CN114903881A - Application of N-acetyl-N' -caffeoyl butanediamine in preparation of preparation for preventing and treating insomnia and related diseases - Google Patents
Application of N-acetyl-N' -caffeoyl butanediamine in preparation of preparation for preventing and treating insomnia and related diseases Download PDFInfo
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/16—Amides, e.g. hydroxamic acids
- A61K31/165—Amides, e.g. hydroxamic acids having aromatic rings, e.g. colchicine, atenolol, progabide
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23L—FOODS, FOODSTUFFS, OR NON-ALCOHOLIC BEVERAGES, NOT COVERED BY SUBCLASSES A21D OR A23B-A23J; THEIR PREPARATION OR TREATMENT, e.g. COOKING, MODIFICATION OF NUTRITIVE QUALITIES, PHYSICAL TREATMENT; PRESERVATION OF FOODS OR FOODSTUFFS, IN GENERAL
- A23L33/00—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof
- A23L33/10—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof using additives
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/20—Hypnotics; Sedatives
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/22—Anxiolytics
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/24—Antidepressants
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23V—INDEXING SCHEME RELATING TO FOODS, FOODSTUFFS OR NON-ALCOHOLIC BEVERAGES AND LACTIC OR PROPIONIC ACID BACTERIA USED IN FOODSTUFFS OR FOOD PREPARATION
- A23V2002/00—Food compositions, function of food ingredients or processes for food or foodstuffs
Abstract
The invention discloses application of N-acetyl-N' -caffeoyl butanediamine in preparing health food and medicine for preventing and treating insomnia, anxiety and depression. The experimental results show that in the dosage range of 1-100mg/kg, N-acetyl-N' -caffeoyl butanediamine can obviously reduce the activity times of the insomnia mice, shorten the sleep latency period of the insomnia mice, prolong the sleep time of the insomnia mice, and obviously regulate the index levels of neurotransmitters such as 5-HT, 5-HIAA, GABA, Glu and the like in the brain tissues of the insomnia mice, and the neurotransmitters are closely related to the mental diseases such as insomnia, anxiety, depression and the like.
Description
Technical Field
The invention relates to the technical field of preparation of medicines or health-care foods, in particular to application of N-acetyl-N' -caffeoyl butanediamine in preparation of a preparation for preventing and treating insomnia, anxiety, depression and related diseases.
Background
Insomnia is one of the more common diseases in life and is closely related to the life work of people. The occurrence of insomnia is related to various factors such as age, sex and disease, and the prevalence of insomnia increases with age. In recent years, social employment pressure is increased, economic requirements are increased day by day, living habits of people are changed, and the incidence rate of insomnia in the social environment is higher and higher. The insomnia can not only cause the mood of the patient such as dysphoria and depression, but also cause various diseases. Therefore, it becomes important to develop a natural drug for treating insomnia. At present, the medicines clinically used for treating insomnia mainly comprise barbiturates and benzodiazepine
And non-benzodiazepines
Sedative-hypnotics; melatonin drugs; an Orexin receptor antagonist; 5-HT2A receptor antagonists; antipsychotic, antidepressant and antiepileptic drugs, etc. The above drugs are chemically synthesized drugs, show more adverse reactions, and may generate drug resistance and dependence after long-term use. In recent years, some newly discovered active monomers of sedative-hypnotic traditional Chinese medicines are also used for research on treatment and improvement of diseases related to sleep disorder. Such as syringic acid, isoliquiritigenin, etc. are proved to have significant improving effect on sleep disorder.
Therefore, the search for active monomer ingredients having sedative-hypnotic effects and useful for preventing and treating insomnia, anxiety and depression from natural drugs has become a problem to be solved by those skilled in the art.
Disclosure of Invention
In view of the above, the present invention provides the use of N-acetyl-N' -caffeoyl butanediamine in the preparation of a formulation for the prevention and treatment of insomnia, anxiety, depression and related diseases.
In order to achieve the purpose, the invention adopts the following technical scheme:
use of N-acetyl-N '-caffeoyl butanediamine in the manufacture of a formulation for the prevention and treatment of insomnia, anxiety, depression and related diseases, said N-acetyl-N' -caffeoyl butanediamine having the structure:
N-acetyl-N' -caffeoyl butanediamine, molecular formula C 15 H 20 N 2 O 4 Molecular weight 292.14, (E) -2-propenamide, N- [4- (acetylamino) butyl)]-3- (3,4-dihydroxyphenyl) -, or 2-propenamide, N- [4- (acetylamino) butyl-]-3- (3,4-dihydroxyphenyl) -, or (E) -N- (4-acetamidobutyl) -3- (3,4-dihydroxyphenyl) acrylamide, or N- (4-acetamidobutyl) -3- (3,4-dihydroxyphenyl) acrylamide, which is called (E) -N-acetyl-N '-caffeoylputrescine for short, or N-acetyl-N' -caffeoylputrescine, is caffeic acid amide separated from medlar. There are few reports on the research on N-acetyl-N '-caffeoyl butanediamine, and there is no report on the biological activity of N-acetyl-N' -caffeoyl butanediamine. Animal experiments show that the N-acetyl-N' -caffeoyl butanediamine has obvious sedative and hypnotic effects. Further, the compound can be developed into health-care food or medicine for preventing and treating insomnia, anxiety and depression, and has great clinical application value.
As a preferable technical scheme of the invention, the preparation is any one of powder, tablets, capsules, emulsion, pills and granules.
In a preferred embodiment of the present invention, the preparation is any one of an oral preparation, an external patch, and an injection.
Another object of the present invention is to provide a pharmaceutical composition comprising N-acetyl-N' -caffeoyl-butanediamine.
As a preferred technical scheme of the invention, the daily application dose of the medicament is 1-100mg/kg calculated by N-acetyl-N' -caffeoyl butanediamine.
Still another object of the present invention is to provide a health food comprising N-acetyl-N' -caffeoyl-butanediamine.
As a preferable technical scheme of the invention, the daily application dose of the health food is 1-100mg/kg calculated by N-acetyl-N' -caffeoyl butanediamine.
According to the technical scheme, compared with the prior art, the application and the pharmaceutical composition of the N-acetyl-N' -caffeoyl butanediamine in the preparation of the health-care food or the medicine for preventing and treating insomnia, anxiety and depression have the following beneficial effects:
(1) the N-acetyl-N' -caffeoyl butanediamine can obviously reduce the number of autonomous activities of insomnia mice.
(2) The N-acetyl-N' -caffeoyl butanediamine can obviously shorten the sleep latency of the insomnia mice.
(3) The N-acetyl-N' -caffeoyl butanediamine can obviously prolong the sleep time of the insomnia mice.
(4) The N-acetyl-N' -caffeoyl butanediamine can call back the level of transmitters such as 5-HT, 5-HIAA, GABA, Glu and the like in brain tissues of insomnia mice.
The invention proves that the N-acetyl-N' -caffeoyl butanediamine has the sedative-hypnotic effect for the first time, and can be used for preparing the medicines or health-care foods for preventing and treating insomnia, anxiety and depression.
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 embodiments or the prior art descriptions will be briefly described below, it is obvious that the drawings in the following description are only embodiments of the present invention, and for those skilled in the art, other drawings can be obtained according to the provided drawings without creative efforts.
FIG. 1 shows the effect of N-acetyl-N '-caffeoyl butanediamine on the test of the autonomic activity of mice, wherein 2 is N-acetyl-N' -caffeoyl butanediamine; G. z, D represent high, medium and low dose groups, respectively; in comparison with the set of models, ** p<0.01， *** p<0.001；
FIG. 2 shows the effect of N-acetyl-N '-caffeoyl butanediamine on sleep latency in mice (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared to normal control group, ### p<0.001; in comparison with the set of models, * p<0.05， *** p<0.001)；
FIG. 3 shows the effect of N-acetyl-N '-caffeoyl butanediamine on sleep time in mice (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared to normal control group, # p<0.05; in comparison with the set of models, ** p<0.01， *** p<0.001)；
FIG. 4 shows the effect of N-acetyl-N '-caffeoyl butanediamine on 5-HT in mouse brain tissue (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared with normal control group, ### p<0.001; in comparison with the set of models, ** p<0.01， *** p<0.001)；
FIG. 5 shows the effect of N-acetyl-N '-caffeoyl butanediamine on 5-HIAA in mouse brain tissue (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared with normal control group, ### p<0.001; in comparison with the set of models, ** p<0.01， *** p<0.001)；
FIG. 6 shows the effect of N-acetyl-N '-caffeoyl butanediamine on GABA in mouse brain tissue (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared with normal control group, ## p<0.01; in comparison with the set of models, ** p<0.01， *** p<0.001)；
FIG. 7 shows the effect of N-acetyl-N '-caffeoyl butanediamine on Glu in mouse brain tissue (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared with normal control group, # p<0.05; in comparison with the set of models, * p<0.05， ** p<0.01， *** p<0.001)；
FIG. 8 shows the effect of N-acetyl-N '-caffeoyl butanediamine on the ratio of Glu/GABA in mouse brain tissue (2 is N-acetyl-N' -caffeoyl butanediamine; G, Z, D represents high, medium and low dose groups respectively; compared with the normal control group, ## p<0.01; in comparison with the set of models, * p<0.05， ** p<0.01， *** p<0.001)。
Detailed Description
The technical solutions in the embodiments of the present invention will be clearly and completely described below with reference to the drawings in the embodiments of the present invention, and it is obvious that the described embodiments are only a part of the embodiments of the present invention, and not all of the embodiments. All other embodiments, which can be derived by a person skilled in the art from the embodiments given herein without making any creative effort, shall fall within the protection scope of the present invention.
Example 1
Investigating the influence of N-acetyl-N' -caffeoyl butanediamine on insomnia, anxiety or depression of mice
The pharmacodynamics evaluation of the sleep improvement effect of N-acetyl-N' -caffeoyl butanediamine is carried out by adopting a model of insomnia, anxiety or depression of mice caused by p-chlorophenylalanine (PCPA) injection. The sedative-hypnotic effect of the N-acetyl-N' -caffeoyl butanediamine on the insomnia mice is observed by behavioral evaluation methods such as the recording of the times of the autonomic activities of the mice, the recording of the body weight, the experiment of inducing the sleep of the mice by the pentobarbital sodium and the like. Brain tissue was used to determine levels of neurotransmitters 5-HT, 5-HIAA, GABA, Glu, and to investigate the possible mechanism of improving sleep, anxiety or depression by N-acetyl-N' -caffeoyl-butanediamine.
1. Laboratory animal
Healthy male ICR mice (18-22g) of SPF grade were provided by the university of ningxia medical center for animal experiments (experimental animal license No. SCXK (university of ningxia medical) 2020-. Adaptively feeding in an SPF standard laboratory, wherein the feeding conditions of all groups of animals are the same: ambient temperature (25 ℃), relative humidity (50% -60%). Free food intake and water intake.
2. Experimental methods
ICR mice were adaptively fed for 3 days before molding, and were randomly divided into 6 groups of a normal control group, a model group, a positive drug group (melatonin), and an N-acetyl-N' -caffeoyl butanediamine group (low dose group 1mg/kg/d, medium dose group 10mg/kg/d, and high dose group 100mg/kg/d) one day before molding, and 10 mice were administered to each group. After adaptive feeding, molding is continuously carried out for 2 days, normal control groups are given physiological saline (0.1mL/10g/d), the PCPA suspension (400mg/kg/d) is injected into the abdominal cavity of other groups, and within 28-30h after injection, the mice do not stop moving in the day, the food intake is reduced, the aggressiveness is enhanced, which indicates that the molding is successful.
After the model building is successful, the normal control group and the model group are administered with equal volume of normal saline (0.1mL/10g/d), the administration dose of the positive drug group melatonin is 10mg/kg/d, and the administration doses of the N-acetyl-N' -caffeoyl butanediamine are 1, 10 and 100mg/kg/d respectively. Each group of mice was dosed at 8:00-12:00 am daily for 7 consecutive days.
3. Observation index
In the research data processing of the invention, SPSS 18.0 is adopted for data analysis and statistics, the obtained results are all represented by mean value plus or minus standard deviation (X plus or minus S), the difference between groups is compared and data processing is carried out by one-way ANOVA, the difference has statistical significance and p is less than 0.05 as a standard.
(1) Number of autonomous activities
After the molding is successful and half an hour after the administration on the 7 th day, the number of autonomous activities of each mouse within 5min is recorded. Mice were first placed in the apparatus to acclimate for 3min before each recording. (results are shown in Table 1 and FIG. 1)
TABLE 1 influence of N-acetyl-N' -caffeoyl-butanediamine on the mouse voluntary Activity experiments
Note: # denotes the pre-dose model group and the normal control groupBy comparison, the process of the first and second steps, # P<0.05, ## P<0.01, ### P<0.001; denotes the comparison after the last administration with the corresponding pre-administration, * P<0.05， ** P<0.01， *** P<0.001。
as can be seen from Table 1 and FIG. 1, the number of autonomic activity increases significantly (p <0.001) in the PCPA insomnia-inducing group before administration, compared with the normal control group (190. + -. 30.85). After the last administration, compared with the administration before, the times of the independent activities of the mice in the normal control group and the model group are not obviously changed, and the times of the independent activities of the mice in each dosage group of the positive drug and the N-acetyl-N '-caffeoyl butanediamine are obviously reduced (p is less than 0.001), which shows that each dosage group of the N-acetyl-N' -caffeoyl butanediamine has obvious improvement effect on insomnia, anxiety or depression.
(2) Body weight
The body weight of each group was recorded before, after, on the 3 rd and 7 th day after molding, respectively, and the body weight change of the mice was observed (see table 2).
TABLE 2 Effect of N-acetyl-N' -caffeoyl-butanediamine on mouse body weight
Note: compared with the method before the mould is manufactured, # P<0.05， ## P<0.01， ### P<0.001; note: in comparison with the set of models, * P<0.05， ** P<0.01， *** P<0.01。
the results show that the body weight of the mice in the normal control group gradually increases (p is less than 0.01) along with the progress of the experiment compared with that before the model building, and the body weight of the mice in the model building group basically has no change and has no statistical difference. On day 3 of administration, the body weight (26.50 + -3.39 g) of the mice in the model group was significantly reduced (p <0.001) compared with that in the normal control group (31.71 + -2.27 g); compared with the model group, the weight of mice in each dose group of the positive drug and the N-acetyl-N' -caffeoyl butanediamine is remarkably increased (p is less than 0.001). On day 7 of administration, the body weight (29.95. + -. 4.07g) of the model group mice was reduced to a small extent as compared with that of the normal control group (32.45. + -. 1.34g), but was not statistically significant; compared with the model group, the weight of mice of each dose group of the positive drug and the N-acetyl-N' -caffeoyl butanediamine is obviously increased (p < 0.05).
(3) Determination of sleep time by flip reflex test
1h after the 7 th day dosing, mice in each group were intraperitoneally injected with pentobarbital sodium suspension (50mg/kg) and the sleep latency and sleep time of the mice were recorded. Recording sleep latency from the end of intraperitoneal injection to the disappearance of mouse righting reflex for more than 1 min; the time to sleep was recorded from when the mice fell asleep to when the mice returned to positive reflex. (the results are shown in Table 3 and FIGS. 2 and 3.)
TABLE 3 Effect of N-acetyl-N' -caffeoyl-butanediamine on sleep latency and sleep time in mice
Note: compared with the normal control group, # P<0.01, ## P<0.01, ### P<0.001; in comparison with the set of models, * P<0.05， ** P<0.01， *** P<0.001。
the results show that the sleep latency time (332.67 +/-62.76 s) of the model group mice is remarkably increased (p is less than 0.001) compared with that of a normal control group (229.00 +/-13.70 s) in the level of the index of the sleep latency time, and the PCPA-induced mouse insomnia model is successful, so that the mice have the phenomena of difficulty in falling asleep, anxiety or depression. Compared with the model group, the sleep latency time of mice in each dose group of the positive drug and the N-acetyl-N '-caffeoyl butanediamine is obviously shortened (p is less than 0.05), which indicates that the positive drug melatonin and the N-acetyl-N' -caffeoyl butanediamine can adjust the sleep latency time of the mice and have an improvement effect on the insomnia, the anxiety or the depression of the mice caused by PCPA. In the aspect of sleep time index level, compared with a normal control group (15.29 +/-7.60 min), the sleep time (7.38 +/-3.81 min) of a mouse in a model group is obviously shortened (p is less than 0.05), which indicates that the model of mouse insomnia caused by PCPA is successful and the sleep time of the mouse is shortened. Compared with the model group, the sleep time of the positive drug and the N-acetyl-N '-caffeoyl butanediamine in the high and medium dose groups is obviously increased (p is less than 0.01), which shows that the positive drug melatonin and the N-acetyl-N' -caffeoyl butanediamine can increase the sleep time of the mice and have an improvement effect on the insomnia, the anxiety or the depression of the mice caused by PCPA.
By combining the experimental results, the phenomena of continuous activity in the daytime, reduced eating and sleep and the like of the mouse after insomnia lead to the increase of the number of times of autonomic activities (p <0.001), the prolongation of the sleep latency (p <0.001), the shortening of the sleep time (p <0.05) and the reduction of the weight growth rate of the mouse. The N-acetyl-N' -caffeoyl butanediamine can reduce the number of the autonomous activities of the insomnia mice to different degrees, shorten the sleep latency, increase the sleep time and improve the reduction of the weight growth rate of the insomnia mice caused by PCPA. The above data indicate that N-acetyl-N' -caffeoyl butanediamine has significant sedative-hypnotic effects.
4. Neurotransmitter level determination
After 7 days of administration, the mice were sacrificed by dislocation of cervical vertebrae, the brains were harvested by cutting the heads on an ice bench, ground uniformly with a tissue homogenizer, and added with physiological saline to prepare a 10% brain tissue homogenate. Centrifuging at 4 deg.C for 15min at 3000r/min, collecting supernatant, and detecting the levels of monoamine neurotransmitters 5-HT and 5-HIAA (see Table 4, figure 4 and figure 5) and amino acid neurotransmitters Glu and GABA (see Table 5, figure 6, figure 7 and figure 8) by ELISA.
TABLE 4 Effect of N-acetyl-N' -caffeoyl-butanediamine on mouse monoamine neurotransmitters
Note: compared with the group of the normal control group, # P<0.05， ## P<0.01， ### P<0.001; in comparison with the set of models, ** P<0.01， *** P<0.001。
table 4 and FIGS. 4 and 5 show that 5-HT (238.66 + -34.66 ng/g) levels in brain tissue of model mice are significantly reduced (p <0.001) compared to normal control (322.96 + -28.00 ng/g), indicating success in the PCPA-induced insomnia, anxiety or depression mouse model. Compared with the model group, the positive drug group and the N-acetyl-N' -caffeoyl butanediamine in the high and medium dose groups have obviously increased 5-HT content (p is less than 0.01) in the mouse brain tissue, and have a certain dose positive correlation, namely, the larger the administration dose is, the higher the 5-HT content is. Compared with a normal control group (34.37 +/-3.71 ng/g), the content of 5-HIAA (29.66 +/-1.74 ng/g) in the brain tissue of the mice in the model group is obviously reduced (p is less than 0.001), which indicates that the mice model with PCPA caused insomnia, anxiety or depression is successful. Compared with the model group, the content of 5-HIAA (37.15 +/-1.56 ng/g) in the brain tissue of the positive medicine group mouse is obviously increased (p is less than 0.001). The 5-HIAA content in the brain tissue of the mice in the high and low dose groups of N-acetyl-N' -caffeoyl butanediamine is obviously increased (p is less than 0.05). In conclusion, the 5-HT and 5-HIAA content in brain tissue is reduced (p <0.05) after insomnia, anxiety or depression in mice. The high-dose group of N-acetyl-N '-caffeoyl butanediamine was able to significantly increase the content of 5-HT and 5-HIAA, and it was speculated that N-acetyl-N' -caffeoyl butanediamine might improve the symptoms of insomnia, anxiety or depression directly by increasing the content of 5-HT and 5-HIAA in the brain tissue of insomnia mice.
TABLE 5 Effect of N-acetyl-N' -caffeoyl-butanediamine on the neurotransmitter of the mouse amino acids
Note: compared with the group of the normal control group, # P<0.05， ## P<0.01， ### P<0.001; in comparison with the set of models, ** P<0.01， *** P<0.001。
table 5 and fig. 6, 7 and 8. Compared with a normal control group (8.47 +/-2.31 nmol/L), the GABA (5.94 +/-0.83 nmol/L) content in the brain tissue of the mouse in the model group is obviously reduced (p is less than 0.01), which indicates that the GABA content in the brain tissue of the mouse with PCPA causing insomnia, anxiety or depression is reduced. Compared with the model group, the GABA (6.89 +/-1.11 nmol/L) content in the brain tissue of the positive drug group mouse is increased, but the statistical significance is not achieved. The GABA content in the brain tissue of mice of each dose group of N-acetyl-N' -caffeoyl butanediamine is obviously increased (p is less than 0.01). Compared with a normal control group (60.31 +/-1.93 mu mol/gprot), the content of Glu (65.56 +/-4.33 mu mol/gprot) in the brain tissue of the mouse in the model group is obviously increased (p is less than 0.05), which indicates that the content of Glu in the brain tissue of the insomnia-causing PCPA mouse is increased. Compared with the model group, the content of Glu (53.52 +/-7.23 mu mol/gprot) in the brain tissue of the mice of the positive drug group is obviously reduced (p is less than 0.001). The N-acetyl-N' -caffeoyl butanediamine can reduce Glu content in brain tissue of mice to different degrees in different dose groups, wherein the low dose and the medium dose have significant difference (p < 0.05). Compared with a normal control group (8.00 +/-1.94), the Glu/GABA value (10.79 +/-1.96) in the brain tissue of the mouse in the model group is obviously increased (p is less than 0.01). Compared with the model group, the brain tissues of mice with different doses of the positive drug and the N-acetyl-N' -caffeoyl butanediamine have significantly reduced Glu/GABA values (p is less than 0.05). In conclusion, after insomnia, anxiety or depression in mice, GABA content in brain tissue decreased (p <0.01), Glu content and Glu/GABA value increased (p < 0.05). The dosage groups of N-acetyl-N' -caffeoyl butanediamine can increase the GABA content in brain tissues of insomnia, anxiety or depression mice, and reduce the Glu content and Glu/GABA value. It is speculated that N-acetyl-N' -caffeoyl butanediamine may improve insomnia, anxiety or depression symptoms by decreasing Glu levels, increasing GABA levels, decreasing Glu/GABA values.
Example 3
An injection for preventing and treating insomnia, anxiety and depression, wherein the dosage of N-acetyl-N' -caffeoyl butanediamine for single application is 1 mg/kg.
Example 4
A health food for preventing and treating insomnia, anxiety and depression comprises N-acetyl-N' -caffeoyl butanediamine in a single application dose of 10 mg/kg.
Example 5
An oral tablet for preventing and treating insomnia, anxiety and depression, wherein the dosage of N-acetyl-N' -caffeoyl butanediamine for single application is 10 mg/kg.
Example 6
A topical patch for preventing and treating insomnia, anxiety and depression is provided, wherein the dosage of N-acetyl-N' -caffeoyl butanediamine for single application is 100 mg/kg.
Example 7
An oral granule for preventing and treating insomnia, anxiety and depression, wherein the dosage of N-acetyl-N' -caffeoyl butanediamine for single application is 10 mg/kg.
The embodiments in the present description are described in a progressive manner, each embodiment focuses on differences from other embodiments, and the same and similar parts among the embodiments are referred to each other.
The previous description of the disclosed embodiments is provided to enable any person skilled in the art to make or use the present invention. Various modifications to these embodiments will be readily apparent to those skilled in the art, and the generic principles defined herein may be applied to other embodiments without departing from the spirit or scope of the invention. Thus, the present invention is not intended to be limited to the embodiments shown herein but is to be accorded the widest scope consistent with the principles and novel features disclosed herein.
Claims (7)
- Use of N-acetyl-N '-caffeoyl butanediamine in the preparation of a formulation for the prevention and treatment of insomnia, anxiety, depression and related diseases, wherein said N-acetyl-N' -caffeoyl butanediamine has the structure:
- 2. the use according to claim 1, wherein the formulation is any one of powder, tablet, capsule, emulsion, pill and granule.
- 3. The use according to claim 1, wherein the preparation is any one of an oral dosage form, an external patch and an injection solution.
- 4. A pharmaceutical comprising N-acetyl-N' -caffeoyl butanediamine.
- 5. The medicament according to claim 5, wherein the medicament is applied in a daily dose of 1-100mg/kg, calculated as N-acetyl-N' -caffeoyl butanediamine.
- 6. A health food characterized by containing N-acetyl-N' -caffeoyl butanediamine.
- 7. The health food according to claim 7, wherein the daily dose of the health food is 1-100mg/kg in terms of N-acetyl-N' -caffeoyl butanediamine.
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| JPS60152454A (en) * | 1984-01-18 | 1985-08-10 | Terumo Corp | Amide derivative and 5-lipoxigenase inhibitor containing said derivative as active component |
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| CN104277081A (en) * | 2013-07-05 | 2015-01-14 | 中国科学院大连化学物理研究所 | Hydroxy cinnamic acid amine compounds and preparation and application thereof |
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| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| JPS60152454A (en) * | 1984-01-18 | 1985-08-10 | Terumo Corp | Amide derivative and 5-lipoxigenase inhibitor containing said derivative as active component |
| JPS6339815A (en) * | 1986-08-05 | 1988-02-20 | Lion Corp | Hypnotic sedative |
| CN104277081A (en) * | 2013-07-05 | 2015-01-14 | 中国科学院大连化学物理研究所 | Hydroxy cinnamic acid amine compounds and preparation and application thereof |
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