التفاصيل البيبلوغرافية
| العنوان: |
Rho Kinase Inhibition by Fasudil Attenuates Adriamycin-Induced Chronic Heart Injury. |
| المؤلفون: |
Yan, Yi, Xiang, Chengyu, Yang, Zhijian, Miao, Dengshun, Zhang, Dingguo |
| المصدر: |
Cardiovascular Toxicology; Aug2020, Vol. 20 Issue 4, p351-360, 10p |
| مصطلحات موضوعية: |
HEART injuries, VENTRICULAR ejection fraction, LACTATE dehydrogenase, CREATINE kinase, CELLULAR aging |
| مستخلص: |
Adriamycin (ADR)-induced chronic heart injury (CHI) is a serious complication of chemotherapy. The present study was designed to assess the ability of fasudil, a Rho kinase inhibitor, to prevent ADR-induced CHI. Forty male 6-week-old C57BL6 mice were randomly divided into the following four groups: (1) control group, (2) CHI induced by adriamycin (ADR group), (3) CHI plus low dose fasudil (ADR + L group), and (4) CHI plus high dose fasudil (ADR + H group). Animals from groups 2–4 received ADR (2.5 mg/kg, i.p.) once a week for 8 weeks, and the control group received saline. Meanwhile, the animals in groups 3–4 received 2 mg/kg/day or 10 mg/kg/day fasudil, respectively. After measurement of cardiac functions, blood samples were collected for biochemical assays. The hearts were excised for histological, immunohistochemistry and western blot study, respectively. Adriamycin produced evident cardiac damage revealed by cardiac functions changes: decreased left ventricular fractional shortening (FS), left ventricular ejection fraction (EF), increased left ventricular volume, cardiac injury marker changes (increased creatine kinase, lactate dehydrogenase), antioxidant enzymes activity changes (decreased superoxide dismutase), and lipid peroxidation (elevated malondialdehyde) to the control group. Fasudil treatment notably ameliorated ADR-induced cardiac damage, restored heart function, suppressed cell apoptosis and senescence, ameliorated redox imbalance, and DNA damage. Fasudil has a protective effect on ADR-induced chronic heart injury, which partially attributed to its antioxidant, anti-apoptotic effects of inhibiting the RhoA/Rho kinase (ROCK) signaling pathway. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
