus, 1g of lactobacillus paracasei, 1g of bifidobacterium breve, 1g of lactobacillus reuteri, 1g of streptococcus thermophilus, 2g of isomaltooligosaccharide, 2g of fructooligosaccharide, 2g of galactooligosaccharide, 2g of stachyose, 2g of inulin, 18g of silicon dioxide and 10g of wall-broken ganoderma lucidum spore powder.
Test for improving learning and memory ability of LPS-induced dementia mice
1.1 laboratory animals
70 male ICR mice, 20-22 g in mass, were offered by Si Bei Fu (Beijing) Biotechnology Co., ltd.
1.2 samples and reagents
A compound probiotic formula; lipopolysaccharide (LPS, sigma Co.); donepezil hydrochloride (guard pharmaceutical company limited);
1.3 laboratory apparatus
DMS-2Morris water maze, DTT-2 mouse diving tower instrument, SBA-2 mouse dark avoidance instrument (national academy of medical science, institute of medicine)
2 method
2.1 grouping, modeling and administration
70 ICR mice were randomly assigned to a blank, sham, model, low, medium, and high dose examples, positive control, 10 per group. Mice in the blank group were not treated at all, and the ventricles of mice in the sham operation group were injected with physiological saline (3. Mu.l/mouse), and the ventricles of mice in the model group and the drug treatment group were injected with an equal volume of LPS solution (5/3. Mu.l/mouse) to establish an AD model. Referring to the stereotactic map of the mouse brain, the injection position of the lateral ventricle is 1mm far to the right of the midpoint of the connecting line of the two eyes and 2mm behind the connecting line of the rear canthus, and the micro-injector is vertically penetrated into the surface of the skull for 2mm after the skin on the surface of the skull is disinfected. The following day after molding, the low, medium and high dose mice of the examples were given probiotic compositions 0.585, 1.17 and 2.34mg/kg each day for gavage, the positive control mice were given 5mg/kg of donepezil each day, and the blank, sham and model mice were given the same volume of physiological saline each day for gavage 1 time a day for continuous gavage for 21d.
2.2Morris Water maze experiments
The Morris water maze test was performed on day 14 after the mice were modeled, 1 test per day, and 4 days continuously. The water maze test was performed in a water pool of 120cm diameter and 50cm height. The pool is provided with 4 quadrants, namely a first quadrant, a second quadrant, a third quadrant and a fourth quadrant, which are used as water inlet points of the mouse water inlet pool. And 1 circular platforms with the diameters of 6cm and the heights of 30cm are arranged in the center of the first quadrant. Before the experiment, water is added until the water surface is 1-2 c m higher than the platform, the water is dyed black by dye, and the water temperature is controlled at (20+/-1). In the experiment, mice were placed into the pool from 4 different quadrants facing the pool wall in sequence, allowed to swim freely to find the platform, and the time required for the mice to find the platform (i.e., escape latency) was recorded. After the mice climbed the platform, the mice were allowed to rest on the platform for 10s. If the platform is not found within 60s, the operator places the mouse on the platform for 10s. The experiment is kept quiet, so that experimental errors caused by external environment interference are reduced.
2.3 the dark avoidance experiment is divided into two stages of learning training and testing. In 1d, the mice are put in the darkroom during learning by utilizing the habit that the mice have darkness and are avoided and prefer to drill holes, and the mice can be shocked when entering the darkroom, if the mice do not enter, the mice are driven to enter, so that memory is generated. And repeating the test after 24 hours, and recording the time of the mice entering the darkroom for the first time and the times of entering the darkroom within 3 minutes as the measurement results.
2.4 bench test is divided into two stages of learning training and testing. After the animals receive electric shock, the normal response is jumping to the platform. Recording the time of the first jump of the rubber table within 3min of the mouse as a learning result, and if the mouse does not jump, inducing the upper table to learn. Testing: after the 2 nd power-on, the mice are placed on the rubber table, and the time of the first jump down of the mice and the times of the jump down of the mice on the rubber table within 3min are recorded as measurement results.
3 results
3.1Morris water maze test results
As shown in table 1, with the extension of the training time, the escape latency time of each group of mice was gradually decreased, and there was no significant difference between the escape latency time of the mice in the blank group and the sham operation group, indicating that there was no significant effect on the lateral ventricle injection operation of the mice; the escape latency was significantly prolonged (P < 0.05) from day 2 to 4 in the model group mice compared to the sham group; the escape latency of the low-dose group and the medium-dose group is obviously shortened (P < 0.05) from day 3 to day 4 compared with that of the model group, and the escape latency of the high-dose group is obviously shortened (P < 0.05) from day 2 compared with that of the model group, so that the probiotic composition can obviously improve the spatial learning and memory functions of AD mice in the range of 0.585-2.34 mg/kg.
Table 1 influence of escape latency on AD mouse water maze experiment (x±s, s, n=10)
(*P<0.05，**P<0.01)
3.2 results of the dark avoidance test on AD mice
There was no significant difference in escape latency between mice in the blank and sham groups, indicating that the operation of lateral ventricle injection had no significant effect on mice. The number of dark errors was significantly increased (P < 0.05) in the model control mice compared to the blank and sham groups; the number of dark errors was significantly reduced (P <0.05, P < 0.01) in mice of the low, medium, high and positive control groups of the control group compared to the model control group. See table 2.
Table 2 effects of dark latency and number of errors in demented mice (x±s, s, n=10)
(*P<0.05，**P<0.01)
3.3 bench jump test results
There was no significant difference in escape latency between mice in the blank and sham groups, indicating that the operation of lateral ventricle injection had no significant effect on mice. Compared with blank group and sham operation group, the diving platform latency of the mice in the model control group is obviously shortened, and the diving platform error frequency is obviously increased (P < 0.01); the number of jump errors in mice in the high dose and positive control groups was significantly reduced (P <0.05, P < 0.01). See table 3.
Table 3 effect on LPS-induced dementia mice diving platform latency and number of errors (x±s, s, n=10)
| Group of | Dosage (g/kg) | Latency/(s) | Error count/(times) |
| Blank group | -- | 133±60 | 0.5±0.6** |
| False operation group | -- | 131±57 | 0.5±0.8** |
| Model group | -- | 15±24 | 4.1±1.9 |
| Implementation group low dose | 0.585 | 24±34 | 3.1±0.5 |
| Dosage in the treatment group | 1.17 | 35±29 | 2.3±0.5* |
| Implementation group high dose | 2.34 | 45±19 | 1.9±0.6* |
| Positive control group | 0.75 | 32±67 | 2.2±0.7* |
(*P<0.05，**P<0.01)
In the water maze experiment test, the model control group has longer escape latency, the number of times of crossing the platform and the retention time of the target quadrant are reduced, which indicates that the model control group has learning and memory disorder, the escape latency of the dementia mice of the embodiment is shortened, the number of times of crossing the platform area and the retention time of the target quadrant are increased, and indicates that the spatial memory capacity of the mice is improved. In the test of the diving tower and dark avoidance experiment, the latency of the model control group is shortened compared with the normal control group, the error frequency is obviously increased, the latency of the embodiment group is prolonged, the error frequency is obviously reduced, and the short-term memory of the administration group is well maintained. The behavioural results show that the compound probiotics of the embodiment can improve the learning and memory capacity of the LPS-induced dementia mice.
Claims (3)
1. A probiotic composition capable of improving cognitive levels in alzheimer's disease, characterized by: the material comprises the following raw materials in parts by weight: 25-30 parts of maltitol, 20-25 parts of resistant dextrin, 5-8 parts of bifidobacterium lactis, 5-8 parts of lactobacillus plantarum, 1-2 parts of lactobacillus acidophilus, 1-2 parts of lactobacillus casei, 1-2 parts of lactobacillus rhamnosus, 1-2 parts of lactobacillus paracasei, 1-2 parts of bifidobacterium breve, 1-2 parts of lactobacillus reuteri, 1-2 parts of streptococcus thermophilus, 2-5 parts of isomaltooligosaccharide, 2-5 parts of fructooligosaccharide, 2-5 parts of galactooligosaccharide, 2-5 parts of stachyose, 2-5 parts of inulin, 18-23 parts of silicon dioxide and 10-15 parts of wall-broken ganoderma lucidum spore powder.
2. A probiotic composition capable of improving cognitive levels in alzheimer's disease according to claim 1, characterized in that: 25 parts of maltitol, 20 parts of resistant dextrin, 5 parts of bifidobacterium lactis, 5 parts of lactobacillus plantarum, 1 part of lactobacillus acidophilus, 1 part of lactobacillus casei, 1 part of lactobacillus rhamnosus, 1 part of lactobacillus paracasei, 1 part of bifidobacterium breve, 1 part of lactobacillus reuteri, 1 part of streptococcus thermophilus, 2 parts of isomaltooligosaccharide, 2 parts of fructooligosaccharide, 2 parts of galactooligosaccharide, 2 parts of stachyose, 2 parts of inulin, 18 parts of silicon dioxide and 10 parts of wall-broken ganoderma lucidum spore powder.
3. Use of a probiotic composition according to claim 1 for the preparation of a medicament for the treatment of alzheimer's disease.
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