Inhibition of Rho‑kinase is involved in the therapeutic effects of atorvastatin in heart ischemia/reperfusion
- Chao Cheng
- Xiao‑Bo Liu
- Shao‑Jie Bi
- Qing‑Hua Lu
- Juan Zhang
Affiliations: Department of Cardiology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250033, P.R. China, Shandong Blood Center, Jinan, Shandong 250012, P.R. China
- Published online on: July 29, 2020 https://doi.org/10.3892/etm.2020.9070
Copyright: © Cheng
et al. This is an open access article distributed under the
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The aim of the present study was to investigate the effects of atorvastatin against heart ischemia/reperfusion (I/R) injury and its potential underlying mechanism. Rats were allocated into the following groups: Sham, I/R, atorvastatin (10 mg/kg daily), fasudil (10 mg/kg daily) and atorvastatin + fasudil in combination. Drugs were administered for 2 weeks prior to I/R injury. I/R was established by ligating the left anterior descending branch (LAD) for 30 min and releasing the ligature for 180 min. The I/R group was found to have increased myocardial infarct size, cardiomyocyte apoptosis, levels of plasma interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α, superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels and Rho‑kinase activity compared with the other treatment groups (P<0.05). Moreover, pretreatment with atorvastatin significantly attenuated Rho‑kinase activity, myocardial infarct size, cardiomyocyte apoptosis, levels of plasma IL‑6 and TNF‑α, SOD activity and MDA levels, and upregulated nitric oxide production. It was also indicated that the specific Rho‑kinase inhibitor, fasudil, had the same effects as atorvastatin in I/R. Therefore, the present results suggested atorvastatin may lead to cardiovascular protection, which may be mediated by Rho‑kinase inhibition in heart I/R injury.