Medicine for preventing and treating cerebral arterial thrombosis

By using a combination of salmon peptides with carriers and edaravone drugs, intravenous injection into the brain, the existing ischemic stroke treatment methods are solved in terms of safety and efficacy, significantly reducing neurological defects and cerebral infarction, and improving patients' neurological function and quality of life.

CN119792487AActive Publication Date: 2025-04-11THE 971ST HOSPITAL OF THE CHINESE PEOPLES LIBERATION ARMY NAVY

Patent Information

Application Number
CN202510113377.6
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2025-01-24
Publication Date
2025-04-11
Estimated Expiration
2045-01-24

AI Technical Summary

Technical Problem

The existing treatment methods for ischemic stroke still have shortcomings in improving treatment effect, reducing side effects and improving post-mortem recovery, especially in terms of safety and efficacy.

Method used

Using a drug composed of salmon polypeptides and a pharmaceutically acceptable carrier, it is quickly transported to the brain by intravenous injection, combined with edaravone as a free radical scavenger, to work synergistically to improve the therapeutic effect.

Benefits of technology

It significantly reduces neurological defects and cerebral infarction caused by ischemic stroke, reduces ischemic damage, promotes nerve regeneration and repair, improves patients' neurological function and quality of life, and improves the safety and effectiveness of treatment.

✦ Generated by Eureka AI based on patent content.

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Abstract

The invention provides a medicine for preventing and treating cerebral arterial thrombosis, and belongs to the technical field of neuromedicine. The medicine comprises salmon polypeptide as shown in SEQ ID NO.1 and a pharmaceutically acceptable carrier, and experimental results show that the salmon polypeptide has good safety, can effectively improve oxygen-glucose deprivation / reoxygenation injury of brain cells, and remarkably reduces neurological impairment and cerebral infarction of mice suffering from cerebral arterial thrombosis. The invention also discloses a pharmaceutical composition for treating cerebral arterial thrombosis. The pharmaceutical composition comprises the salmon polypeptide and edaravone. The composition shows a remarkable synergistic effect, compared with the single use of the salmon polypeptide or edaravone, the composition can more remarkably reduce neurological impairment and cerebral infarction, and the actual effect is obviously superior to the theoretical superposition effect. Therefore, the invention provides a novel and more effective treatment scheme for the treatment of cerebral arterial thrombosis.
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Description

Technical Field

[0001] The invention belongs to the technical field of neuromedicine, and in particular relates to a medicine for preventing and treating ischemic stroke. Background Art

[0002] Cerebrovascular Accident (CVA), also commonly known as stroke, is an acute disease caused by interruption or abnormality of cerebral blood supply, which leads to brain tissue dysfunction. The occurrence of stroke usually causes serious damage to the patient's neurological function, and as the course of the disease prolongs, the degree of brain damage worsens and the possibility of recovery decreases.

[0003] Stroke can be divided into two categories: ischemic stroke and hemorrhagic stroke. Among them, ischemic stroke accounts for about 80% of all strokes. Ischemic stroke is caused by vascular stenosis, blockage or thrombosis, which leads to interruption of blood flow in some brain areas, and then causes brain tissue hypoxia, metabolic disorders, and ultimately brain cell death. At present, although some treatments are available to relieve the symptoms of ischemic stroke, there is still a great demand for improving treatment effects, reducing side effects, and improving recovery after illness. Therefore, the development of new drugs and treatment options, especially neuroprotective drugs with higher safety and efficacy, is the focus of current research.

[0004] Salmon polypeptide (amino acid sequence: TPEVHIAVDKF, SEQ ID NO.1) is a bioactive polypeptide successfully extracted from Atlantic salmon byproducts through a specific technology. In existing scientific research, it has been clearly confirmed that the polypeptide has a significant hyaluronidase inhibitory effect. This discovery provides an important theoretical basis for its application in the biomedical field. However, based on the current literature, there are no public literature reports on whether the salmon polypeptide TPEVHIAVDKF can play a role in the treatment of stroke and its specific mechanism of action. This also makes its application prospects in the treatment of stroke full of unknowns, which needs further in-depth research. Summary of the invention

[0005] The purpose of the present invention is to provide a drug for preventing and treating ischemic stroke and a pharmaceutical composition composed thereof, so as to achieve better therapeutic effect while achieving higher safety.

[0006] In order to achieve the above-mentioned purpose, the present invention provides the following technical solutions:

[0007] First, the present invention provides a drug for preventing and treating ischemic stroke, wherein the drug is composed of a salmon polypeptide and a pharmaceutically acceptable carrier; the amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.1.

[0008] The pharmaceutically acceptable carrier includes solvents: water, physiological saline, glucose solution, etc.; fillers: starch, microcrystalline cellulose, etc.; binders: starch slurry, hydroxypropyl methylcellulose, etc.; antioxidants: sodium sulfite, vitamin C, vitamin E, etc.

[0009] Preferably, the drug is a liquid drug, and the concentration of salmon polypeptide in the drug is greater than or equal to 80 μg / ml.

[0010] Preferably, in the drug, the concentration of salmon polypeptide is 80 μg / ml-160 μg / ml;

[0011] The pharmaceutically acceptable carrier is physiological saline, and the drug is administered by intravenous injection so as to quickly achieve the therapeutic purpose through the blood circulation;

[0012] Preferably, in order to enhance the efficacy, the concentration of salmon polypeptide is preferably 160 μg / ml.

[0013] Secondly, the present invention provides an application of a salmon polypeptide in the preparation of a drug for preventing and treating ischemic stroke, wherein the amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.1.

[0014] Preferably, the drug is a liquid drug prepared from physiological saline, the concentration of salmon polypeptide in the drug is 80 μg / ml-160 μg / ml, and the drug is administered by intravenous injection.

[0015] Preferably, the concentration of salmon polypeptide in the drug is 160 μg / ml.

[0016] Preferably, the drug can reduce neurological deficits and cerebral infarction caused by ischemic stroke, thereby alleviating ischemic damage, promoting nerve regeneration and repair, and significantly improving the patient's neurological function and quality of life.

[0017] Again, the present invention provides a pharmaceutical composition for treating ischemic stroke, wherein each 300 μl of the pharmaceutical composition is composed of 150 μl of a salmon polypeptide drug at a concentration of 160 μg / ml and 150 μl of an edaravone drug at a concentration of 500 μg / ml, and the amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.1. Edaravone, as a known free radical scavenger, can effectively reduce oxidative stress and protect nerve cells from damage. The combined use of edaravone and salmon polypeptide can exert a synergistic effect, thereby improving the therapeutic effect.

[0018] Preferably, the solvent of the salmon polypeptide drug and the edaravone drug is normal saline;

[0019] The pharmaceutical composition is administered by intravenous injection;

[0020] The pharmaceutical composition synergistically reduces neurological deficits and cerebral infarction caused by ischemic stroke.

[0021] Finally, the present invention provides an application of a composition in the preparation of a drug for treating ischemic stroke, wherein each 300 μl of the composition consists of 150 μl of a salmon polypeptide solution with a concentration of 160 μg / ml and 150 μl of an edaravone solution with a concentration of 500 μg / ml, and the amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.1.

[0022] Preferably, the solvent of the salmon polypeptide solution and the edaravone solution is physiological saline;

[0023] The drug is administered by intravenous injection;

[0024] The drug synergistically reduces neurological deficits and cerebral infarction caused by ischemic stroke through salmon peptides and edaravone.

[0025] The beneficial effects of the present invention are:

[0026] First, the present invention provides a new treatment option for ischemic stroke. The present invention discloses for the first time the use of the salmon polypeptide (amino acid sequence: TPEVHIAVDKF) shown in SEQID NO.1 in preventing and / or treating ischemic stroke. In the prior art, there is no report on the use of the salmon polypeptide in the field of stroke treatment. The discovery of the present invention provides a new treatment strategy and drug selection for the treatment of ischemic stroke, expanding the application field of the polypeptide.

[0027] Secondly, the hemolytic activity and cytotoxicity experimental results of Example 1 show that within the effective concentration range, the salmon polypeptide provided by the present invention does not have obvious hemolytic activity and cytotoxicity (such as Figure 1 This indicates that it has good safety and can be used for drug preparation, reducing the potential risks of clinical application.

[0028] Finally, the study of Example 3 also found that the combination of salmon polypeptide and the known free radical scavenger edaravone can produce significant synergistic effects. Compared with the use of salmon polypeptide or edaravone alone, the combined use can more significantly reduce the neurological deficit score and the percentage of cerebral infarction (Table 1 and Table 2), and the actual effect is significantly better than the theoretical superposition effect. This shows that the pharmaceutical composition of the present invention can more effectively intervene in the pathophysiological process of ischemic stroke through a multi-target mechanism of action, thereby significantly improving the therapeutic effect. BRIEF DESCRIPTION OF THE DRAWINGS

[0029] Figure 1 This is a diagram showing the results of the drug safety test of salmon peptides;

[0030] in, Figure 1 (a) is the result of hemolytic activity test, Figure 1 (b) is the result of cytotoxicity test;

[0031] Figure 2 This is a graph showing the therapeutic effect of salmon peptides on brain cell oxygen-glucose deprivation / reoxygenation damage;

[0032] Figure 1 middle, △△△ Compared with the control group, P < 0.001; * Compared with the oxygen-glucose deprivation / reoxygenation group, P < 0.05; ** Compared with the oxygen-glucose deprivation / reoxygenation group, P < 0.01. DETAILED DESCRIPTION

[0033] Embodiments of the present invention are described in detail below, and the examples of the embodiments are shown in the accompanying drawings, wherein the same or similar reference numerals represent the same or similar elements or elements with the same or similar functions from beginning to end. The embodiments described below by reference to the accompanying drawings are exemplary, are intended to be used to explain the present invention, and are not to be construed as limitations of the present invention. Those who do not indicate specific techniques or conditions in the embodiments are carried out according to the techniques or conditions described in the documents in this area or according to the product specification. Those who do not indicate the manufacturer of reagents or instruments used are all conventional products that can be obtained commercially.

[0034] Example 1

[0035] Conducting drug safety testing on salmon peptides

[0036] (A) Hemolytic activity test of salmon peptides

[0037] First, the cells were grouped as follows:

[0038] In the negative control group, red blood cells were diluted to 1×10 8 / ml, and then 200 μl was added to a 96-well plate;

[0039] In the positive control group, red blood cells were diluted to 1×10 8 / ml, and 200 μl was added to a 96-well plate;

[0040] Treatment group 1 was treated with PBS containing salmon peptide (synthesized by GenScript Biotech Co., Ltd.) at a final concentration of 10 μg / ml. 8 / ml, and then take 200μl and add it to a 96-well plate;

[0041] Treatment group 2 used PBS containing salmon peptide at a final concentration of 20 μg / ml to dilute the red blood cells to 1×10 8 After 100 μl was added to a 96-well plate;

[0042] Treatment group 3 was treated with PBS containing salmon peptide at a final concentration of 40 μg / ml. 8 / ml, and then 200 μl was added to a 96-well plate;

[0043] Treatment group 4 used PBS containing salmon peptide at a final concentration of 80 μg / ml to dilute red blood cells to 1×10 8 / ml, take 200μl and add it to a 96-well plate;

[0044] Treatment group 5 used PBS containing salmon peptide at a final concentration of 160 μg / ml to dilute the red blood cells to 1×10 8 / ml, take 200μl and add it to 96-well plate.

[0045] After the grouping and loading, the 96-well plate was placed in a 37°C constant temperature incubator for 30 minutes. After the incubation, the solution was collected and centrifuged at 1000 rpm for 5 minutes. After the centrifugation, 100 μl of supernatant was taken out from each well and transferred to a new 96-well plate. Finally, the new 96-well plate was placed in an ELISA reader and the absorbance value was detected at OD540. The results are shown in the figure. Figure 1 (a) shown.

[0046] (B) Cytotoxicity assay

[0047] First, BV2 microglial cells in the logarithmic growth phase were inoculated into 96-well plates and placed in a cell culture incubator for culture. When the cells were cultured to a cell density greater than 90%, the cells were treated according to the following groupings:

[0048] The control group was added with 100 μl of DMEM culture solution;

[0049] Treatment group 1 was added with 100 μl of salmon peptide solution (prepared in DMEM) with a final concentration of 10 μg / ml;

[0050] Treatment group 2 was added with 100 μl of salmon peptide solution (prepared in DMEM) with a final concentration of 20 μg / ml;

[0051] Treatment group 3 was added with 100 μl of salmon peptide solution (prepared in DMEM) with a final concentration of 40 μg / ml;

[0052] Treatment group 4 was added with 100 μl of salmon peptide solution (prepared in DMEM) with a final concentration of 80 μg / ml;

[0053] To treatment group 5, 100 μl of salmon peptide solution (prepared in DMEM) with a final concentration of 160 μg / ml was added.

[0054] After the grouping and sample addition, the 96-well plate was placed in a cell culture incubator at 37°C and 5% CO2 for 24 hours. After the incubation, 20 μL of MTT solution (pH = 7.4) was added to each well and incubated for another 4 hours at 37°C and 5% CO2. Then, the culture supernatant in the well was carefully aspirated, 150 μL of DMSO was added, and after shaking for 10 minutes, the well was placed in an ELISA reader and the absorbance value was detected at OD570. The results are shown in the figure. Figure 1 (b) as shown.

[0055] from Figure 1 (a) and Figure 1 (b) It can be seen that salmon peptides did not cause lysis of red blood cells at different concentrations, proving that they do not produce hemolysis. In addition, through cell culture experiments ( Figure 1 (b)) It can be seen that salmon peptides have no significant inhibitory effect on the growth and survival of nerve cells, indicating that they are not cytotoxic. These results show that salmon peptides, as a bioactive substance, have good biocompatibility and are suitable for drug preparation.

[0056] Example 2

[0057] Detecting the therapeutic effect of salmon peptides on brain cell oxygen-glucose deprivation / reoxygenation injury

[0058] BV2 cells in the logarithmic growth phase were inoculated into 6-well culture plates, and subsequent experiments were performed when the cell density reached about 80%. The cells were grouped as follows:

[0059] Control group: high-glucose DMEM medium was used for normal culture at 37°C and 5% CO2;

[0060] Oxygen-glucose deprivation / reoxygenation group: The cells were cultured in a cell culture incubator at 37°C, 0.3% O2, and 5% CO2 for 6 h using sugar-free DMEM medium, then replaced with high-glucose DMEM medium and placed in a cell culture incubator at 37°C, 21% O2, and 5% CO2 for 24 h.

[0061] Treatment group 1: cultured in a 37°C, 0.3% O2 ​​and 5% CO2 cell culture incubator for 6 h using sugar-free DMEM medium, then replaced with a high-glucose medium containing 10 μg / ml salmon peptides and placed in a 37°C, 21% O2 and 5% CO2 cell culture incubator for 24 h of resugar and reoxygenation;

[0062] Treatment group 2: cultured in a 37°C, 0.3% O2 ​​and 5% CO2 cell culture incubator for 6 h using sugar-free DMEM medium, then replaced with a high-glucose medium containing 20 μg / ml salmon peptides and placed in a 37°C, 21% O2 and 5% CO2 cell culture incubator for 24 h of resugar and reoxygenation;

[0063] Treatment group 3: cultured in a 37°C, 0.3% O2 ​​and 5% CO2 cell culture incubator for 6 h using sugar-free DMEM medium, then replaced with a high-glucose medium containing 40 μg / ml salmon peptides and placed in a 37°C, 21% O2 and 5% CO2 cell culture incubator for 24 h of resugar and reoxygenation;

[0064] Treatment group 4: cultured in a cell culture incubator at 37°C, 0.3% O2 ​​and 5% CO2 for 6 h using sugar-free DMEM medium, then replaced with high-glucose medium containing 80 μg / ml salmon peptides, and cultured in a cell culture incubator at 37°C, 21% O2 and 5% CO2 for 24 h with resugar and reoxygenation;

[0065] Treatment group 5: cultured in a 37°C, 0.3% O2 ​​and 5% CO2 cell culture incubator for 6 h using sugar-free DMEM medium, then replaced with a high-glucose medium containing 160 μg / ml salmon peptides and placed in a 37°C, 21O2 and 5% CO2 cell culture incubator for 24 h of resugar and reoxygenation;

[0066] After the incubation, 20 μL of MTT solution (pH=7.4) was added to each well, and the cells were incubated for 4 hours at 37°C and 5% CO2. Then, the culture supernatant in the well was carefully removed, 150 μL of DMSO was added, and the cells were shaken for 10 minutes, and then placed in a microplate reader to detect the absorbance at OD570 and calculate the relative cell survival rate.

[0067] exist Figure 2The relative cell survival rate of the oxygen-glucose deprivation / reoxygenation group was 69.03%. Among the treatment groups, the relative cell survival rate of treatment group 1 was 69.59%, the relative cell survival rate of treatment group 2 was 70.32%, the relative cell survival rate of treatment group 3 was 71.29%, the relative cell survival rate of treatment group 4 was 75.99%, and the relative cell survival rate of treatment group 5 was 80.06%.

[0068] From the above results, it can be observed that the relative cell survival rates of treatment groups 1-3 were improved to a certain extent compared with the oxygen-glucose deprivation / re-glucose reoxygenation group, but the differences were not statistically significant. The relative cell survival rates of treatment groups 4 and 5 were higher than those of the oxygen-glucose deprivation / re-glucose reoxygenation group, and the differences met the statistical requirements, indicating that the use of 80 or 160 μg / ml salmon peptides to treat oxygen-glucose deprivation / re-glucose reoxygenation neurons can effectively improve the recovery ability of cells, and the effect of 160 μg / ml salmon peptides is more significant.

[0069] At the same time, it can be seen that although 160μg / ml salmon peptide can improve the cell recovery ability of the stroke cell model, the effect can only achieve a good effect. This shows that the use of salmon peptide alone can effectively treat stroke, but its effect needs to be further improved.

[0070] Example 3

[0071] Detection of the therapeutic effect of salmon peptide combined with edaravone on the mouse model of cerebral ischemia-reperfusion

[0072] 60 C57BL / 6 mice of about 8 months old, with an average weight of about 25g, half male and half female, were selected and adaptively raised for 3 days before the experiment. Then, the mice were randomly divided into 5 groups, 12 in each group, namely, sham operation group, model group, salmon peptide group, edaravone group and combination group (salmon peptide + edaravone), and the mice except the sham operation group were modeled with cerebral ischemia reperfusion model.

[0073] The detailed modeling process is as follows:

[0074] After the mice were anesthetized with sodium pentobarbital, a longitudinal incision was made in the midline of the neck to expose the right common carotid, external carotid and pterygopalatine arteries. The external carotid, pterygopalatine and common carotid arteries were ligated with silk thread at the proximal end, and the artery was temporarily clamped near the bifurcation.

[0075] Make a small incision about 4 mm away from the bifurcation of the common carotid artery, insert the nylon thread that has been melted into a ball at the top, remove the artery clamp, and slowly send the thread through the internal carotid artery to the skull to the starting point of the middle cerebral artery. The length is about 9 to 10 mm, and stop when you feel an obstruction.

[0076] Ligation was performed at the bifurcation, and the neck incision was sutured, leaving 4 mm of the thread plug stump. After ligation (ischemia) for 1.5 h, the nylon thread plug was loosened to achieve blood reflow (reperfusion). After MCAO / R surgery, the mice were resuscitated on a hot pad for 2 h, and then the model mice that met the experimental requirements were returned to a warm cage with food and water. The sham operation group did not insert nylon thread, and the rest of the operations were the same as the model mice.

[0077] 2 hours after surgery, the mice in the sham operation group and the model group were intravenously injected with 150 μl of normal saline twice; the salmon peptide group was injected with 150 μl of normal saline containing 160 μg / ml salmon peptide and 150 μl of normal saline without drug; the edaravone group was injected with 150 μl of normal saline containing 500 μg / ml edaravone and 150 μl of normal saline without drug; the combined group was injected with 150 μl of normal saline containing 160 μg / ml salmon peptide and 150 μl of normal saline containing 500 μg / ml edaravone; the drugs were administered once a day, for a total of 7 times.

[0078] (A) Neurological function scores were performed 7 days after treatment:

[0079] Zea Longa neurological function scoring criteria:

[0080] Rating 0:

[0081] Normal: The mice do not have any neurological damage and exhibit normal activities and behaviors.

[0082] Rating 1:

[0083] Mild injuries: Mice showed mild motor impairments, such as a slight unsteady gait or a slight leaning to one side when walking.

[0084] Rating 2:

[0085] Moderate impairment: Mice show significant motor impairment and are unable to walk normally. This is usually manifested by an inability to walk freely, an inability to stand in balance, or significant rotational movements.

[0086] Rating 3:

[0087] Severe Injury: The mouse is clearly unable to walk or exhibits severe paralysis. The mouse may have little or no movement.

[0088] Rating 4:

[0089] Complete injury: The mouse is completely paralyzed and loses most or all of its voluntary movement functions. It usually manifests as complete motor paralysis, inability to perform any activities, and may have difficulty breathing or appear to be in a dying state.

[0090] The results of the neurological deficit scores of mice are shown in Table 1.

[0091] Table 1 Neurological deficit scores in mice

[0092]

[0093] Note: a means P < 0.05 compared with the model group, b means P < 0.01 compared with the model group, c means P < 0.001 compared with the model group, d means P < 0.001 compared with the salmon peptide group, and e means P < 0.001 compared with the edaravone group.

[0094] From the results in Table 1, it can be seen that the score of the salmon peptide group is lower than that of the model group, indicating that the use of salmon peptide alone can effectively treat neurological deficits caused by ischemic stroke, further verifying that salmon peptide can be used to treat ischemic stroke.

[0095] Further observations revealed that compared with the use of salmon peptides or edaravone alone, the score of the combined group was significantly reduced, and the magnitude of the decrease was significantly higher than the theoretical sum of the two: compared with the model group, the score of the salmon peptide group decreased by 0.69, the score of the edaravone group decreased by 1.08, and the combined group decreased by 2.7. The theoretical effect of the sum of the two was a decrease of 1.77 compared with the model group, and the actual combined effect was 1.52 times the theoretical effect. This result shows that the combined use of salmon peptides and edaravone can produce a synergistic treatment for ischemic stroke. The possible reason is that ischemic stroke involves a variety of different mechanisms, and salmon peptides and edaravone produce a synergistic effect by acting on different mechanisms.

[0096] (B) TTC staining assay

[0097] After the neurological scoring, the mice were killed, the brain tissue was removed and placed on a mouse brain mold, and coronal sections were made every 2 mm from 2 mm behind the bregma of the frontal pole. The brain slices were placed in a freshly prepared 1% TTC solution, stained for 30 minutes in the dark, and then fixed in 4% paraformaldehyde. According to the formula, white is the infarct focus, and red is the normal brain tissue. The cerebral infarction area was measured and multiplied by the thickness to obtain the cerebral infarction volume. The percentage of the infarct focus in the total cerebral hemisphere was calculated to obtain the infarction percentage.

[0098] The percentage of cerebral infarction in mice is shown in Table 2.

[0099] Table 2 Percentage of cerebral infarction in mice

[0100]

[0101]

[0102] Note: c indicates P < 0.05 compared with the model group, d indicates P < 0.001 compared with the salmon peptide group, and e indicates P < 0.001 compared with the edaravone group.

[0103] From the results in Table 2, it can be seen that compared with the model group, the percentage of cerebral infarction in the salmon peptide group was reduced by 8.33%, the edaravone group was reduced by 10.8%, and the percentage of cerebral infarction in the combined group decreased more significantly, reaching 28.97%. This result further proves that drugs containing salmon peptides can significantly reduce the incidence of cerebral infarction in the treatment of ischemic stroke mice, thereby effectively alleviating the damage caused by cerebral ischemia.

[0104] At the same time, it can be seen that the effect of the combined group is significantly better than the theoretical additive effect of salmon peptide and edaravone (19.13%). This result shows that the combined use of salmon peptide and edaravone can synergistically reduce the incidence of cerebral infarction in ischemic stroke mice through multi-target treatment.

Claims

1. A drug for preventing and treating ischemic stroke, characterized in that: The drug consists of a salmon polypeptide and a pharmaceutically acceptable carrier; the amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.

1.

2. The drug according to claim 1, characterized in that The medicine is a liquid medicine, and the concentration of salmon polypeptide in the medicine is greater than or equal to 80 μg / ml.

3. The drug according to claim 2, characterized in that In the drug, the concentration of salmon polypeptide is 80 μg / ml-160 μg / ml; The pharmaceutically acceptable carrier is physiological saline, and the drug is administered by intravenous injection.

4. Use of a salmon polypeptide in the preparation of a drug for preventing and treating ischemic stroke, characterized in that: The amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.

1.

5. The use according to claim 4, characterized in that: The medicine is a liquid medicine prepared from physiological saline, the concentration of salmon polypeptide in the medicine is 80 μg / ml-160 μg / ml, and the administration method of the medicine is intravenous injection.

6. The use according to claim 4, characterized in that: The drug can reduce neurological deficits and cerebral infarction caused by ischemic stroke.

7. A pharmaceutical composition for treating ischemic stroke, characterized in that: Every 300 μl of the pharmaceutical composition is composed of 150 μl of a salmon polypeptide drug with a concentration of 160 μg / ml and 150 μl of an edaravone drug with a concentration of 500 μg / ml. The amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.

1.

8. The pharmaceutical composition according to claim 7, characterized in that The solvent of the salmon polypeptide drug and the edaravone drug is normal saline; The pharmaceutical composition is administered by intravenous injection; The pharmaceutical composition synergistically reduces neurological deficits and cerebral infarction caused by ischemic stroke.

9. Use of a composition in the preparation of a drug for treating ischemic stroke, characterized in that: Each 300 μl of the composition consists of 150 μl of a salmon polypeptide solution with a concentration of 160 μg / ml and 150 μl of an edaravone solution with a concentration of 500 μg / ml. The amino acid sequence of the salmon polypeptide is shown in SEQ ID NO.

1.

10. The use according to claim 9, characterized in that: The solvent of the salmon polypeptide solution and the edaravone solution is normal saline; The drug is administered by intravenous injection; The drug synergistically reduces neurological deficits and cerebral infarction caused by ischemic stroke through salmon peptides and edaravone.

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