KR102213913B1 - Pharmaceutical composition for preventing or treating myocardial damage comprising Spinochrome D - Google Patents

Abstract

The present invention relates to a composition for preventing or treating myocardial damage containing spinochrome D as an active component, wherein the spinochrome D is confirmed to inhibit the generation of reactive oxygen species generated by cardiotoxic drugs and restores mitochondrial dysfunction to exhibit an effect of inhibiting the death of myocardial cells. Therefore, the composition containing the spinochrome D as the active component is provided as a pharmaceutical composition and health food for preventing or treating myocardial damage caused by cardiotoxic drugs.

Description

Pharmaceutical composition for preventing or treating myocardial damage comprising Spinochrome D as an active ingredient {Pharmaceutical composition for preventing or treating myocardial damage comprising Spinochrome D}

The present invention relates to a composition for preventing or treating myocardial damage containing spinochrome D as an active ingredient.

The myocardium is a muscle that makes up the heart and becomes the body of heart contraction, and is metabolically active. In these myocardium, aerobic metabolism is essential because mitochondria are present in more than 30% of the volume of individual fibers, and the reserve of high-energy phosphate is very insufficient.

Cardiomyocyte death proceeds as adenosine triphosphate (ATP) levels are very low and anaerobic glycolysis is substantially stopped. Recently, the increase in side effects caused by the administration of therapeutic agents for various diseases has been a problem.In particular, such as doxorubicin, a quinone-based compound anticancer agent, and sodium nitroferricyanide (SNP), a vasodilator, which exhibits an inhibitory effect on signal transduction between cells. As the drug induces death of cardiomyocytes by increasing intracellular reactive oxygen species and decreasing mitochondrial function, it may cause a decrease in heart function and various heart diseases. However, mammalian cardiomyocytes are potentially limited in proliferation and do not undergo sufficient regeneration if severely damaged.

As a treatment method for damaged myocardium, there is a treatment through irreversible damage cell removal through an inflammatory reaction after reperfusion injury, but it is difficult to completely heal because the regeneration of myocardial cells is difficult. Therefore, it is the best way to protect heart cells against damage-causing factors and prevent loss of heart cells through them.

Spinochrome D (SpD) is a derivative isolated from marine natural products extracted from sea urchin shells. So far, no reports on the effects of Spinochrome D on drug toxicity or heart damage caused by free radicals have been reported.

Republic of Korea Patent Registration No. 10-1499355 (announced on March 6, 2015)

The present invention provides a composition containing spinochrome D as an active ingredient to provide a composition for preventing or treating heart damage to protect heart cells from toxicity of drugs that cause heart damage.

The present invention provides a pharmaceutical composition for preventing or treating myocardial damage, containing Spinochrome D as an active ingredient.

In addition, the present invention provides a health food for preventing or improving myocardial damage, which contains Spinochrome D as an active ingredient.

According to the present invention, spinochrome D inhibits the production of reactive oxygen species caused by cardiotoxic drugs and restores mitochondrial degradation, thereby inhibiting the death of cardiomyocytes, the spinochrome D It is intended to provide a composition containing as an active ingredient as a pharmaceutical composition and health food for preventing or treating myocardial damage caused by cardiotoxic drugs.

1 is a compound structure of spinochrome D (SpD).
Figure 2 is a result of confirming the cytotoxicity of spinochrome D, Figures 2A and 2B are normal cells, human cardiomyocytes AC16 and mouse cardiomyocytes H9c2 treated with spinochrome D for 24 hours at 1, 10 and 100 μM concentration After confirming the cell viability, FIG. 2C is a result of confirming the cell viability after treating spinochrome D at 1, 5 and 10 μM concentrations under the condition of reducing the fetal bovine serum (FBS) concentration, and FIG. 2D This is the result of confirming the change in intracellular pH by spinochrome D treatment at concentrations of 1, 10 and 100 μM.
3 is a result of confirming the inhibitory effect of spinochrome D on the production of active oxygen. FIG. 3A is 0 in culture conditions in which active oxygen was generated by treating human cardiomyocytes (AC16) with 1 mM hydrogen peroxide (H ₂ O ₂ ). , 1 and 10 μM concentration of spinochrome D is a result of confirming the intracellular active oxygen level, and FIG. 3B is 0 in culture conditions in which active oxygen was generated by treatment with cobalt chloride (CoCl ₂ ) that induces intracellular stress. This is the result of confirming the level of active oxygen in the cells by treatment with μM concentration of Spinochrome D.
4 is a result of confirming the level of ATP production by SpD treatment in human cardiomyocytes AC16. FIG. 4A is a result of inhibiting glycolysis occurring in the cytoplasm by treatment with 10 mM galactose, and then 10 μM of SpD for 24 hours. It is a result of confirming the ATP level produced by the mitochondria by treatment, and FIG. 4B is a result of confirming the oxygen consumption rate (OCR) of cardiomyocytes under the same conditions, and FIG. 4C is a 1 mM hydrogen peroxide (H ₂ O ₂ ) The result of confirming the ATP production level by treating the 10 μM concentration of SpD under conditions in which reactive oxygen species were generated by treatment, and FIG. 4D is a result of confirming the ATP production level in the cardiomyocytes treated with 0.1 μM concentration of doxorubicin. As a result of confirming the production level, # means that the value increased significantly compared to the galactose treatment group ( p <0.05).
5 is a result of confirming the effect of SpD on the membrane potential of mitochondria inhibited by doxorubicin in human cardiomyocyte AC16.
Figure 6 is a result of confirming the cytotoxicity of spinochrome D (SpD) and ethinochrome A (EchA) in human cardiomyocytes AC16, treatment with SpD and EchA at 1, 10 and 100 μM concentrations, and confirming cell viability , * Represents p<0.05.
7 is a result of confirming the cardiomyocyte protective effect and active oxygen inhibitory effect of EchA and SpD from doxorubicin toxicity. FIG. 7A shows cell survival after treatment alone or in combination with doxorubicin at a concentration of 0.1 μM and SpD and EchA at a concentration of 10 μM for 24 hours. Fig. 7B is a result of confirming the effect of removing active oxygen in cells by treatment with 1 mM hydrogen peroxide to increase the intracellular active oxygen concentration and then treatment with 1 and 10 μM EchA or SpD, respectively.
8 is a result of confirming the ATP production level by treating EchA and SpD at a concentration of 10 μM in the presence or absence of 10 mM galactose in human cardiomyocytes AC16 and mouse cardiomyocytes H9c2.
9 is a result of confirming the amount of oxygen consumption (OCR) in human cardiomyocytes AC16 treated with EchA and SpD at a concentration of 10 μM, and * means p <0.05.

Hereinafter, the present invention will be described in more detail.

The present inventors confirmed the effect of inhibiting the death of heart cells and restoring mitochondrial function from the toxicity that occurs when the anticancer agent treatment of spinochrome D isolated from marine natural products extracted from sea urchin shells, the spinochrome D damages cardiomyocytes. The present invention was completed to treat myocardial damage by preventing and treating.

The present invention can provide a pharmaceutical composition for preventing or treating myocardial damage containing Spinochrome D as an active ingredient.

The myocardial damage may be induced by cardiomyocyte death by cardiotoxic drugs.

The cardiotoxic drug may be an anticancer agent, and the anticancer agent is vinblastine, mitomycin, cisplatin, doxorubicin, etoposide, tamoxifen, campto It may be selected from the group consisting of camptothecin, inostamycin, and neocarzinostatin, more preferably doxorubicin, but is not limited thereto.

The spinochrome D may inhibit the production of reactive oxygen species induced by cardiotoxic drugs and restore mitochondrial deterioration to inhibit the death of cardiomyocytes.

In one embodiment of the present invention, the pharmaceutical composition for preventing or treating myocardial damage containing spinochrome D as an active ingredient is an appropriate carrier, excipient, disintegrant, sweetener, coating agent, swelling agent, which is commonly used in the manufacture of pharmaceutical compositions. It may further include one or more additives selected from the group consisting of lubricants, lubricants, flavoring agents, antioxidants, buffers, bacteriostatic agents, diluents, dispersants, surfactants, binders and lubricants.

Specifically, carriers, excipients and diluents are lactose, dextrose, sucrose, sorbitol, mannitol, xylitol, erythritol, maltitol, starch, gum acacia, alginate, gelatin, calcium phosphate, calcium silicate, cellulose, methyl cellulose, microcrystalline Cellulose, polyvinyl pyrrolidone, water, methylhydroxybenzoate, propylhydroxybenzoate, talc, magnesium stearate, and mineral oil can be used, and solid preparations for oral administration include tablets, pills, powders, granules, capsules. And the like, and these solid preparations may be prepared by mixing at least one excipient, for example, starch, calcium carbonate, sucrose or lactose, gelatin, and the like in the composition. In addition to simple excipients, lubricants such as magnesium stearate and talc can also be used. Liquid preparations for oral use include suspensions, liquid solutions, emulsions, syrups, etc.In addition to water and liquid paraffin, which are commonly used simple diluents, various excipients such as humectants, sweeteners, fragrances, and preservatives may be included. Preparations for parenteral administration include sterilized aqueous solutions, non-aqueous solutions, suspensions, emulsions, lyophilized preparations, suppositories, and the like. Propylene glycol, polyethylene glycol, vegetable oils such as olive oil, injectable esters such as ethyloleate, etc. may be used as the non-aqueous solvent and suspension. As a base material for the suppository, witepsol, macrogol, tween 61, cacao butter, laurin paper, glycerogelatin, and the like may be used.

According to an embodiment of the present invention, the pharmaceutical composition is intravenous, intraarterial, intraperitoneal, intramuscular, intraarterial, intraperitoneal, intrasternal, transdermal, intranasal, inhalation, topical, rectal, oral, intraocular or intradermal It can be administered to a subject in a conventional manner via the route.

The preferred dosage of spinochrome D may vary depending on the condition and weight of the subject, the type and extent of the disease, the form of the drug, the route and duration of administration, and may be appropriately selected by those skilled in the art. According to an embodiment of the present invention, although not limited thereto, the daily dosage may be 0.01 to 200 mg/kg, specifically 0.1 to 200 mg/kg, and more specifically 0.1 to 100 mg/kg. Administration may be administered once a day or may be divided into several doses, whereby the scope of the present invention is not limited.

In the present invention, the'subject' may be a mammal including a human, but is not limited to these examples.

In addition, the present invention can provide a health food for preventing or improving myocardial damage, which contains Spinochrome D as an active ingredient.

The health food is used with other foods or food additives other than the spinochrome D, and may be appropriately used according to a conventional method. The mixing amount of the active ingredient may be appropriately determined according to the purpose of use, for example, prevention, health or therapeutic treatment.

The effective dose of the compound contained in the health food may be used in accordance with the effective dose of the therapeutic agent, but in the case of long-term intake for the purpose of health and hygiene or health control, it may be less than the above range, and is effective It is clear that the component can be used in an amount beyond the above range because there is no problem in terms of safety.

There is no particular limitation on the kind of health food, for example, meat, sausage, bread, chocolate, candy, snacks, confectionery, pizza, ramen, other noodles, gum, dairy products including ice cream, various soups, beverages, tea, Drinks, alcoholic beverages, and vitamin complexes.

Hereinafter, examples will be described in detail to aid understanding of the present invention. However, the following examples are for illustrative purposes only, and the scope of the present invention is not limited to the following examples. The embodiments of the present invention are provided to more completely explain the present invention to those of ordinary skill in the art.

The following experimental examples are intended to provide experimental examples commonly applied to each of the examples according to the present invention.

< Experimental example 1> Cell culture

AC16 cells, human cardiomyocytes, H9c2 cells, mouse cardiomyocytes, MCF-7, human breast cancer cells, and HeLa, cervical cancer cells, were purchased from ATCC (American Type Culture Collection). All cells were cultured in DMEM (Dulbecco's modified Eagle's medium) containing 10% FBS (Fetal Bovine Serum). Galactose (D-(+)-Galactose, Sigma) was added to the medium at a concentration of 10 mM according to the experimental conditions.

< Experimental example 2> Cell activity analysis

Cell activity was confirmed by reacting to 2×10 ⁵ cells (cells/well) using a CCK-8 assay kit (Cell counting kit-8; Dojindo Molecular Technologies) and at 450 nm wavelength (SpectraMax M2, Moleclular Devices, USA). I did.

< Experimental example 3> Confirmation of active oxygen in cells

Cells cultured under the given conditions were reacted with DCF-DA at a concentration of 20 μM for 30 minutes at 37° C., washed twice in saline (Phosphate buffered saline, PBS), and measured at _EX 480/ _Em 535 wavelength.

< Experimental example 4> ATP check

After culturing 2×10 ⁴ to 2×10 ⁵ cells (cells/well) under each condition for 24 hours using a 96 well plate for cell culture, the ATP level was checked using the ATP Detection Assay kit of Cayman (USA). I did.

< Experimental example 5> Check Oxygen Consumption Rate (OCR)

After culturing 2×10 ⁴ to 2×10 ⁵ cells (cells/well) under each condition using a 96-well plate for cell culture, oxygen consumption rate (OCR) using the Oxygen Consumption Rate Assay kit of Cayman (USA) ) Was confirmed.

< Experimental example 6> Check the fluorescence microscope

After culturing 2×10 ⁵ cells (cells/well) using a 48-well plate under each condition, an image obtained using an Olympus IX71 (Olympus, Japan) fluorescence microscope was analyzed with MetaVue5.0.

< Example 1> Spinochrome D ( Sphinochrome D, SpD ) Ready

Spinochrome D was isolated from the sea urchin astropy radiata collected at a depth of 10-15 m. In addition , it can be isolated from Strongylocentrotus intermedius, Echinothrix calamaris, Echinothrix diadema, Echinarachnius parma, and Scaphechinus mirabilis .

Sea urchin (2.8 kg) was prepared by washing the intestines and rinsing with water (H ₂ O). The crushed skin and spine were thoroughly extracted with ethanol (EtOH) containing H ₂ SO ₄ (10%), and the resulting extract was centrifuged to remove high molecular weight compounds and concentrated in vacuo. , Separated between water and ethanol.

The ethanol fraction was concentrated in vacuo and chromatographed on polychrome using water-ethanol. Evaporate the ethanol fraction and perform chromatography on a Toyopearl HW-40 (Toyo Soda, Japan) column using an ethanol-water solvent containing formic acid (0.01%) having an ethanol gradient increasing from 10% to 50%. Performed.

Chromatographic fractionation and separation compounds were analyzed by HPLC-MS on an LCMS-2020 instrument (Shimadzu, Japan) equipped with a diode array matrix and mass spectrometry detector.

Samples were acetic acid with a Discovery HS C18 column (150×2.1mm, 3μm, Waters, USA) and an acetonitrile (MeCN) gradient increasing from 5% to 100% at a flow rate of 0.2 mL/min and a column temperature of 40°C. (AcOH, 0.2%)-was analyzed using acetonitrile.

Mass spectra were recorded in the range of m/z 100-800 using electrospray ionization at atmospheric pressure. NMR spectra were recorded with a Bruker Avance III 700 spectrometer (700 MHz for 1H and 176 MHz for 13C).

Spinochrome D (2,3,5,6,8-pentahydroxy-1,4-naphthoquinone) ; C ₁₀ H ₆ O ₇ ; Red powder; Sublimation without melting at temperatures above 286°C; absorption spectrum (H ₂ O-CH ₃ CN), λ _max , nm: 251, 327, 463; IR-spectrum (CHCl ₃ ), ν, cm ^-1 : 1626, 1521, 1499, 1409, 1279, 1085. ¹ Н NMR-spectrum (500 MHz, acetone-d ₆ ) δ, ppm: 6.56 (1H, s, Н-7), 9.11 (3Н, br.s, ОН-2, ОН-3, ОН-6), 12.37 (1Н, s, ОН-8), 12.55 (1Н, br.s, α-ОН-5) ). ¹³ C NMR-spectrum (126 MHz, acetone-d ₆ ) δ, ppm: 103.2 (С-9), 109.6 (С-7), 110.2 (С-10), 140.0 (С-3), 141.9 (С- 2), 151.2 (С-6), 157.4 (С-5), 162.2 (С-8), 180.4 (С-1), 182.8 (С-4). Mass-spectra: ESI-MS, m/z: 237 [М-Н] ^- , 239 [М+Н] ⁺ .

Spinochrome D can also be obtained synthetically. When the known 2,3 dichloronaphthazarin is used as the starting compound, a three step synthesis of spinochrome D is carried out in a yield of 62-65%.

< Example 2> Spinochrome D ( Sphinochrome D, SpD ) Confirmation of cell activity effect by treatment

In order to confirm the effect of spinochrome D (SpD) on cellular activity, human cardiomyocyte AC16 cells and rat cardiomyocyte H9c2 cells were treated with SpD at 1, 10 and 100 μM concentrations for 24 hours, followed by CCK-8 assay kit ( Cell counting kit-8; Dojindo Molecular Technologies) was used to react with each 2×10 ⁴ cells (cells/well), and cell activity was confirmed at 450 nm wavelength (SpectraMax M2, Moleclular Devices, USA).

As a result, as shown in FIGS. 2A and 2B, spinochrome D did not show any effect on cardiomyocyte activity.

In addition, after reducing fetal bovine serum (FBS), which is a nutrient to the cardiomyocyte culture medium, from 10% to 0.2% (v/v), SpD was added at 0, 1, 5 and 10 μM concentrations to The activity was confirmed.

As a result, it was confirmed that the cell activity increased in a SpD concentration-dependent manner as shown in FIG. 2C.

On the other hand, BCECF (2', 7'-Bis-(2-Carboxyethyl)-5-(and-6)-Carboxyfluorescein, Acetoxymethyl Ester) was used in cells according to SpD treatment at concentrations of 0.1, 1, 10 and 100 μM. The pH change was confirmed.

As a result, as shown in Fig. 2D, SpD-treated cells did not show any significant change compared to the control, and from the results, it was confirmed that SpD concentrations of 0.1, 1, 10 and 100 μM did not affect cell activity.

< Example 3> Spinochrome D ( Sphinochrome D, SpD ) Confirmation of production of active oxygen in cells by treatment

DCF-DA (2'-7' dichlorofluorescin diacetate, which reacts with free radicals after culturing human cardiomyocytes AC16 in a culture condition that generates reactive oxygen by treating 1 mM hydrogen peroxide (H ₂ O ₂ ) and shows fluorescence. ) _Was treated to check the level of active oxygen in the cells in _Ex 485/ _Em 535.

As a result, as shown in Fig. 3A, it was confirmed that the level of active oxygen in the cells was decreased, which was caused by hydrogen peroxide according to the concentration of SpD.

In addition, 10 μM of cobalt chloride (CoCl ₂ ), which induces endoplasmic reticulum stress (ER-stress) in cells, was treated in a culture medium in which the glucose concentration was increased to 22.5 mM and 33.3 mM to increase active oxygen in the cells. In the culture environment, 10 μM of SpD was treated with cardiomyocyte AC16.

As a result, as shown in FIG. 3B, in the cell group treated with SpD at a concentration of 10 μM, the level of intracellular active oxygen was significantly decreased.

< Example 4> Spinochrome D ( Sphinochrome D, SpD ) Confirmation of ATP generation by processing

To confirm the level of ATP production by spinochrome D (SpD) treatment, cardiomyocyte AC16 was treated with 10 mM galactose to inhibit glycolysis occurring in the cytoplasm, and then SpD 10 μM was treated and cultured for 24 hours. The level of ATP produced by mitochondria was confirmed.

Since galactose is converted to 1-phosphate galactose, one molecule of glucose in the form of uridine diphosphate glucose is used in the glycolysis process, it is converted into the form of glucose 1-phosphate and participates, so there is an effect of slowing the reaction rate of the glycolysis process in the cytoplasm.

As a result, it was confirmed that the ATP level was increased in the SpD-treated cell group as shown in FIG. 4A.

In addition, the oxygen consumption rate (OCR) of cardiomyocytes was confirmed under the same conditions as above.

As a result, it was confirmed that the oxygen consumption rate increased by SpD as shown in FIG. 4B.

From the above results, it can be suggested that the oxidative phosphorylation of mitochondria was affected by SpD.

In addition, it was confirmed that the ATP level of the SpD-treated cardiomyocytes AC16 was significantly increased even in the reactive oxygen environment caused by hydrogen peroxide as shown in FIG. 4C, and as shown in FIG. 4D, the cardiomyocytes reduced by doxorubicin by the treatment of SpD. It was confirmed that the ATP level was also significantly increased.

< Example 5> Spinochrome D ( Sphinochrome D, SpD ) Of mitochondria

Cardiomyocytes handle doxorubicin 0.1 and 1 μM on AC16 24 hours, after processing the SpD 10 μM were stained cardiomyocytes in _{TMRE (Tetramethylrhodamine ethyl ester) Ex 550} / Em at 590nm wavelength of the mitochondrial membrane potential (mitochondrial membrane potential, and ΔΨm ) Was measured and confirmed with a fluorescence microscope to confirm the mitochondrial protective effect of spinochrome D.

As a result, as shown in FIG. 5, it was confirmed that the mitochondrial membrane potential was reduced at the same time as the cell death in a concentration-dependent manner of doxorubicin, but the mitochondrial membrane potential was recovered in the SpD-treated cardiomyocytes.

From the above results, it was confirmed that spinochrome D exhibits an effect of increasing the mitochondrial membrane potential inhibited by doxorubicin.

< Example 6> Spinochrome D and Ethinochrome Of A Cardiomyocyte Protection effect check

The effects of Spinochrome D (SpD) and Echinochrome A were compared and analyzed using human cardiomyocytes AC16 and mouse cardiomyocytes H9c2.

1. Cell activity check

Human cardiomyocytes AC16 were treated with EchA or SpD at concentrations of 1, 10 and 100 μM, respectively, and the difference in the degree of cell activity according to the concentration between EchA and SpD was confirmed by CCK-8.

As a result, it was confirmed that EchA and SpD increased the formation of WST-8 formazan by enhancing NAD/NADH activity in cardiomyocytes when administered more than 10 μM as shown in FIG. 6, and cardiomyocytes treated with 100 μM SpD It was confirmed that the activity of EchA was significantly increased than that of cardiomyocytes treated with EchA (*: p<0.05).

2. Cardiomyocyte Checking the protective effect

From doxorubicin toxicity, the cardiomyocyte protective effect and free radical control effect of EchA and SpD were confirmed.

Cardiomyocytes AC16 were treated with doxorubicin at a concentration of 0.1 μM and EchA and SpD at a concentration of 10 μM for 24 hours, and then cell viability was confirmed.

As a result, cell viability of 50-60% was confirmed in the cell group treated with doxorubicin alone, as shown in FIG. 7A, whereas the cell viability improved to 70-80% in the cell group treated with doxorubicin and EchA or SpD was confirmed. , There was no statistically significant difference in the effect of enhancing cellular activity between EchA and SpD.

In addition, cardiomyocytes were treated with hydrogen peroxide at a concentration of 1 mM to increase the active oxygen concentration in the cells, and then treated with EchA or SpD at concentrations of 1 and 10 μM, and DCF-DA was used to confirm the free radical control effect.

As a result, in the case of the cells treated with EchA as shown in FIG. 7B, there was no difference in the effect of removing active oxygen in the cells according to the treatment concentration, whereas in the group of cells treated with SpD, the effect of removing active oxygen in the cells was increased depending on the concentration of SpD. It was confirmed that the reduction of free radicals in cells showed a statistically significant difference between EchA and SpD. The above results may be suggested to be related to showing that the ethyl group of carbon 6 of EchA is vulnerable to nucleophilic attack in the environment of active oxygen.

3. Check the effect of ATP generation

The effect of ATP production by EchA and SpD treatment was confirmed in human cardiomyocytes AC16 and mouse cardiomyocytes H9c2. Cardiomyocytes AC16 and H9c2 were treated with 10 mM galactose to inhibit glycolysis occurring in the cytoplasm, and then EchA and SpD 10 μM were each treated for 24 hours incubation, and the ATP levels produced in mitochondria were confirmed.

As a result, it was confirmed that the ATP production level of the heart cell group treated with 10 μM of EchA or SpD was improved by 10-20% compared to the control, as shown in FIG. 8, but when 10 mM galactose was added, it was improved than EchA in the 10 μM SpD group. It was confirmed to indicate an increased level of ATP.

4. Check the oxygen consumption rate

Human cardiomyocytes AC16 2×10 ⁴ cells were treated with EchA and SpD at a concentration of 10 μM, incubated at 37° C. for 1 hour, and then the oxygen consumption rate (OCR) was confirmed.

As a result, as shown in FIG. 9, it was confirmed that the oxygen consumption rate of the SpD-treated cells showed a statistically significant difference.

From the above results, it was confirmed that Spinochrome D (SpD) exhibits a superior cardiac cell protective effect than Echinochrome A.

As described above, specific parts of the present invention have been described in detail, and for those of ordinary skill in the art, it is obvious that these specific techniques are only preferred embodiments, and the scope of the present invention is not limited thereby. something to do. Therefore, it will be said that the practical scope of the present invention is defined by the appended claims and their equivalents.

Claims (5)

A pharmaceutical composition for the prevention or treatment of myocardial damage containing Spinochrome D as an active ingredient. The pharmaceutical composition for preventing or treating myocardial damage according to claim 1, wherein the myocardial damage is induced by cardiomyocyte death by cardiotoxic drugs. The pharmaceutical composition for preventing or treating myocardial damage according to claim 2, wherein the cardiotoxic drug is an anticancer agent. The method of claim 1, wherein the spinochrome D inhibits the production of reactive oxygen species induced by cardiotoxic drugs and restores mitochondrial deterioration, thereby inhibiting the death of cardiomyocytes. Pharmaceutical composition. A health food for preventing or improving myocardial damage that contains Spinochrome D as an active ingredient.

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