Application of sodium tyrosol sulfate and derivative tyrosol compound in preparation of brain health product

Abstract

The invention belongs to the technical field of biological medicines, and provides application of sodium tyrosol sulfate and a derivative tyrosol compound in preparation of brain health products. The structure of the sodium tyrosol sulfate and the derivative tyrosol compound is shown as a formula I. The sodium tyrosol sulfate and the derivative tyrosol compound can effectively reduce the infarction area after cerebral ischemia and relieve encephaledema caused by cerebral ischemia, and have wide application in the aspects of resisting cerebral ischemia and improving encephaledema and cerebral infarction caused by cerebral ischemia. Meanwhile, learning and memory abilities can be effectively improved, brain function recovery is promoted, and the traditional Chinese medicine composition can be widely applied to treatment of behavior / cognitive dysfunction diseases such as cerebral trauma, cerebrovascular accidents, Alzheimer's disease and Parkinson's disease. And the formula I of the # imgabs0 # is shown in the specification.

Description

Technical Field

[0001] The present invention belongs to the field of biomedicine technology, and particularly relates to the application of sodium tyrosol sulfate and derived tyrosol compounds in the preparation of brain health products. Background Art

[0002] Cognitive impairment is a common complication of various chronic diseases, including stroke, cerebral palsy, and diabetes. It has a high incidence, and early identification and intervention are crucial for recovery. Clinical treatments include increasing cerebral blood flow to alleviate cerebral ischemia, improving brain oxygen supply, inhibiting lipid peroxidation, and scavenging free radicals. Commonly used medications include dihydroergotamine preparations, neurotrophic drugs, and calcium antagonists, but evidence-based medical evidence is still lacking.

[0003] Tyrosol (p-hydroxyphenylethanol) was first isolated and discovered from olive oil. It is one of the important antioxidant components in olive oil, present in relatively high concentrations. It is also widely found in plants such as Rhodiola rosea, Ligustrum lucidum, and grape seeds. It is the aglycone component of salidroside, the main active ingredient in the traditional Chinese medicine Rhodiola rosea. Its chemical structure exhibits certain reactive properties, including substitution reactions on the benzene ring and the hydroxyl group. A series of tyrosol derivatives can be prepared through biosynthesis and chemical synthesis. Hydroxytyrosol has been the most extensively studied of these compounds.

[0004] For example, Chinese invention patent application CN101674817A discloses that hydroxytyrosol can enhance chondrocyte proliferation and increase extracellular matrix synthesis, and also serves as an effective micronutrient for cartilage repair and regeneration. Chinese invention patent CN103961338B discloses the use of hydroxytyrosol in combating doxorubicin-induced cardiotoxicity. Hydroxytyrosol demonstrates significant resistance to doxorubicin-induced cardiotoxicity and exhibits a strong protective effect on cardiomyocytes.

[0005] For example, Chinese invention patent application CN105213356A discloses the use of hydroxytyrosol in the preparation of drugs against vascular dementia, and verifies that hydroxytyrosol can alleviate neurological deficits, reduce the scope of cerebral infarction and the degree of cerebral edema, effectively inhibit the morphological changes of neural tissue in rats with vascular dementia, improve the cognitive, learning and memory abilities of rats with vascular dementia, and alleviate dementia symptoms.

[0006] However, tyrosol or hydroxytyrosol has limited efficacy in improving cognitive impairment caused by cerebral ischemia. Studies on tyrosol derivatives without a hydroxyl group at the 3rd position of the benzene ring are relatively limited. Studies have shown that tyrosol and its derivatives, such as sodium tyrosol sulfate, tyrosol glucuronic acid, and tyrosol fatty acid esters, also possess anti-inflammatory and antioxidant activities, but their applications remain to be further explored. Summary of the Invention

[0007] To address the above-mentioned issues, the present invention provides the use of sodium tyrosol sulfate and its derivatives in the preparation of brain health products. This invention proposes, for the first time, the use of sodium tyrosol sulfate and its derivatives in health foods or pharmaceutical preparations for improving brain function, such as combating cerebral ischemia and hypoxia, improving learning and memory, and addressing cerebral edema caused by cerebral ischemia.

[0008] To achieve the above object, the technical solution of the present invention is as follows: The present invention provides the use of sodium tyrosol sulfate and derived tyrosol compounds in the preparation of brain health products.

[0009] Furthermore, the sodium tyrosol sulfate and the derived tyrosol compounds have the following general structural formula:

[0010] Wherein, R1 (phenolic hydroxyl substituent) is a C1-C18 alkyl group, -COR', -SO3Na, a saccharyl group or a glucuronic acid; R2 (alcoholic hydroxyl substituent) is H or -COR''; and R' and R'' are each independently selected from any one of a C1-C18 alkyl group (i.e., -COR' is specifically a tyrosol ester compound formed by formic acid, acetic acid, fumaric acid, succinic acid, tartaric acid, caprylic acid, capric acid, lauric acid, myristic acid, palmitic acid, stearic acid, arachidic acid, etc. with a phenolic hydroxyl group; -COR'' is specifically a tyrosol ester compound formed by formic acid, acetic acid, fumaric acid, succinic acid, tartaric acid, caprylic acid, capric acid, lauric acid, myristic acid, palmitic acid, stearic acid, arachidic acid, etc. with an alcoholic hydroxyl group).

[0011] Furthermore, the glycosyl group is a group formed by glucose, galactose, arabinose or rhamnose without a hydroxyl group (ie, -OR1 is a glycoside formed by glucose, galactose, arabinose or rhamnose and the phenolic hydroxyl group of tyrosol).

[0012] In some embodiments of the present invention, the sodium tyrosol sulfate and the derived tyrosol compounds are compounds in which only the alcoholic hydroxyl position is substituted, that is, in the general formula, R1 is any one of a C1-C18 alkyl group, -COR', -SO3Na, a saccharyl group or glucuronic acid; R2 is H, wherein R' is a C1-C18 alkyl group.

[0013] Preferably: 、 、 、 or .

[0014] In other embodiments of the present invention, the sodium tyrosol sulfate and the derived tyrosol compounds are compounds in which both the alcoholic hydroxyl group and the phenolic hydroxyl group are substituted, that is, in the general formula, R1 is any one of a C1-C18 alkyl, -COR', -SO3Na, a saccharyl group or glucuronic acid; and R2 is -COR''.

[0015] Preferably, R1 is -SO3Na; R2 is -COR''; and R'' is any one of a C1-C18 alkyl group (i.e., -COR' specifically includes: tyrosol ester compounds formed by formic acid, acetic acid, fumaric acid, succinic acid, tartaric acid, caprylic acid, capric acid, lauric acid, myristic acid, palmitic acid, stearic acid, arachidic acid, etc. and an alcoholic hydroxyl group).

[0016] More preferably: .

[0017] Furthermore, the brain health product includes any one of products for resisting cerebral ischemia, improving cerebral edema caused by cerebral ischemia, improving cerebral infarction caused by cerebral ischemia, resisting cerebral hypoxia and improving behavioral / cognitive dysfunction.

[0018] Furthermore, the behavioral / cognitive dysfunction includes any one of brain trauma, cerebrovascular accident, Alzheimer's disease and Parkinson's disease.

[0019] Furthermore, the brain health product is a pharmaceutical preparation or a health food.

[0020] The present invention also provides a pharmaceutical preparation, wherein the active ingredients of the pharmaceutical preparation include sodium tyrosol sulfate and a tyrosol-derived compound; the sodium tyrosol sulfate and the tyrosol-derived compound have the following general structural formula:

[0021] Wherein, R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid; R2 is H or -COR''; R' and R'' are each independently selected from any one of the C1-C18 alkyl groups; the glycosyl is a group formed by losing a hydroxyl group of glucose, galactose, arabinose or rhamnose.

[0022] Furthermore, the pharmaceutical preparation also includes one or more of pharmaceutically acceptable salts, solvates, hydrates and polymorphs of the derived tyrosol compound.

[0023] Furthermore, the pharmaceutical preparation also includes medically acceptable excipients.

[0024] Furthermore, the pharmaceutical preparation is any one of tablets, capsules, pills, granules, powders, ointments, mixtures, suspensions, injections and transdermal absorbers.

[0025] The present invention also provides a brain health food, which comprises sodium tyrosol sulfate and a tyrosol-derived compound; the sodium tyrosol sulfate and the tyrosol-derived compound have the following general structural formula:

[0026] Wherein, R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid; R2 is H or -COR''; R' and R'' are each independently selected from any one of the C1-C18 alkyl groups; the glycosyl is a group formed by losing a hydroxyl group of glucose, galactose, arabinose or rhamnose.

[0027] Furthermore, the brain health food also includes food-acceptable auxiliary materials.

[0028] Compared with the prior art, the present invention has the following beneficial effects: Compared with tyrosol, the sodium tyrosol sulfate and its derivative tyrosol compounds (especially the derivative tyrosol compounds C and E containing sulfate groups) provided by the present invention are more effective in resisting cerebral ischemia, alleviating cerebral infarction, reducing cerebral edema, resisting cerebral hypoxia, and improving learning and memory. They are widely used in products for resisting cerebral ischemia, resisting cerebral hypoxia, improving cerebral edema and cerebral infarction caused by cerebral ischemia, and improving behavioral / cognitive dysfunction. BRIEF DESCRIPTION OF THE DRAWINGS

[0029] Figure 1 The results show the effect of compound C on the neurobehavioral score of MCAO rats; Figure 2 The results show the effect of compound C on cerebral infarction in MCAO rats; Figure 3 The results show the effect of compound C on brain edema in MCAO rats; Figure 4 The results show the effect of compound C on the escape latency of MCAO rats in the Morris water maze test; Figure 5 The results show the effect of compound C on the number of platform shuttles in MCAO rats in the Morris water maze test; Figure 6 The results show the effect of compound C on the time ratio of MCAO rats in the target quadrant during spatial exploration in the Morris water maze test. Figure 7 This is the swimming route diagram of the escape latency of rats in the Sham group, MCAO group and drug-treated group (Compound C) on the 5th day of the Morris water maze experiment; Figure 8 This is the result of the protective effect of sodium tyrosol sulfate and its derivative tyrosol compounds on neurons; compared with the normal group, *p <0.05, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01; Figure 9 The results show that sodium tyrosol sulfate and its derivative tyrosol compounds have protective effects on astrocytes; compared with the normal group, * p <0.05, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01. DETAILED DESCRIPTION

[0030] To make the purpose, technical solutions, and advantages of the embodiments of the present invention more clear, the technical solutions in the embodiments of the present invention will be clearly and completely described below. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without making creative efforts are within the scope of protection of the present invention.

[0031] The present invention uses compounds AH in Table 1 as experimental drugs to verify the brain health-improving effects of sodium tyrosol sulfate and its derivative tyrosol compounds.

[0032] Table 1 Structural information of sodium tyrosol sulfate and its derivative tyrosol compounds

[0033] Compound E was prepared according to the method reported in the literature Exploring the Biological Potential of Hydroxytyrosoland Derivatives: Synthetic Strategies and Evaluation of Antiproliferative, Antioxidant, and Antimicrobial Activities (J. Agric. Food Chem. 2024, 72, 48, 26699-26710).

[0034] Experimental Example 1: Study on the protective effect of sodium tyrosol sulfate and its derivative tyrosol compounds on the brain nerves of rats with middle cerebral artery occlusion (MCAO) model (1) Experimental animals: Male SD rats, SPF grade, weighing 220±10 g.

[0035] (2) Experimental method: Anesthesia was performed by intraperitoneal injection of 4% chloral hydrate, and a suture was inserted into the internal carotid artery. Reperfusion was performed 90 minutes after the suture insertion. Blood could enter the middle cerebral artery again through the circle of Willis, achieving reperfusion of brain blood vessels.

[0036] The experimental rats were scored twice according to the principle of random blinding. The first score was performed 2 hours after the rats woke up after surgery, and the second score was performed 24 hours later. The 5-point scoring system of Longa et al. is as follows: 0 points: normal, no neurological signs; 1 point: the animal cannot fully extend its left forelimb; 2 points: The animal's left limbs are paralyzed, it circles to the left when walking, and it chases its tail; 3 points: The animal walks to the left and falls, or the animal cannot stand or roll over; 4 points: No spontaneous activity, impaired consciousness.

[0037] A neurological deficit score of 1-3 points was considered a successful model. Except for the sham-operated group, animals with a score of 0 (unsuccessful model) or 4 (excessive injury, death within 24 hours) in each group were excluded. Animals from the excluded groups were supplemented in subsequent experiments to ensure the number of animals in each group.

[0038] (3) Experimental grouping and drug administration: The rats with successful modeling were randomly divided into 10 groups. After the insertion of the thread plug, the rats were immediately given intraperitoneal injections of low-dose (10 mg / kg) and high-dose (20 mg / kg) of compound AH (prepared with normal saline to a concentration of 10 mg / ml), respectively. The sham operation group (Sham) and the model group (MCAO) were given an equal amount of normal saline and were killed 24 hours later.

[0039] (4) Experimental results: 4.1 The results of neurobehavioral scores of MCAO rats are shown in Table 2. Among them, the neurobehavioral scores of the sham group, model group, and low-dose and high-dose compound C groups after 2h and 24h were compared. Figure 1 shown.

[0040] Table 2 Neurobehavioral score results of rats in each group ( , n=10)

[0041] Note: Compared with the sham operation group, ** p <0.01; compared with the model group, # p <0.05,## p <0.01.

[0042] As can be seen from the table above: compared with the MCAO group, compound BH can reduce the neurobehavioral score of rats with cerebral ischemia, among which compound C and compound E at a dose of 10 mg / kg are significantly better than compound A in reducing the neurobehavioral score of rats with cerebral ischemia after 2 hours of action ( p <0.01).

[0043] 4.2 Cerebral infarction area: 24 h after MCAO, rats were anesthetized with intraperitoneal injection of chloral hydrate and quickly decapitated. The brain was removed by craniotomy. The blood and cerebrospinal fluid on the surface were gently absorbed with filter paper. The brain was promptly cut into 5 slices along the coronal axis. The brain slices were then stained with 1% TTC, and photos of the distribution of infarct foci in the brain slices were taken. The TTC staining results of the sham operation group, model group, and low-dose and high-dose compound C groups are shown in Figure 2. Figure 2 As shown in Figure A; Image Pro Plus software was used to plot the ischemic area of each brain slice and the area of the whole brain slice, and the cerebral infarction area was calculated. Cerebral infarction area (%) = cerebral infarction area / whole brain slice area × 100%. The results are shown in Table 3. Among them, TCC staining images of the sham operation group, MCAO model group, and low-dose and high-dose compound C groups are shown in Figure 2 As shown in Figure B.

[0044] Table 3 Results of cerebral infarction area in rats in each group ( , n=10)

[0045] Note: Compared with the sham operation group, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01.

[0046] Depend on Figure 2 As can be seen from the table above: there are significant cerebral infarction foci after cerebral ischemia. Compared with the MCAO group, compound BH can reduce the infarction area. Among them, compound CH can significantly reduce the cerebral infarction area at a dose of 10 mg / kg ( p <0.05 or p <0.01), it can be seen that compounds CH have better effects in improving cerebral infarction, especially compound E.

[0047] Experimental Example 2: Study on the improvement of brain edema in rats with middle cerebral artery occlusion (MCAO) model by sodium tyrosol sulfate and its derivative tyrosol compounds The experimental animals, experimental methods, and grouping and drug administration were the same as those in Experimental Example 1.

[0048] The rats were killed 24 hours after modeling and drug administration. The whole brain was weighed and weighed in wet weight. The dry weight was weighed after baking at 60℃ for 24 hours. The water weight of brain tissue was calculated by wet-dry method. The rat body weight and whole brain wet weight (accurate to 0.001g) were obtained by weighing with an electronic balance. Brain index (%) = whole brain wet weight / rat body weight × 100%; brain water content (%) = (wet weight - dry weight) / wet weight × 100%; the results are shown in Table 4. Among them, the comparison of brain edema in the sham operation group, model group, low-dose group and high-dose group of compound C was as follows: Figure 3 shown.

[0049] Table 4 Brain index and brain water content of rats in each group ( , n=10)

[0050] Note: Compared with the sham operation group, ** p <0.001; compared with the model group, # p <0.05, ## p <0.01.

[0051] As can be seen from the table above, compared with the MCAO group, compound CH showed different degrees of effect in reducing brain edema caused by local cerebral ischemia, and at the same time reduced the brain index; among them, compounds C, D, E, and H were better (at a dose of 10 mg / kg, p <0.01), followed by compounds F and G.

[0052] Experimental Example 3: Effects of sodium tyrosol sulfate and its derivative tyrosol compounds on learning and memory in rats with multiple cerebral infarctions (1) Experimental animals: Male SD rats, SPF grade, weighing 220±10 g.

[0053] (2) Experimental method: Morris water maze test, anesthetized with 4% chloral hydrate intraperitoneally, 0.2 mL of fluorescent microspheres were injected from the external carotid artery to the internal carotid artery with a syringe, and then the arterial clamp was released. At this time, the fluorescent microspheres were dispersed from the internal carotid artery to the various arteries of the brain with the blood flow. After the operation, low doses (10 mg / kg) and high doses (20 mg / kg) of compound AH (prepared with saline to a concentration of 10 mg / ml) were intraperitoneally injected for 28 consecutive days. After 28 days, acquisition training of the Morris water maze test was performed. During the training test, each rat was trained in quadrants one, two, three, and four every day, and the order was randomized every day.

[0054] At the beginning of each quadrant trial, rats were placed in the water, facing one side of the pool wall. Once in the water, rats were allowed 90 seconds to locate the escape platform. If they failed to find it after 120 seconds, they were guided to the platform. Once on the platform, rats were allowed to rest for 10 seconds (if less than 10 seconds, they needed to be guided again) while observing spatial cues on the platform. A video tracking system was used to record the time and distance traveled before the rats found the hidden platform. The rats were then removed from the water maze. After completing training in the first quadrant, they were released into a new quadrant, ensuring that each rat had at least 5 minutes of rest to recover its body temperature and strength. The water maze exploration experiment was repeated for five consecutive days, with the sixth day conducting the experiment. The platform was removed, and rats were placed in the third quadrant. The distance and time taken for the rats to swim through the first quadrant were recorded over a 90-second period. During this period, the rats, instinctively avoiding water for survival, would search for the escape platform based on their memory from the acquisition experiment. During the acquisition training, the escape platform was placed in the center of the first quadrant.

[0055] (3) Experimental results: The results of the Morris water maze test are shown in Tables 5 to 7. The escape latency, platform shuttle times, time ratio in the target quadrant of the spatial exploration test, and the swimming route diagram of the escape latency of rats in the sham operation group, model group, low-dose group, and high-dose group of each compound in the Morris water maze test are shown in Tables 5 to 7. Figure 4-Figure 7 .

[0056] Table 5 Escape latency results of rats in Morris water maze test ( , n=10)

[0057] Note: Compared with the sham operation group, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01.

[0058] Table 6 Effects of sodium tyrosol sulfate and its derivative tyrosol compounds on the number of platform shuttles in rats with cerebral ischemia ( , n=10)

[0059] Note: Compared with the sham operation group, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01.

[0060] Table 7 Effects of sodium tyrosol sulfate and its derivative tyrosol compounds on the time ratio of rats with cerebral ischemia in the target quadrant ( , n=10)

[0061] Note: Compared with the sham operation group, ** p <0.01; compared with the model group, # p <0.05, ## p <0.01.

[0062] The above results show that as the test time increases, the escape latency of the MCAO group rats is significantly longer than that of the Sham group (starting from the first day, p <0.01). Compared with the MCAO group, the escape latency of rats in each drug-treated group (except compound A) was significantly shortened with the increase in the number of training times. At the dose of 20 mg / kg, the escape latency of rats in each group was significantly different from that of the model group from the second day ( p <0.05), among which compounds C and E were the best, followed by compounds B and D. The escape latency of rats in the groups treated with compounds F, G, and H was also shortened to varying degrees.

[0063] In addition, compared with the MCAO group, except for the low-dose group of compound A and compound B, the number of platform shuttles of rats in other drug-treated groups was significantly reduced, and the percentage of time in the platform quadrant was significantly increased. The action trends of each compound showed a similar trend in reducing the escape latency. Overall, compounds C, D, and E were the best, followed by F, G, and H.

[0064] Experimental Example 4: Protective Effects of Sodium Tyrosol Sulfate and Its Derivative Tyrosol Compounds on Neurons (1) Experimental method: Human neuroblastoma SH-SY5Y cells were used for oxygen glucose deprivation (OGD) induction experiments.

[0065] OGD-induced model: Sugar-free DMEM medium, pre-saturated with a 95% N₂-5% CO₂ mixture for 15 minutes, was added to each well of a 96-well plate. The plate was then placed in a hypoxic chamber and aerated with a 95% N₂-5% CO₂ mixture. An oxygen meter monitored the outlet oxygen concentration in real time. When the oxygen concentration reached 1%, ventilation was stopped, the inlet and outlet tubes were closed, and the hypoxic chamber was placed in a cell culture incubator for 4 hours of hypoxic culture. Reoxygenation: The hypoxic chamber was opened, the 96-well plate was removed, the hypoxic solution was aspirated, and sugar-free AMEM medium was added to each well. The cells were then placed in an incubator and cultured for a further 2 hours. Sugar-free DMEM medium without hypoxia-reoxygenation treatment served as a blank control (normal group). Except for the model group, the drug-treated groups were administered 25μM, 50μM, and 100μM of Compound AH simultaneously with hypoxia.

[0066] (2) Experimental results: like Figure 8 As shown in Figure 2, after OGD induction, compared with the model group, compound E at a concentration of 25 μM can significantly increase the activity of damaged cells ( p <0.01), compounds C, F, G, and H at 50 μM can significantly enhance the activity of damaged cells ( p <0.05); Compounds A, B and D at a high concentration of 100 μM had a significant improvement effect on OGD-induced SH-SY5Y cell damage ( p <0.05). The results showed that E had the strongest neuroprotective effect, followed by C, F, G, and H, but the effective concentrations of these ingredients were lower than those of tyrosol and salidroside.

[0067] Example 5: Protective Effects of Sodium Tyrosol Sulfate and Its Derivative Tyrosol Compounds on Astrocytes (1) Experimental method: Human astrocytes SVGp12 were used for glucose-oxygen deprivation (OGD) induction experiments. The method was the same as that of Experimental Example 4.

[0068] (2) Experimental results: like Figure 9 As shown in Figure 2, after OGD induction, both compound C and compound D at 50 μM can significantly increase the activity of damaged cells ( p <0.01), compound E at 50 μM significantly increased the activity of damaged cells ( p <0.05); A, B, G and F have a significant protective effect on astrocytes against hypoxia and hypoxia damage at 100 μM ( p <0.05). The above results show that compounds C, D and E of the present invention have better protective effects on astrocytes.

[0069] Finally, it should be noted that the above content is only used to illustrate the technical solution of the present invention, rather than to limit the scope of protection of the present invention. Simple modifications or equivalent substitutions of the technical solution of the present invention by ordinary technicians in this field do not deviate from the essence and scope of the technical solution of the present invention.

Claims

1. Application of sodium tyrosol sulfate and its derivative tyrosol compounds in the preparation of brain health products, characterized in that: The sodium tyrosol sulfate and the derived tyrosol compounds have the following general structural formula: Wherein, R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid; R2 is H or -COR''; R' and R'' are each independently selected from any one of the C1-C18 alkyl groups; the glycosyl is a group formed by losing a hydroxyl group of glucose, galactose, arabinose or rhamnose.

2. The use according to claim 1, characterized in that R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid, and R2 is H, wherein R' is a C1-C18 alkyl; Or R1 is -SO3Na; R2 is -COR''; wherein R'' is a C1-C18 alkyl group.

3. The use according to claim 2, characterized in that The sodium tyrosol sulfate and the derived tyrosol compound are any one of the following structures: 、 、 、 、 or .

4. The use according to claim 1, characterized in that The brain health product includes any one of products for resisting cerebral ischemia, improving cerebral edema caused by cerebral ischemia, improving cerebral infarction caused by cerebral ischemia, and improving behavioral / cognitive dysfunction.

5. The use according to claim 4, characterized in that The behavioral / cognitive dysfunction includes any one of brain trauma, cerebrovascular accident, Alzheimer's disease and Parkinson's disease.

6. The use according to any one of claims 1 to 5, characterized in that: The brain health product is a pharmaceutical preparation or a health food.

7. A pharmaceutical preparation, characterized in that The active ingredients of the pharmaceutical preparation include one or more of sodium tyrosol sulfate and its derivative tyrosol compounds; the sodium tyrosol sulfate and its derivative tyrosol compounds have the following general structural formula: Wherein, R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid; R2 is H or -COR''; R' and R'' are each independently selected from any one of the C1-C18 alkyl groups; the glycosyl is a group formed by losing a hydroxyl group of glucose, galactose, arabinose or rhamnose.

8. The pharmaceutical preparation according to claim 7, characterized in that The sodium tyrosol sulfate and the derived tyrosol compounds are one or more of their pharmaceutically acceptable salts, solvates, hydrates and polymorphs.

9. The pharmaceutical preparation according to claim 7, characterized in that The pharmaceutical preparation is any one of tablets, capsules, pills, granules, powders, ointments, mixtures, suspensions, injections and transdermal absorbers.

10. A brain health food, characterized in that: It comprises sodium tyrosol sulfate and its derivative tyrosol compound and food-acceptable auxiliary materials; the sodium tyrosol sulfate and its derivative tyrosol compound have the following general structural formula: Wherein, R1 is a C1-C18 alkyl, -COR', -SO3Na, a glycosyl or glucuronic acid; R2 is H or -COR''; R' and R'' are each independently selected from any one of the C1-C18 alkyl groups; the glycosyl is a group formed by losing a hydroxyl group of glucose, galactose, arabinose or rhamnose.

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