The Cardioprotective Effects of Valsartan in Septic Rats and Its Possible Mechanism

Abstract: The objection of this study was to investigate the effect of valsartan on myocardial protection of rats with sepsis and its mechanism. Sepsis in rats was induced via cecal ligation and puncture (CLP). Sixty-five rats were randomly divided into five groups， followed by control group (group C， C)， sham group (group S， S)， model group (group M， M)， small dose of valsartan group (group A， A)， large dose of valsartan group (group B， B). At 24 hours， blood was drawn from the abdominal aorta to detect changes in troponin I (TNI) levels. The left ventricle was stained with HE and TUNEL staining to measure pathologic changes and apoptosis index of myocardium. The remaining tissue was used to detect activation of p38 MAPK by Western blot. We measured variation in expression of tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) via ELISA. The results showed that comparing with group C and S， the content of TnI， TNF-α， MDA and the specific value of p-p38 MAPK/p38 MAPK of group M increased significantly (P<0.05)， and the pathological damage and apoptosis index also exacerbated obviously. While there were no statistical differences (P>0.05) of the specific value of p-p38 MAPK/p38 MAPK and the content of MDA of group A compared to group M. But the content of TnI， TNF-α， MDA and the specific value of p-p38 MAPK/p38 MAPK of group B all decreased significantly than group M (P<0.05). We could conclude that large-dose valsartan reduced myocardial injury in septic rats through inhibit the p38 MAPK pathway. But the protective effect of small doses of valsartan was not significant.

CSTR: 32200.14.cjcb.2018.05.0009