Small molecule peptide and application thereof in preparation of anti-Alzheimer disease medicine

Abstract

The invention provides a small molecule peptide and application thereof in preparation of an anti-Alzheimer disease drug, and relates to the technical field of biological medicine. Firstly, the invention provides the small molecule peptide EGATETSFSHA with a brand new structure, the small molecule peptide shows a remarkable paralysis inhibition effect on AD model caenorhabditis elegans, meanwhile, the behavioristics of APP / PS1 mice can be remarkably improved, and A beta deposition in APP / PS1 mice brain tissues is effectively inhibited; the small molecule peptide provided by the invention shows obvious pharmaceutical activity in the aspect of resisting the Alzheimer disease. In addition, the small molecule polypeptide has a remarkable inhibition effect on IgE secreted by U266 cells. The small molecule peptide provided by the invention has dual drug activity of resisting Alzheimer's disease and allergy, and can be further developed and applied as a multifunctional drug capable of simultaneously treating Alzheimer's disease and allergy.

Description

Technical Field

[0001] This invention belongs to the field of biomedical technology, specifically relating to a small molecule peptide and its application in the preparation of anti-Alzheimer's disease drugs. Background Technology

[0002] Alzheimer's disease (AD) is a common, irreversible neurodegenerative disease in the elderly, clinically manifested as progressive memory and cognitive decline, language impairment, and psychomotor abnormalities. Oxidative stress, a major factor in the progression of Alzheimer's disease, promotes pathological formation by causing neuronal mitochondrial dysfunction, macromolecular oxidation, the production of reactive oxygen species (ROS) through the binding of metal ions to Aβ plaques, and the upregulation of tau protein and Aβ synthesis due to hyperphosphorylation. Currently approved AD treatments, such as the cholinesterase inhibitor donepezil and the NMDA receptor antagonist memantine, can only temporarily relieve symptoms by regulating neurotransmitter levels, failing to curb disease progression and accompanied by relatively serious side effects.

[0003] Food allergy is an abnormal reaction mediated by the immune system to specific food proteins. It is a serious public health problem affecting the quality of life of adults and children worldwide. The most common pathogenesis is type I hypersensitivity mediated by immunoglobulin E (IgE), specifically referring to the binding of IgE antibodies to specific food proteins (such as peanuts, milk, and eggs), inducing mast cells and basophils to release inflammatory mediators such as histamine, leading to symptoms in multiple systems including the skin, respiratory tract, digestive tract, and cardiovascular system. In severe cases, it can cause anaphylactic shock and even death. Current treatment primarily relies on strict avoidance of allergens and the use of antihistamines, corticosteroids, or adrenaline to relieve acute symptoms. However, these methods only control the reaction, not interrupt it, and long-term use carries risks such as drug resistance and metabolic disorders. While desensitization strategies such as oral immunotherapy can gradually improve tolerance, their efficacy is unstable, treatment time is long, and these strategies are desensitization rather than a cure. Therefore, there is an urgent need to find new drugs for allergies that can inhibit IgE responses and precisely regulate immune responses. Summary of the Invention

[0004] (a) Technical problems to be solved

[0005] To address the shortcomings of existing technologies, this invention provides a small molecule peptide that simultaneously possesses anti-Alzheimer's disease and anti-allergy activities.

[0006] (II) Technical Solution

[0007] To achieve the above objectives, the present invention provides the following technical solution:

[0008] In a first aspect, the present invention provides a small molecule peptide, wherein the amino acid sequence of the small molecule peptide is EGATETSFSHA.

[0009] Secondly, the invention provides the application of a small molecule peptide as an active ingredient in the preparation of a drug for treating or alleviating Alzheimer's disease, wherein the amino acid sequence of the small molecule peptide is EGATETSFSHA.

[0010] Thirdly, the present invention provides the application of a small molecule peptide as an active ingredient in the preparation of a drug for treating or relieving allergies, wherein the amino acid sequence of the small molecule peptide is EGATETSFSHA.

[0011] Fourthly, the present invention provides the application of a small molecule peptide as an active ingredient in the preparation of a drug that inhibits or reduces IgE content, wherein the amino acid sequence of the small molecule peptide is EGATETSFSHA.

[0012] Furthermore, the above-mentioned drug uses the small molecule peptide described in claim 1 as the active ingredient and is formulated into a pharmaceutically acceptable dosage form using a pharmaceutically acceptable carrier excipient; the dosage form includes tablets, capsules, powders, injections, oral liquids, powders, and lyophilized powders.

[0013] (III) Beneficial Effects

[0014] 1. This invention provides a novel structural small molecule peptide, EGATETSFSHA. This small molecule peptide has no adverse effects on the survival rate of nematodes and cells. This small molecule polypeptide is safe and has no toxic side effects, and can be further developed and studied as a drug.

[0015] 2. First, the effects of the small molecule peptide of this invention on the paralysis model of CL4176 nematode were investigated. The experimental results showed that the small molecule peptide could significantly reduce the paralysis rate of CL4176 nematode and reduce the occurrence of paralysis. Furthermore, the small molecule peptide of this invention could significantly improve the behavior of APP / PS1 mice and effectively inhibit Aβ deposition in the brain tissue of APP / PS1 mice. The small molecule peptide provided by this invention showed significant pharmacological activity in the treatment of Alzheimer's disease and can be used as a new drug for the treatment of Alzheimer's disease.

[0016] 3. In addition, we also investigated the effect of this small molecule peptide on U266 cells that specifically express IgE. The experimental results showed that the small molecule peptide has a significant inhibitory effect on the secretion of IgE by U266 cells. This small molecule peptide can achieve anti-allergic drug activity by inhibiting the production of IgE, and can be used as a new anti-allergic drug. Attached Figure Description

[0017] Figure 1The results of high performance liquid chromatography analysis of the purity of the synthesized small molecule peptide EGATETSFSHA; RT: 10.097 min; Area: 2027100; Height: 396885.

[0018] Figure 2 The results are from mass spectrometry analysis of the small molecule peptide EGATETSFSHA.

[0019] Figure 3 The effect of different concentrations of small molecule peptides on the survival rate of nematodes; Note: ns indicates no significant difference compared with the control group, P>0.05.

[0020] Figure 4 The paralysis rate of nematodes in each group; Note: * This indicates a comparison with the model group. * P < 0.05 ** P < 0.01, *** P < 0.001.

[0021] Figure 5 The effect of different concentrations of peptides on cell viability is given by ns, where ns indicates no significant difference compared to the control group (P>0.05). Detailed Implementation

[0022] To make the objectives, technical solutions, and advantages of the embodiments of the present invention clearer, the technical solutions of the embodiments of the present invention will be clearly and completely described below in conjunction with the embodiments of the present invention. Obviously, the described embodiments are only some embodiments of the present invention, not all embodiments. Based on the embodiments of the present invention, all other embodiments obtained by those skilled in the art without creative effort are within the scope of protection of the present invention.

[0023] Example 1

[0024] Peptide Synthesis and Identification

[0025] This embodiment describes the solid-phase synthesis of the small molecule peptide EGATETSFSHA (assisted by Nanjing Jietai Biotechnology Co., Ltd.), and the purity of the synthesized small molecule peptide was analyzed and identified by mass spectrometry. Figure 1 As shown, in the small molecule peptides of this invention, the main peak accounts for the majority, with almost no impurity peaks, and the purity is above 95%. Figure 2 As shown, the [M+H] of the small molecule peptides of this invention H+ The molecular weight was 1137.27 Da, which is basically consistent with its theoretical molecular weight (1136.12 Da). These results indicate that the purity of the synthesized small molecule peptide EGATETSFSHA in this embodiment meets the requirements for subsequent experiments.

[0026] Example 2

[0027] The effect of the small molecule peptide EGATETSFSHA on the paralysis model of CL4176 nematode. This small molecule peptide was prepared in Example 1.

[0028] I. Experimental Materials

[0029] MgSO4 was purchased from Shanghai Maclean Biochemical Technology Co., Ltd.; agar powder, yeast powder, cholesterol, tryptone, NaCl, and CaCl2 were all purchased from Beijing Solarbio Science & Technology Co., Ltd.; Na2HPO4·12H2O and KH2PO4 were all purchased from Sinopharm Chemical Reagent Co., Ltd.; the transgenic AD model of Caenorhabditis elegans (C. elegans) CL4176 [dvIs27 [myo-3p::A-Beta (1-42)::let-851 3'UTR) + rol-6(su1006)] X] and the uracil-deficient Escherichia coli OP50 were both purchased from the Caenorhabditis elegans Genetic Center in the United States.

[0030] II. Solution Preparation

[0031] M9 buffer: Weigh 0.6g disodium hydrogen phosphate, 0.3g potassium dihydrogen phosphate, 0.5g sodium chloride, and 0.025g magnesium sulfate (dehydrated), dissolve in 100mL deionized water, sterilize at high temperature, and set aside for use.

[0032] NGM culture plate: Weigh 3.0g sodium chloride, 2.5g tryptone, and 17g agar into an Erlenmeyer flask, add 975mL deionized water, and autoclave. When the temperature of the sterilized solution drops to approximately 55℃, add 0.5mL of 1M calcium chloride solution, 1mL of 5mg / mL cholesterol solution, 1mL of 1M magnesium sulfate solution, and 25mL of potassium phosphate buffer solution sequentially. Use a pipette to add the prepared culture medium liquid to the corresponding petri dishes or well plates, and allow to cool and solidify overnight.

[0033] Stock solution of small molecule peptide to be tested: Weigh an appropriate amount of small molecule peptide and dissolve it in DMSO to prepare a 50mM solution.

[0034] III. Experimental Methods

[0035] 1. Effects of small molecule peptides on the survival rate of wild-type Caenorhabditis elegans

[0036] Small molecule peptide stock solutions were diluted with M9 buffer to 0.1 mM, 1 mM, and 10 mM, respectively. 500 μL of each solution was evenly spread onto freshly prepared NGM plates and allowed to air dry at room temperature. 50 μL of OP50 bacterial suspension was added to the center of each plate, and the plates were dried overnight. Wild-type *C. elegans* were inoculated onto the drug-containing plates. A control group without the small molecule peptide was also included. After 48 hours of culture, the effect of different peptide concentrations on the survival rate of wild-type *C. elegans* was observed. Each group contained at least 30 nematodes, and each experiment was repeated three times. The 48-hour survival rate was calculated.

[0037] 48-hour nematode survival rate % = (Total number of surviving nematodes after 48 hours / Total number of surviving nematodes at 0 hours) × 100%

[0038] 2. Effects of small molecule peptides on the transgenic AD model Caenorhabditis elegans strain CL4176

[0039] The small molecule peptide stock solution was diluted with M9 buffer to 0.1 mM, 1 mM, and 10 mM. 500 μL of each solution was then evenly spread onto freshly prepared NGM plates and allowed to air dry at room temperature. 50 μL of OP50 bacterial suspension was added to the center of each plate, and the plates were dried overnight. Synchronized CL4176 *C. elegans* nematodes were inoculated onto the drug-containing plates. A group without the small molecule peptide was also set up as a model group.

[0040] CL4176 *C. elegans*, after being synchronized, were cultured at 16°C for 48 hours, reaching the L3 stage. The culture plate was then transferred to 25°C to induce Aβ gene transcription. Under these conditions, the number of paralyzed *C. elegans* within 36 hours was observed and recorded. Paralyzed individuals exhibited stiffness in the trunk, leading to motor impairment or even loss of motor function; the head could be twisted. Each group contained at least 30 nematodes, and each experiment was repeated three times. The paralysis rate at 36 hours was calculated as follows: 36-hour paralysis rate % = (Number of paralyzed nematodes / Total number of nematodes) × 100%.

[0041] 3. Statistical Analysis

[0042] Data are expressed as mean ± SD. The t-test was used for comparisons between groups, and P < 0.05 was considered statistically significant.

[0043] IV. Experimental Results

[0044] 1. Effects of small molecule peptides on the survival rate of wild-type Caenorhabditis elegans

[0045] The survival rate of nematodes at different small molecule peptide concentrations for 48 hours is as follows: Figure 3 As shown, compared with the control group, there was no significant difference in the survival rate of wild-type nematodes under different concentrations of peptide culture (P>0.05), indicating that the small molecule peptides provided by the present invention are safe and have no side effects.

[0046] 2. Effects of small molecule peptides on the transgenic AD model Caenorhabditis elegans strain CL4176

[0047] Transgenic CL476 nematodes can induce human Aβ at 25°C. 1-42 In muscle expression, with Aβ 1-42 As the nematodes accumulate, they gradually become paralyzed and lose their ability to move. Therefore, the CL4176 transgenic nematode is widely used as a biological model to explore the anti-Alzheimer's disease effects of drugs.

[0048] Results of nematode paralysis rate detection within 36 hours are as follows Figure 4 As shown in the figure, compared with the model group, the paralysis rate of nematodes in different concentrations of small molecule peptide groups was significantly reduced (P < 0.05, P < 0.01, P < 0.001), and a good dose-response relationship was observed. These results indicate that the small molecule peptides provided by this invention can effectively inhibit the occurrence of paralysis in the AD model *C. elegans*, exhibiting significant anti-AD activity, and are expected to be further developed as a drug for treating AD.

[0049] Example 3

[0050] Effects of small molecule peptides on APP / PS1 mice

[0051] 1. Grouping and administration of experimental animals

[0052] Six-month-old SPF-grade male APP / PS1 mice and age-matched C57BL / 6J mice, weighing 20-30 g, were purchased from Beijing Huafukang Laboratory Animal Co., Ltd. They were provided with free access to water and food, and underwent 12-hour light exposure day and night for 7 days before the experiments were conducted.

[0053] APP / PS1 mice were randomly divided into two groups: a model group (APP / PS1 group) and small molecule peptide groups (low, medium, and high dose groups), with 12 mice in each group. C57BL / 6J mice were acclimatized for one week and then became the normal control group (WT group). Appropriate amounts of small molecule peptides were prepared into solutions of 7.5 μg / mL, 15 μg / mL, and 30 μg / mL, respectively. The small molecule peptide groups were administered the peptides at doses of 50 μg / kg, 100 μg / kg, and 200 μg / kg (approximately 0.2 ml). The normal control group and the model group were given the same volume of physiological saline daily, once daily, for 8 weeks. The small molecule peptides were prepared as described in Example 1.

[0054] 2. Behavioral testing

[0055] 2.1 Morris Water Maze

[0056] The Morris water maze can assess an animal's spatial learning and memory abilities. The maze setup is a circular, temperature-controlled water tank with an inner diameter of 120 cm and a height of 50 cm. The tank is divided into four quadrants, labeled Quadrant I, Quadrant II, Quadrant III, and Quadrant IV. A hidden platform is placed in the center of Quadrant II, less than 1 cm above the water surface. The water temperature is maintained at approximately 23°C to prevent mice from becoming too comfortable and prolonging their swimming time, or to avoid the risk of death due to excessively low water temperature. The entire experiment is video-recorded, and a SMART system is used to set up the tracking program and record data. The water maze experiment lasts for 6 days, with the first 5 days being a navigation experiment. Mice are placed in the water from the midpoint of the tank wall in each of the four quadrants and allowed to explore freely for 1 minute. Recording stops automatically when a mouse finds a platform and stays there for more than 3 seconds, or when it fails to find a platform after 1 minute of exploration. If the mouse fails to find a platform within 1 minute, the experimenter guides it to the platform and allows it to stay there for 10 seconds. Each mouse is trained 4 times per day, and the time taken to find the platform each time is recorded as the escape latency period. Day 6 was the spatial exploration experiment. Before the experiment, the underwater hidden platform was removed, and the mice were uniformly placed into the water from the fourth quadrant. The mice were allowed to explore freely for 1 minute, and their swimming trajectories were recorded. The number of times the mice crossed the platform and the time spent in the target quadrant were counted. The percentage of time spent in the target quadrant was calculated as follows: Target quadrant time ratio (%) = Target quadrant time / Non-target quadrant time × 100%.

[0057] 2.2 Y Maze

[0058] The Y-maze reflects an animal's spatial recognition and memory abilities. The Y-maze consists of three arms, each 30 cm long, 8 cm wide, and 15 cm high, with each arm forming a 120° angle with the others. The entire experiment was video-recorded and analyzed using the SMART system. During the test, mice were placed in the center of the Y-maze and allowed 5 minutes of free exploration. The number of times each mouse entered a maze arm was recorded. A single successful spontaneous alternation was defined as a mouse entering three different maze arms consecutively. After each mouse's test, excrement was cleaned, odor was eliminated with 75% alcohol, and the mice were dried to prevent odor from affecting subsequent tests. The accuracy rate of spontaneous alternation was calculated as: Accuracy rate (%) = [Number of spontaneous alternations / (Total number of arm entries - 2)] * 100%

[0059] 2.3 Measurement of Aβ1-42 levels in brain tissue

[0060] After drug administration, five mice from each group were randomly selected, euthanized by cervical dislocation, and their brain tissue was extracted. The Aβ1-42 level in the brain tissue was measured according to the ELISA kit instructions. The specific procedures were as follows: Standard wells and sample wells were prepared on the sample plate. 50 μL of different concentrations of standard solution were added to each standard well. 10 μL of the sample to be tested was added to each sample well, followed by 40 μL of sample diluent (i.e., a 5-fold dilution). No diluent was added to the blank wells. Except for the blank wells, 100 μL of horseradish peroxidase (HRP)-labeled detection antibody was added to each of the standard and sample wells. The reaction wells were sealed with sealing film and incubated at 37°C for 60 min in a water bath or incubator. The liquid was discarded, and the plates were patted dry on absorbent paper. Each well was filled with washing buffer, allowed to stand for 1 min, the washing buffer was discarded, and the plates were patted dry on absorbent paper. This washing process was repeated 5 times (or a plate washer could be used). 50 μL each of substrates A and B were added to each well, and the plates were incubated at 37°C in the dark for 15 min. Add 50 μL of stop solution to each well, and measure the OD value of each well at a wavelength of 450 nm within 15 min. Establish a standard curve based on the OD values, and calculate the Aβ1-42 level in the sample using the standard curve.

[0061] 3. Statistical Analysis

[0062] Data are expressed as mean ± SD. The t-test was used for comparisons between groups, and P < 0.05 was considered statistically significant.

[0063] 4. Results

[0064] APP / PS1 mice are a commonly used transgenic animal model for Alzheimer's disease (AD), widely recognized internationally and used for research on AD pathogenesis and drug screening. Using APP / PS1 mice as a disease model, the small molecule peptide prepared in Example 1 was administered to further verify its anti-AD activity.

[0065] Compared with the normal group, the escape latency of mice in the model group was significantly increased, while the number of platform crossings, the target quadrant dwell time ratio, and the accuracy of spontaneous alternation were all significantly decreased (P<0.01, P<0.001). Mice in the model group exhibited obvious behavioral regression characteristics. Compared with the model group, the escape latency of the low-dose small molecule peptide group was reduced, while the number of platform crossings, the target quadrant dwell time ratio, and the accuracy of spontaneous alternation were all increased to varying degrees, but the differences were not statistically significant (P>0.05). Compared with the model group, the escape latency of the medium- and high-dose small molecule peptide groups was significantly reduced, while the number of platform crossings, the target quadrant dwell time ratio, and the accuracy of spontaneous alternation were all significantly increased, with statistically significant differences (P<0.05, P<0.01, P<0.001). These results indicate that the small molecule peptides of this invention can improve the behavioral behavior of an AD disease model. The results are shown in Table 1.

[0066] Table 1. Results of behavioral measurements in each group of mice

[0067] Group Avoiding the incubation period (s) Number of times the platform was traversed (times) Target quadrant dwell time ratio (%) Accuracy rate of autonomous alternation (%) normal group 25.25±10.72 4.87±0.87 36.67±6.50 51.88±4.96 Model group 48.54±9.24** 2.15±0.58** 13.77±4.02** 21.13±1.63*** Small molecule peptide group (50μg / kg) <![CDATA[43.74±10.53 # ]]> <![CDATA[2.83±0.79 ns ]]> <![CDATA[18.83±6.27 ns ]]> <![CDATA[35.02±5.18 # ]]> Small molecule peptide group (100μg / kg) <![CDATA[37.28±4.73 ns ]]> <![CDATA[3.12±0.84 # ]]> <![CDATA[25.87±6.16 ns ]]> <![CDATA[38.52±4.13 # ]]> Small molecule peptide group (200μg / kg) <![CDATA[28.40±6.35 ## ]]> <![CDATA[4.25±0.58 ## ]]> <![CDATA[30.13±7.52 ## ]]> <![CDATA[45.54±7.35 ### ]]>

[0068] Note: Compared with the normal group, *P<0.05, **P<0.01; compared with the model group, nsP>0.05. # P<0.05, ## P<0.01, ### P<0.01.

[0069] Furthermore, we investigated the Aβ1-42 levels in the brain tissue of mice in each group, and the results are shown in Table 2. Compared with the normal group, the Aβ1-42 levels in the brain tissue of mice in the model group were significantly increased (P<0.001). Compared with the model group, the Aβ1-42 levels in the brain tissue of mice in the low-dose small molecule peptide group were decreased, but the difference was not statistically significant; compared with the model group, the Aβ1-42 levels in the brain tissue of mice in the medium- and high-dose small molecule peptide groups were significantly decreased, and the differences were statistically significant (P<0.05, P<0.001). These results indicate that the small molecule peptides described in this invention can effectively inhibit Aβ deposition and achieve anti-AD drug activity. The results are shown in Table 2.

[0070] Table 2. Aβ1-42 levels in the brain tissue of mice in each group

[0071] Group Aβ1-42 concentration (ng / mg) normal group 3.76±0.91 Model group 263.12±9.43*** Small molecule peptide group (50μg / kg) <![CDATA[243.62±11.26 ns ]]> Small molecule peptide group (100μg / kg) <![CDATA[183.27±10.37 # ]]> Small molecule peptide group (200μg / kg) <![CDATA[126.19±9.86 ### ]]>

[0072] Note: Compared with the normal group, *P<0.05, **P<0.01; compared with the model group, nsP>0.05. # P<0.05, ## P<0.01, ### P<0.01.

[0073] Example 4

[0074] Study on the IgE inhibitory activity of small molecule peptides of this invention

[0075] I. Experimental Materials

[0076] Small molecule peptide stock solution: Weigh the small molecule peptide synthesized in Example 1 and prepare a 50 mM solution with DMSO. Store at 4°C. Dilute with DMSO according to the required concentration during the experiment.

[0077] Phosphate-buffered saline (PBS), fetal bovine serum (FBS), RPMI 1640 medium, trypan blue, and dimethyl sulfoxide (DMSO) were all purchased from Beijing Solarbio Science & Technology Co., Ltd. U266 cell lines were obtained from the laboratory of Henan University of Traditional Chinese Medicine, and IgE detection kits were purchased from Mabtech.

[0078] II. Experimental Methods

[0079] U266 cryopreserved cell lines were revived in a 37°C water bath. After adding 10 mL of PBS and centrifuging to remove DMSO, the cells were resuspended in RPMI 1640 medium containing 10% FBS and cultured in a 37°C, 5% CO2 incubator. Once the cells regained their growth state, the U266 cell density was counted using a cell counting chamber, and the cells were diluted to 1×10⁶ cells / mL using pre-prepared RPMI 1640 complete medium (without antibiotics) containing 10% fetal bovine serum. 5 The 96-well plates were divided into groups: a blank group, a model group, and experimental groups with different concentrations. Each group had three replicates. The blank group was treated with 100 μL of complete culture medium, while the model and experimental groups were treated with 100 μL of 1×10⁻⁶ medium. 5 Cell suspensions of U266 cells / mL were prepared. Different treatments were then applied: the blank and model groups were supplemented with 100 μL of complete culture medium, while the experimental groups were supplemented with 100 μL of complete culture medium containing the tested peptide stock solution, bringing the final drug concentrations in the 96-well plates to 0.1 mM, 1 mM, and 10 mM, respectively. The culture plates were incubated at 37°C for 72 h. After incubation, U266 cells were in suspension. 50 μL of the mixture from each well was removed, and trypan blue staining was used to determine cell viability after treatment with different drug concentrations. The culture plates were then centrifuged at 1000 rpm for 5 min, and the supernatant was collected. Total IgE levels were measured using an ELISA kit, and the IgE inhibition rate was calculated.

[0080] Cell viability (%) = (Total number of live cells / (Total number of live cells + Total number of dead cells)) × 100%

[0081] IgE experimental data are expressed as inhibition rate (I), where E 实验 E represents the detected value of IgE in each experimental group. 模型 E represents the average IgE level in the U266 cell group of the model group. 空白 The formula representing the blank group detection value is as follows:

[0082] Inhibition rate Ic for each group = 100% - (E 实验 - E 空白 ) / (E 模型 -E 空白 )×100%.

[0083] III. Experimental Results

[0084] Results of U266 cell viability detection at different small molecule peptide concentrations are as follows: Figure 5As shown, compared with normally cultured U266 cells, there was no significant difference in the survival rate of U266 cells cultured with different concentrations of small molecule peptides, indicating that the small molecule peptides provided by the present invention are safe and have no toxic side effects.

[0085] As shown in Table 1, within the concentration range of 0.1-10 mM, the small molecule peptide significantly inhibited IgE secretion from U266 cells, exhibiting a favorable dose-response relationship. These results indicate that the small molecule peptide can achieve anti-allergic drug activity by inhibiting IgE production, and thus holds promise as a novel anti-allergy drug.

[0086] Table 1. Inhibition rate of IgE by different concentrations of peptides

[0087]

[0088] The above embodiments are only used to illustrate the technical solutions of the present invention, and are not intended to limit it. Although the present invention has been described in detail with reference to the foregoing embodiments, those skilled in the art should understand that modifications can still be made to the technical solutions described in the foregoing embodiments, or equivalent substitutions can be made to some of the technical features. Such modifications or substitutions do not cause the essence of the corresponding technical solutions to deviate from the spirit and scope of the technical solutions of the embodiments of the present invention.

Claims

1. A small molecule peptide, characterized in that, The amino acid sequence of the small molecule peptide is EGATETSFSHA.

2. The application of a small molecule peptide as an active ingredient in the preparation of drugs for treating or alleviating Alzheimer's disease, characterized in that, The amino acid sequence of the small molecule peptide is EGATETSFSHA.

3. The application of a small molecule peptide as an active ingredient in the preparation of drugs for treating or relieving allergies, characterized in that, The amino acid sequence of the small molecule peptide is EGATETSFSHA.

4. The application of a small molecule peptide as an active ingredient in the preparation of drugs that inhibit or reduce IgE expression, characterized in that, The amino acid sequence of the small molecule peptide is EGATETSFSHA.

5. The application according to claim 2 or claim 4, characterized in that, The drug uses the small molecule peptide of claim 1 as the active ingredient and is formulated into a pharmaceutically acceptable dosage form using a pharmaceutically acceptable carrier excipient; the dosage form includes tablets, capsules, powders, injections, oral liquids, powders, and lyophilized powders.

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