CN114288285A - Application of epigallocatechin gallate in preparing medicine for preventing or treating systemic poisoning of medusa toxin - Google Patents

Abstract

The invention relates to the field of biological medicine, in particular to application of epigallocatechin gallate (EGCG) in preparing a medicine for preventing or treating systemic poisoning caused by jellyfish toxin. The invention provides a new application of EGCG, EGCG injection administration can play an obvious role in preventing and treating jellyfish toxin systemic poisoning animal models, and experimental results show that EGCG injection administration can effectively prevent and treat jellyfish toxin systemic poisoning, so that an effective candidate drug is provided for developing a medicine for preventing or treating jellyfish sting systemic poisoning, and a reference is provided for clinical research of new application of the medicine.

Description

Application of epigallocatechin gallate in preparing medicine for preventing or treating systemic poisoning of medusa toxin

Technical Field

The invention relates to the field of biological medicine, in particular to application of epigallocatechin gallate (EGCG) in preparing a medicine for preventing or treating medusa toxin systemic poisoning.

Background

The jellyfishes are low-grade invertebrate zooplankton in aquatic environment and have the characteristics of multiple types, large quantity, wide distribution and the like. Under the influence of global warming, over-fishing, biodiversity change and other factors, jellyfish outbreak frequently occurs in various sea areas in the world, and the safety and health of economic development and sea-related operators in coastal areas are seriously damaged.

In general, jellyfish stings cause local symptoms such as pain, flagellate red swelling or pruritus immediately; when the toxin is further absorbed into the blood, general symptoms such as nausea, vomiting or headache can occur; if a large amount of toxins enter the body, acute lethal symptoms such as dyspnea, sudden cardiac arrest, and liver and kidney failure may also occur. The complex and diverse toxicosis symptoms caused by jellyfish sting are mainly caused by jellyfish toxin, and the jellyfish toxin is found to have hemolytic toxicity, cardiovascular toxicity, neurotoxicity, skin and muscle toxicity and various enzyme activities. Hemolytic toxicity and enzyme activity commonly exist in the jellyfish toxin, are main reasons of symptoms such as local blister, hemolysis and multi-organ injury after jellyfish sting, and can also aggravate cardiotoxicity of the jellyfish toxin to cause death symptoms such as acute pulmonary edema and respiratory and cardiac arrest. At present, the treatment measures of jellyfish sting are mainly symptomatic treatment, and no specific antibacterial drug with definite curative effect exists.

Epigallocatechin gallate (EGCG) with molecular formula of C₂₂H₁₈O₁₁The catechin monomer is separated from tea leaves, is the main active and water-soluble component of green tea, accounts for about 50-70% of the total polyphenol content of green tea, and has almost no toxic action on normal human bodies. A large number of experiments and epidemiological researches show that EGCG has the biological activities of resisting tumor, oxidation, bacteria, ultraviolet radiation and the like, and can prevent various chronic diseases, such as heart disease, diabetes and neurodegenerationType diseases and cancers, etc. At present, catechin is widely applied to a plurality of fields such as food, daily necessities, health care products, medicines and the like. For example, the catechin has good bactericidal effect, so that the catechin can be widely added into health care products to play roles in resisting decayed teeth and inhibiting bacteria; in view of the good anti-tumor and anti-atherosclerosis effects of catechin, catechin is also used for the adjuvant treatment of various diseases.

To date, no relevant reports on the use of EGCG for the prevention or treatment of systemic toxicity of aequorin have been found.

Disclosure of Invention

The invention aims to provide a new medical application of epigallocatechin gallate (EGCG), in particular to an application of EGCG injection administration in preventing or treating medusa toxin (NnV) systemic poisoning.

The research of the invention finds that the EGCG injection administration can effectively antagonize the general poisoning effect of the aequorin and reduce the death rate of poisoned mice. The discovery not only widens the application range of EGCG, but also provides reference for treating the poisoning caused by jellyfish sting.

In order to realize the purpose, the invention adopts the following technical scheme:

(1) and establishing an animal model. Mice were injected intravenously with different doses of NnV (0.35 mg/kg-0.6 mg/kg) and observed for symptoms of intoxication and survival. When the toxin dose reaches 0.5mg/kg, the poisoned mice have symptoms of tachypnea, accelerated heartbeat, hypodynamia, cachexia, crouching and the like at the early stage, and then gradually have convulsion and death, and the death rate is 100 percent within 12 h. Therefore, the invention selects the dose to make a mouse model of the systemic toxicity of the aequorin.

(2) The EGCG has effect in preventing systemic poisoning due to jellyfish toxin. Different doses of EGCG (10 mg/kg-100 mg/kg) and NnV (0.5mg/kg) were pre-incubated for half a minute, and then the mice were administered into the tail vein. The result shows that when the dose of EGCG is more than or equal to 20mg/kg, the symptoms of cachexia, crouching, labored state and the like of the mice are obviously improved, and the mice survive for 7 days. Then NnV 0.5.5 mg/kg and EGCG 20mg/kg are selected for next pathological observation, a toxin group (NnV), a negative control group (normal saline) and a drug treatment group (EGCG + NnV) are arranged, and the heart, the lung, the liver and the kidney of the mouse are respectively taken for histopathological examination 10min and 1h after administration. In addition, the toxin dose is reduced to 0.42mg/kg, a toxin group, a negative control group and a drug treatment group are also arranged, and the heart, the lung, the liver and the kidney of the mouse are taken 12 hours after the drug administration for histopathological examination. The results show that extensive liver lobular diffuse bleeding, liver cell swelling, liver cell cord rupture and blood stasis of the heart appear in the early poisoning stage of the toxin group mice; advanced liver lesions are more severe with bridging necrosis between the regions of the junction, coagulative necrosis of hepatocytes and inflammatory cell infiltration. The pathological changes are not found in EGCG treatment groups.

(3) Antagonism of hemolytic activity of NnV by EGCG. Hemolytic components of aequorin rapidly initiate erythrolysis, produce large amounts of potassium and lactic acid causing hyperkalemia and acidemia, and aggravate cardiovascular toxicity and myotoxicity of aequorin, and thus hemolytic toxicity is also a major cause of acute death after systemic toxicity of aequorin. In vitro hemolysis experiment shows that NnV has significant hemolysis activity, and when the toxin concentration is 0.05. mu.g/ml, the hemolysis rate reaches 84.34%. When 0.05mg/ml of EGCG is added into a hemolysis system and NnV is added, the hemolysis rate is remarkably reduced, which indicates that EGCG can remarkably inhibit NnV hemolysis.

(4) Therapeutic effects of EGCG on systemic toxicity of aequorin. Mouse tail vein injection NnV (0.5mg/kg) is used for establishing a model of jellyfish toxin systemic poisoning. EGCG (20mg/kg) was then injected intravenously at various intervals and mice were observed for signs of toxicity and survival. The result shows that EGCG can play a good role in treatment within 5min after the poisoning of the mice, and the mice almost completely survive; EGCG can play a certain treatment effect after being given for 5-10 min, the survival time of the mice is obviously prolonged, and half of the mice can survive; after 10min, EGCG was administered, although the survival time of the mice was somewhat prolonged, the survival rate of the mice could not be improved.

Based on the technical scheme. In a first aspect of the invention, there is provided the use of epigallocatechin gallate (EGCG) in the manufacture of a medicament for the prevention or treatment of systemic poisoning by aequorin.

The molecular formula of the EGCG is C₂₂H₁₈O₁₁The structure is shown as the following formula I:

further, the drug for preventing or treating the systemic toxicity of the aequorin is EGCG as the only active ingredient or a pharmaceutical composition containing the EGCG.

Furthermore, the medicament for preventing or treating the aequorin systemic poisoning is an injection.

Further, the injection is prepared by adding 0.5g of the above-mentioned compound to 50ml of 0.9% sodium chloride solution.

Further, the dosage of EGCG is 20 mg/kg.

Furthermore, the administration time of the medicine is within 5min after the aequorin is poisoned.

Furthermore, the EGCG greatly improves the survival rate of the jellyfish toxin after poisoning and obviously improves the blood pressure drop after poisoning; remarkably inhibiting the hemolytic activity of the aequorin; obviously improve early heart and liver injury and late liver and kidney injury caused by the jellyfish toxin.

In a second aspect of the present invention, there is provided a medicament for preventing or treating systemic toxicity of aequorin, wherein the medicament comprises EGCG as the sole active ingredient or a pharmaceutical composition comprising EGCG.

Further, the medicine is injection, and 0.5g of EGCG is added into 50ml of 0.9% sodium chloride solution. The administration dosage is 20mg/kg, and can be changed according to the disease condition.

Experiments prove that the EGCG and the lethal dose of the aequorin (NnV) are injected and administered after being pre-hatched, so that the survival rate of mice can be greatly improved. In vitro hemolytic test shows that EGCG can obviously inhibit the hemolytic activity of NnV. The pathological examination result shows that EGCG and NnV can obviously improve early heart and liver injury and late liver and kidney injury of mice caused by the aequorin after pre-hatching and injection administration.

The treatment effect of EGCG on the general poisoning of the aequorin is observed by establishing an aequorin mouse poisoning model and injecting EGCG at different time intervals after poisoning. The result shows that the survival rate of the poisoned mice is obviously improved by using the EGCG as the therapeutic drug, and the earlier the drug is administrated after the poisoning, the better the therapeutic effect is.

Compared with the prior art, the invention has the advantages that:

1. the invention provides a new application of EGCG, EGCG injection administration can play a role in obviously preventing and treating a whole body poisoning animal model of aequorin, and particularly EGCG can be injected into a mouse after being pre-hatched with lethal dose of aequorin, so that the survival rate of the mouse can be obviously improved; after EGCG and lethal dose of jellyfish toxin are pre-hatched, a rat is injected, so that the condition of blood pressure reduction of the rat caused by the toxin can be improved; after the mouse is poisoned by the aequorin, the EGCG is injected, so that the survival rate of the mouse can be obviously improved; EGCG has also been found to significantly inhibit the hemolytic activity of aequorin. The results show that EGCG injection administration can effectively prevent and treat jellyfish toxin systemic poisoning, which provides an effective candidate drug for developing a medicine for preventing or treating jellyfish sting systemic poisoning and also provides a reference for clinical research on new application of the medicine.

2. The long-term drinking history and habits of China exist, and the EGCG is used as the main component of green tea, so that the safety is guaranteed, and therefore, the EGCG green tea has good clinical application and popularization values.

Drawings

FIG. 1: survival of mice injected intravenously with aequorin.

FIG. 2: effect of EGCG on survival in mouse intoxication models.

FIG. 3: hemolytic activity of various concentrations of aequorin.

FIG. 4: the inhibitory effect of EGCG on the hemolytic activity of aequorin.

FIG. 5: the mouse is injected with NnV (0.5mg/kg), NnV (0.5mg/kg) + EGCG (20mg/kg) intravenously at tail for 1h, and the morphology of heart, liver, lung and kidney change. (A) Normal heart tissue; (B) heart tissue after NnV injection, eosinophilic degeneration of cardiomyocytes (black arrows), increased cytoplasmic eosinophilia, and cytostasis; congestion is seen in the interstitial capillaries (herringbone white arrows); (C) the heart tissue after NnV + EGCG mixed injection has no obvious abnormality; (D) normal liver tissue; (E) liver tissue after NnV injection, moderate swelling of tissue hepatocytes (black arrows), loose and pale cytoplasma, mixed with small amounts of round fat vacuoles (grey arrows); extensive lobular diffuse bleeding (white arrow with a herringbone pattern), with ruptured hepatocyte cords; (F) the liver tissue after NnV + EGCG mixed injection has clear liver lobule structure and wide liver cell mild vacuolization; (G) normal lung tissue; (H) the lung tissue injected with NnV has little epithelial cell hyperplasia, little neutrophil infiltration (triangle white arrow) (I) and no obvious abnormality after NnV + EGCG mixed injection; (J) normal kidney tissue; (K) no obvious abnormality was seen in the kidney tissue after NnV injection; (L) renal tissue after NnV + EGCG mixed injection, no obvious abnormality was observed.

FIG. 6: the mouse is injected with NnV (0.42mg/kg), NnV (0.42mg/kg) + EGCG (20mg/kg) via tail vein, and the morphology of heart, liver, lung and kidney changes after 12 h. (A) Normal heart tissue; (B) no obvious abnormality was seen in the heart tissue after NnV injection; (C) the heart tissue after NnV + EGCG mixed injection has no obvious abnormality; (D) normal liver tissue; (E) liver tissue after NnV injection, bridging necrosis between extensive regions of the assembled duct, hepatocellular coagulative necrosis, increased cytoplasmic eosinophilia, nuclear disappearance with mild bleeding (white arrow with a herringbone pattern), small neutrophil infiltration (white arrow with a triangular pattern), severe vacuolar degeneration of individual surrounding hepatocytes (black arrow), and more common microvesicle steatosis of surrounding hepatocytes (grey arrow); (F) the liver tissue after NnV + EGCG mixed injection has clear liver lobule structure, extensive severe vacuolar degeneration of liver cells (black arrow), cell swelling, loose and light staining of cytoplasm, more ballooning change (herringbone white arrow), and no obvious inflammatory cell infiltration; (G) normal lung tissue; (H) NnV injected lung tissue has no obvious abnormality; (I) the lung tissue after NnV + EGCG mixed injection has no obvious abnormality; (J) normal kidney tissue; (K) in the kidney tissue after NnV injection, more renal tubular epithelial cells are subjected to steatosis (black arrows), tiny round vacuoles are visible in cytoplasm, and no obvious inflammatory cell infiltration is observed; (L) renal tissue after NnV + EGCG mixed injection, no obvious abnormality was observed.

FIG. 7: effect of therapeutic administration of EGCG (20mg/kg) on survival in mouse models of intoxication.

Detailed Description

The following examples are provided to illustrate specific embodiments of the present invention. The following examples are carried out on the premise of the technical scheme of the invention, and detailed embodiments and specific operation procedures are given, but the scope of the invention is not limited to the following examples.

Example 1 investigation of lethal doses of mouse intravenous injection of jellyfish toxin (NnV)

1. Experimental methods

ICR mice were randomly divided into 5 groups (n ═ 3), and different doses of NnV (0.42mg/kg, 0.5mg/kg, 0.6mg/kg, 0.72mg/kg, 0.86mg/kg, solvent was physiological saline, and the volume was made 0.1ml) were injected into the tail vein, and the effect of different doses of NnV on the survival of the mice was observed.

2. Results of the experiment

When the toxin dose is more than or equal to 0.6mg/kg, the mice die continuously within 2 h. At toxin doses of 0.5mg/kg, mice survived for an extended period of time, but eventually all died within 1 d. At a toxin dose of 0.42mg/kg, some mice survived for more than 1 week.

Example 2: NnV survival analysis of poisoned mice

1. Experimental methods

Based on the results of example 1, the NnV dose range was re-established and the number of mice per group was expanded. ICR mice were randomly divided into 5 groups (n ═ 10), and different doses of NnV (0.35mg/kg, 0.42mg/kg, 0.45mg/kg, 0.5mg/kg, 0.6mg/kg, solvent was physiological saline, and the volume was made 0.1ml) were injected into the tail vein, and the effect of different doses of NnV on the survival of the mice was observed.

2. Results of the experiment

As shown in FIG. 1, when the toxin dose is less than or equal to 0.42mg/kg, the mice show an excitatory response at an early stage, and after 10min, the mice gradually become cachectic, slow in response and crouched, and part of the mice die continuously within 3 d. When the toxin dose is 0.45mg/kg or 0.5mg/kg, the mice have tachypnea, heart beat enhancement, hypodynamia, cachexia and crouching in the early stage, and gradually have convulsion and death. When the toxin dose reached 0.6mg/kg, the mice immediately developed convulsions and died rapidly.

Example 3: the effective dose range of EGCG antagonistic lethal dose NnV is searched

1. Experimental methods

EGCG was dissolved in 10mg/ml physiological saline. ICR mice were randomly divided into 5 groups (n ═ 2) different doses of EGCG (100mg/kg, 80mg/kg, 40mg/kg, 20mg/kg, 10mg/kg) were mixed with 0.5mg/kg NnV, made up to 0.2ml with physiological saline, injected tail vein, and observed for mouse response and survival time.

2. Results of the experiment

Except for the 10mg/kg EGCG group, one mouse died, and the remaining mice survived for 7 d. Mice in the group with the dosage of more than 20mg/kg show mild excitability state in the early stage and return to normal after about 2 hours.

Example 4: prevention effect of EGCG injection administration on NnV systemic poisoning

1. Experimental methods

According to the results of example 3, ICR mice were randomly divided into 4 groups (n is 10), different doses of EGCG (5mg/kg, 10mg/kg, 20mg/kg) were mixed with 0.5mg/kg NnV, and the control group was treated with NnV alone, all of which were made up to 0.1ml with physiological saline, injected into tail vein, and observed for mouse response and survival time.

2. Results of the experiment

As shown in FIG. 2, the survival rate of the poisoned mice can be improved by pre-incubating EGCG with NnV when the dose of EGCG reaches 5 mg/kg. When the dose of EGCG reaches 20mg/kg, the acute toxic effect of 0.5mg/kg NnV on mice can be completely antagonized.

Example 5: NnV hemolytic Activity test

1. Experimental methods

A 2% concentration mouse red blood cell suspension was prepared: eyeball hemorrhaging method the whole blood of mice is dripped into a 15ml centrifuge tube, 8ml PBS is added, after gentle mixing, the mixture is centrifuged at 1000 Xg for 10min at 4 ℃, and the supernatant is discarded. And adding 8ml of PBS, uniformly mixing, centrifuging, discarding the supernatant, and repeating for 2-3 times. Then 200. mu.l of red blood cells were added to 9800. mu.l of physiological saline to prepare a 2% suspension of red blood cells.

Mu.l of 2% erythrocyte suspension was mixed with NnV 400. mu.l of different concentrations, and a negative control group (400. mu.l of 0.9% sodium chloride solution + 400. mu.l of 2% erythrocyte suspension) and a positive control group (400. mu.l of deionized water + 400. mu.l of 2% erythrocyte suspension) were set, incubated in warm water at 37 ℃ for 30min, centrifuged at 1000 Xg at 4 ℃ for 10min, 200. mu.l of the supernatant was dropped into a 96-well microtiter plate, and 3 replicate wells per system were used to determine the absorbance at 450 nm.

2. Results of the experiment

As shown in FIG. 3, NnV has obvious hemolytic effect on mouse erythrocytes, and the higher the toxin concentration, the stronger the hemolytic effect, and NnV reached 0.5. mu.g/ml, which means that the hemolytic rate exceeded 100%.

Example 6: inhibition of NnV hemolytic activity by EGCG

1. Experimental methods

According to the results of the NnV hemolytic assay, 0.2. mu.g/ml NnV was selected as the toxin concentration to test the inhibitory effect of EGCG on NnV hemolytic activity. 0.16 mu g of NnV and different doses of EGCG are premixed, and the mixture is made up to 400 mu l by using physiological saline, and then mixed with 400 mu l of 2% erythrocyte suspension, at the same time, a negative control group (400 mu l of 0.9% sodium chloride solution and 400 mu l of 2% erythrocyte suspension), a positive control group (400 mu l of deionized water and 400 mu l of 2% erythrocyte suspension) and a single jellyfish toxin group are arranged, incubated in warm water at 37 ℃ for 30min, centrifuged at 4 ℃ for 10min at 1000 Xg, 200 mu l of supernatant is dropped into a 96-well microtiter plate, 3 duplicate wells of each system are used, and the absorbance at 450nm is measured.

2. Results of the experiment

The experimental result shows that EGCG has obvious inhibition effect on NnV hemolytic activity. As shown in FIG. 4, the hemolysis rate of 0.05mg/ml EGCG-treated group was only 2.23%, almost completely inhibiting the hemolysis of NnV.

Example 7: protective effect of EGCG and NnV pre-hatched injection administration on mouse viscera I

1. Experimental methods

ICR mice were randomly divided into 3 groups: the normal saline control group, the NnV group of 0.5mg/kg, and the EGCG group of 0.5mg/kg NnV +20mg/kg, 10min after injection administration, the heart, liver, lung, and kidney tissues of each group of mice were fixed with 4% paraformaldehyde, and histopathological examination was performed.

2. Results of the experiment

As shown in figure 5, the aequorin poisoning mouse model has obvious early hepatic tissue lesion, moderate tissue hepatocyte swelling, loose and lightly stained cytoplasm, small amount of round fat vacuoles, large-scale hepatic lobular diffuse bleeding and hepatic cell cord rupture. The change of heart tissue is slight, the change of myocardial cell eosinophilia, the increase of cytoplasmic eosinophilia, the nuclear fixation and contraction, the blood stasis of interstitial capillary vessels can be seen, and the change of lung and kidney is basically absent. The pathological changes are obviously improved in the EGCG treatment group.

Example 8: protective effect of EGCG and NnV pre-hatched injection administration on mouse viscera II

1. Experimental methods

ICR mice were randomly divided into 3 groups: the physiological saline control group, the NnV group of 0.42mg/kg, and the EGCG group of 0.42mg/kg NnV +20mg/kg, were injected for 12 hours, and the heart, liver, lung, and kidney tissues of each group of mice were fixed with 4% paraformaldehyde for histopathological examination.

2. Results of the experiment

As shown in fig. 6, the advanced liver tissue lesion of the jellyfish sting poisoning mouse model is more serious, the necrosis is bridged between the extensive regions of the tissue, the liver cell coagulative necrosis, the eosinophilia of cytoplasm is enhanced, the nucleus disappears, the mild hemorrhage is accompanied, a small amount of neutrophil infiltration is realized, the peripheral individual liver cells are severely vacuolated and degenerated, the peripheral liver cells are mostly subjected to microvesicle steatosis, the kidney has more renal tubular epithelial cell steatosis, and the heart and lung are basically unchanged. The pathological changes are obviously improved in the EGCG treatment group.

Experimental example 9: therapeutic Effect of EGCG injection administration on NnV systemic poisoning I

1. Experimental methods

NnV (0.5mg/kg) is injected into tail vein of ICR mice, a model of systemic toxication of the mouse aequorin is established, the mice are randomly divided into 3 groups (n is 5), different doses of EGCG (20mg/kg, 40mg/kg and 60mg/kg) are injected into tail vein after 5min, and the response and survival analysis of the mice are observed.

2. Results of the experiment

The mice developed symptoms of accelerated heartbeat and weakness in the early stage, but with EGCG administration, the symptoms were gradually relieved and all mice survived.

Experimental example 10: therapeutic Effect of EGCG injection administration on NnV systemic poisoning II

1. Experimental methods

NnV (0.5mg/kg) is injected into tail vein of ICR mice, a model of the systemic toxication of the mouse aequorin is established, the model is randomly divided into 3 groups (n is 10), 20mg/kg EGCG is injected into tail vein respectively 5min, 10min and 20min after toxin administration, and the response and survival analysis of the mice are observed.

2. Results of the experiment

As shown in fig. 7, the symptoms of mice were effectively alleviated by EGCG injection within 5min after toxin administration, and the survival rate of jellyfish toxin systemically poisoned mice was 90%; EGCG is given at intervals of 10min, and the survival rate of the jellyfish toxin systemic poisoning mouse is reduced to 50%; EGCG was given at 20min intervals and only slightly prolonged survival. EGCG has a certain therapeutic effect on the systemic toxicity of the aequorin, but needs to be injected as soon as possible.

While the preferred embodiments of the present invention have been described in detail, it will be understood by those skilled in the art that the invention is not limited thereto, and that various changes and modifications may be made without departing from the spirit of the invention, and the scope of the appended claims is to be accorded the full range of equivalents.

Claims (9)

1. Application of epigallocatechin gallate in preparing medicine for preventing or treating systemic poisoning of medusa toxin is provided.

2. The use of epigallocatechin gallate according to claim 1 in the preparation of a medicament for the prevention or treatment of systemic toxicity of medusa toxin, wherein the medicament for the prevention or treatment of systemic toxicity of medusa toxin is epigallocatechin gallate as the sole active ingredient or a pharmaceutical composition comprising epigallocatechin gallate.

3. The use of epigallocatechin gallate according to claim 1, wherein said medicament for preventing or treating systemic toxicity of aequorin is in the form of injection.

4. The use of epigallocatechin gallate according to claim 3, wherein said injection is prepared by adding 0.5g of epigallocatechin gallate to 50ml of 0.9% sodium chloride solution.

5. The use of epigallocatechin gallate according to claim 1 in the preparation of a medicament for the prevention or treatment of aequorin systemic poisoning, wherein said epigallocatechin gallate is administered at a dose of 20 mg/kg.

6. The use of epigallocatechin gallate according to claim 1 in the preparation of a medicament for the prevention or treatment of systemic medroxobin intoxication, wherein the administration time of said medicament is within 5min after medroxobin intoxication.

7. The use of epigallocatechin gallate according to claim 1 in the preparation of a medicament for the prevention or treatment of systemic toxicity of medusa toxin, wherein said epigallocatechin gallate substantially increases the survival rate of medusa toxin after poisoning; remarkably inhibiting the hemolytic activity of the aequorin; obviously improve early heart and liver injury and late liver and kidney injury caused by the jellyfish toxin.

8. A medicine for preventing or treating the systemic poisoning of medusa toxin is characterized in that the medicine takes epigallocatechin gallate as the only active component or is a medicine composition containing epigallocatechin gallate.

9. The medicament for preventing or treating the systemic poisoning by medusa toxin according to claim 8, wherein the medicament is an injection prepared by adding 0.5g of epigallocatechin gallate to 50ml of 0.9% sodium chloride solution; the dose administered was 20 mg/kg.

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