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Fasudil protects against adriamycin-induced acute heart injury by inhibiting oxidative stress, apoptosis and cellular senescence.

BACKGROUND
The clinical utility of Adriamycin (ADR) is limited due to its toxicity, particularly cardiotoxicity. Therefore, effective cardioprotective adjuvants to minimize ADR-induced acute cardiotoxicity are urgently needed. Our previous studies have demonstrated protective roles of fasudil on tissue injury. And here we further to explore whether inhibition of Rho-kinase could alleviate the acute heart injury induced by ADR.


METHODS
C57BL6 mice were randomly divided into the following four groups: ①ADR group;②low-dose fasudil ( ADR+L);③high-dose fasudil ( ADR+H); and ④control group(CON). Animals were injected i.p 20 mg/kg ADR once in group①~③. And animals were injected i.p fasudil (2 or 10 mg/kg/day ) daily for consecutive 6 days in group ②and ③,respectively. Blood samples and heart tissues were collected for assays. H9C2 cells were treated with fasudil for 30mins and then incubated with ADR for 24 hours. Cells were collected for immunohistochemistry and western blot study, respectively. Results In the mouse model, administration of fasudil significantly ameliorated ADR-induced cardiac damage, suppressed cell apoptosis and senescence, ameliorated redox imbalance and DNA damage. In vitro, fasudil treatment ameliorated ADR-induced immunofluorescence reaction of 8-OHdG, decreased the expression of TUNEL cells and proteins of Bax、Caspase-3 and p53,and increased the expression of proteins of Bcl-2 and SIRT 1. Conclusion Fasudil has the protective effect on ADR induced acute cardiotoxicity, which partially attributed to its antioxidant, anti-senescence, and anti-apoptotic effects.