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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.5
- 수록면
- 483 - 489 (7page)
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초록· 키워드
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Background: Korean Red Ginseng (KRG) has been known to possess many ginsenosides. These ginsenosides are used for curing cardiovascular problems. The present study show the protective potential of KRG against doxorubicin (DOX)einduced myocardial dysfunction, by assessing electrocardiographic, hemodynamic, and biochemical parameters and histopathological findings.
Methods: Animals were fed a standard chow and adjusted to their environment for 3 days before the experiments. Next, the rats were equally divided into five groups (n ¼ 9, each group). The animals were administered with KRG (250 and 500 mg/kg) for 10 days and injected with DOX (20 mg/kg, subcutaneously, twice at a 24-h interval) on the 8th and 9th day. Electrocardiography and echocardiography were performed to study hemodynamics. Plasma levels of superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were measured. In addition, the dose of troponin I and activity of myeloperoxidase in serum and cardiac tissue were analyzed, and the histopathological findings were evaluated using light microscopy.
Results: Administration of KRG at a dose of 250 and 500 mg/kg recovered electrocardiographic changes, ejection fraction, fractional shortening, left ventricular systolic pressure, the maximal rate of change in left ventricle contraction (þdP/dtmax), and left ventricle relaxation (-dP/dtmax). In addition, KRG treatment significantly normalized the oxidative stress markers in plasma, dose dependently. In addition, the values of troponin I and myeloperoxidase were ameliorated by KRG treatment, dose dependently. And, KRG treatment showed better histopathological findings when compared with the DOX control group.
Conclusion: These mean that KRG mitigates myocardial damage by modulating the hemodynamics, histopathological abnormality, and oxidative stress related to DOX-induced cardiomyopathy in rats. The results of the present study show protective effects of KRG on cardiac toxicity.
Methods: Animals were fed a standard chow and adjusted to their environment for 3 days before the experiments. Next, the rats were equally divided into five groups (n ¼ 9, each group). The animals were administered with KRG (250 and 500 mg/kg) for 10 days and injected with DOX (20 mg/kg, subcutaneously, twice at a 24-h interval) on the 8th and 9th day. Electrocardiography and echocardiography were performed to study hemodynamics. Plasma levels of superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were measured. In addition, the dose of troponin I and activity of myeloperoxidase in serum and cardiac tissue were analyzed, and the histopathological findings were evaluated using light microscopy.
Results: Administration of KRG at a dose of 250 and 500 mg/kg recovered electrocardiographic changes, ejection fraction, fractional shortening, left ventricular systolic pressure, the maximal rate of change in left ventricle contraction (þdP/dtmax), and left ventricle relaxation (-dP/dtmax). In addition, KRG treatment significantly normalized the oxidative stress markers in plasma, dose dependently. In addition, the values of troponin I and myeloperoxidase were ameliorated by KRG treatment, dose dependently. And, KRG treatment showed better histopathological findings when compared with the DOX control group.
Conclusion: These mean that KRG mitigates myocardial damage by modulating the hemodynamics, histopathological abnormality, and oxidative stress related to DOX-induced cardiomyopathy in rats. The results of the present study show protective effects of KRG on cardiac toxicity.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
참고문헌 (39)
참고문헌 신청
Minotti G / 2004 / Anthracyclines : Molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity / Pharmacol Rev 56:185~229
Bast A / 2007 / Protection by flavonoids against anthracycline cardiotoxicity : from chemistry to clinical trials / Cardiovasc Toxicol 7:154~159
Saeki K / 1998 / Doxorubicin directly binds to the cardiac-type ryanodine receptor / Life Sci 19:450~457
Olson RD / 1990 / Doxorubicin cardiotoxicity analysis of prevailing hypotheses / FASEB J 4:3076~3086
Akimoto H / 1993 / Effect of verapamil on doxorubicin cardiotoxicity : altered muscle gene expression in cultured neonatal rat cardiomyocytes / Cancer Res 53:4658~4664
Bast A / 2007 / Protection by flavonoids against anthracycline cardiotoxicity : from chemistry to clinical trials / Cardiovasc Toxicol 7:154~159
Saeki K / 1998 / Doxorubicin directly binds to the cardiac-type ryanodine receptor / Life Sci 19:450~457
Olson RD / 1990 / Doxorubicin cardiotoxicity analysis of prevailing hypotheses / FASEB J 4:3076~3086
Akimoto H / 1993 / Effect of verapamil on doxorubicin cardiotoxicity : altered muscle gene expression in cultured neonatal rat cardiomyocytes / Cancer Res 53:4658~4664
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UCI(KEPA) : I410-ECN-0101-2020-524-000843033