Abstract
To investigate the impacts and related mechanisms of penehyclidine hydrochloride (PHC) on ischemia/reperfusion (I/R)-induced myocardial injury. A rat model of myocardial I/R injury was established by the ligation of left anterior descending coronary artery for 30 min followed by 3 h perfusion. Before I/R, the rats were pretreated with or without PHC. Cardiac function was measured by echocardiography. The activities/levels of myocardial enzymes, oxidants and antioxidant enzymes were detected. Evans blue/TTC double staining was performed to assess infarct size. Cardiomyocyte apoptosis was evaluated by TUNEL assay. The release of inflammatory cytokines and inflammatory mediators was detected by ELISA. Western blot was performed to analyze the expression of COX-2, IκB, p-IκB and NF-κB. Meanwhile, the rats were given a single injection of H-PHC before I/R. The effects of PHC on myocardial infarct and cardiac function were investigated after 7 days post-reperfusion. We found that PHC remarkably improved cardiac function, alleviated myocardial injury by decreasing myocardial enzyme levels and attenuated oxidative stress in a dose-dependent manner. Additionally, PHC preconditioning significantly reduced infarct size and the apoptotic rate of cardiomyocytes. Administration of PHC significantly decreased serum TNF-α, IL-1β, IL-6 and PGE2 levels and myocardium COX-2 level. Meanwhile, the expression levels of p-IκB and NF-κB were downregulated, while IκB expression was upregulated. H-PHC also exerted long-term cardioprotection in a rat model of I/R injury by decreasing infarct size and improving cardiac function. These results suggest that PHC can efficiently protect the rats against I/R-induced myocardial injury.
Highlights
Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality [1]
We investigated the impacts of Penehyclidine hydrochloride (PHC) on cardiac function
There were no significant differences in ejection fraction (EF) (Fig 1A), fractional shortening (FS) (Fig 1B), left ventricular end-diastolic pressure (LVEDP) (Fig 1C) and left ventricular systolic pressure (LVSP) (Fig 1D) between the Sham group and the Sham+high dose of penehyclidine hydrochloride (H-PHC) group, indicating that H-PHC administration had no adverse effects on these parameters
Summary
Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality [1]. More than 700,000 people reportedly die from this disease every year in China [2]. AMI may cause insufficient blood supply and increase the myocardial necrosis area [3]. AMI diagnosis in old people is difficult because of dementia and dysphasia [4]. Reperfusion therapy with primary percutaneous coronary intervention (PCI) effectively reduces mortality.
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