动物造模,心肌缺血再灌注损伤 z-bio 2022-06-16 453

　　Objective To investigate the effect of pancreatic kininogenase on myocardial injury, oxidative stress and fibrosis in rats with myocardial ischemia-reperfusion injury.

　　Methods SD male rats were divided into sham operation group, model group and model drug-added group. The heart rate (HR), left ventricular systolic blood pressure (LVSP) and short-axis shortening rate (FS) were detected and recorded in each group. HE staining was used to observe the degree of myocardial pathological damage. The contents of creatine kinase isoenzyme (CK-MB), myoglobin (Mb) and cardiac troponin I (cTnI) were detected by ELISA. The kit detects the content of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH). Western blot was used to detect the expression levels of mitochondrial pathway apoptosis-related proteins and fibrosis marker proteins. Masson staining was used to observe myocardial fibrosis. RT-PCR was used to detect the expression levels of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1) and fibronectin (FN).

　　Results Compared with the model group, the HR, LVSP and FS of the rats in the 3 and 6 U/kg PKase groups were significantly increased (P<0.05), the myocardial tissue pathological damage was significantly improved, and the contents of CK-MB, Mb, cTnI and MDA were significantly increased. decreased (P<0.05), SOD and GSH contents increased (P<0.05), myocardial fibrosis was significantly improved, Bax/Bcl-2, cas-9, cas-3, α-SMA, TGF The expression levels of -β1 and FN were significantly decreased (P<0.05).

　　Conclusion Pancreatic kallikrein can alleviate myocardial injury, oxidative stress and fibrosis in rats with myocardial ischemia-reperfusion injury.