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Updated: Dec 23, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Increased ROCK1 not ROCK2 in circulating leukocytes in rats with myocardial ischemia/reperfusion
Chao Cheng1, Xiao-Bo Liu2, Dong-Ling Xu1
1Department of Cardiology, The Second Hospital of Shandong University, Jinan, China.
Insights
Increased Rho-associated protein kinase 1 (ROCK1) in circulating leukocytes contributes to myocardial ischemia/reperfusion injury. Inhibiting ROCK1 with fasudil offers cardioprotection, suggesting ROCK1 as a potential biomarker.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Immunology
Background:
- Rho-associated protein kinase (ROCK) is implicated in cardiovascular diseases and myocardial ischemia/reperfusion.
- The specific role of ROCK in circulating leukocytes during this injury is not well understood.
Purpose of the Study:
- To investigate ROCK activity in circulating leukocytes following myocardial ischemia/reperfusion injury in a rat model.
- To assess the therapeutic potential of ROCK inhibition in this context.
Main Methods:
- Myocardial ischemia/reperfusion was induced in Wistar rats.
- ROCK activity in circulating leukocytes was measured via substrate phosphorylation.
- ROCK1 and ROCK2 levels were analyzed.
- The effects of the ROCK inhibitor fasudil were evaluated.
Main Results:
- ROCK activity and ROCK1 levels were significantly elevated in circulating leukocytes post-ischemia/reperfusion.
- Fasudil treatment reduced infarct size, myocyte apoptosis, and inflammatory cytokines (IL-6, TNF-α).
- Fasudil also improved nitric oxide production.
Conclusions:
- Elevated ROCK1 in circulating leukocytes contributes to myocardial ischemia/reperfusion injury.
- Inhibiting ROCK1 in leukocytes mediates fasudil's cardioprotective effects.
- ROCK1 in circulating leukocytes may serve as a novel biomarker for this injury.
Background:
Rho-associated protein kinase (ROCK) plays a vital role in the pathogenesis of many cardiovascular diseases. Previous studies have demonstrated that ROCK is overactivated and involved in myocardial ischemia/reperfusion in vivo. But the role of ROCK in circulating leukocytes during myocardial ischemia/reperfusion is not well studied.
Material And Methods:
This study was performed to evaluate ROCK activity in circulating leukocytes in rats with myocardial ischemia/reperfusion injury. Myocardial ischemia/reperfusion Wistar rats were subjected to 30-min ischemia followed by 180-min reperfusion. ROCK activity in circulating leukocytes was examined by the phosphorylation state of myosin phosphatase targeting subunit 1, a substrate of ROCK.
Results:
ROCK activity significantly increased in leukocytes in rat ischemia/reperfusion models compared to the sham group. ROCK1 not ROCK2 level in circulating leukocytes was significantly elevated in ischemia/reperfusion. Administration of the selective inhibitor of ROCK, fasudil, significantly reduced myocardial infarct size, myocyte apoptosis, and inflammatory cytokine, including interleukin 6 and tumor necrosis factor α. Furthermore, fasudil upregulated ischemia/reperfusion-induced reduction of nitric oxide production.
Conclusion:
Increased ROCK1 not ROCK2 in circulating leukocytes plays a role in the pathogenesis of myocardial ischemia/reperfusion injury. Inhibition of ROCK1 in circulating leukocytes has an important role in fasudil-induced cardioprotective effects. ROCK1 in circulating leukocytes might be a new biomarker in myocardial ischemia/reperfusion injury.
