Abstract

Objective To investigate the effect of a novel lymphotoxin with selectively binding to p55 tumor necrosis factor receptor (p55TNFR) on myocardial ischemia -reperfusion injury in rats in order to explore the mechanism. Methods A total of 40 SD rats were randomly (random number) assigned into four groups (n =10 in each) , namely sham operation group (group A), I/R group (group B), wild type rhLTα treatment group (group C), and p55TNFR selective rhLTα (rhLTα-Q107E) treatment group (group D). After I/R model rats were established, various therapeutic agents or saline were given by continuous intravenous infusion for 24 h via a micropump. After 24 hours of treatment, serum myocardial zymogram, such as aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK), as well as superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were determined. Myocardial infarction size (MIS) was measured by nitro blue tetrazolium chloride (NBT) staining. Results Compared to sham operation group, MIS, AST, LDH, CK, MDA were increased, while the activities of SOD and GSH-Px were decreased. However, all the effects were significantly reversed by treatment with rhLTα-Q107E (P 0.05). Conclusions The rhLTα-Q107E plays a role in the protection against myocardial ischemia -reperfusion injury in rats by the mechanism of scavenging oxygen free radicals and increasing the activity of endogenous antioxidant system. Key words: p55TNFR; Ischemia-reperfusion; Myocardial injury; Oxidative stress

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