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ERK1/2 signal pathWay mediated propofol protected on cultured rat cardiomyocytes damaged by H2 O2
Author(s): 
Pages: 257-260
Year: Issue:  5
Journal: Qilu Pharmaceutical Affairs

Keyword:  PropofolCardiomyocytesH2O2;
Abstract: Objective To investigate the influence and mechanism of propofol on cardiomyocytes damaged by H2 O2 . Methods Cardiomyocytes from the hearts of 1 ~ 3 - day - old neonatal rats were prepared by a modified method. Treated cultured rat cardiomyocytes by H2 O2 ,propofol(12. 5,25,50 μmol·L - 1 ). MTT was used to detect cell viability. Malondial-dehyde(MDA)was determined by measuring thiobarbituric acid - reactive substances. Superoxide dismutase(SOD)was assayed by xanthine oxidase method. The rates of apoptosis of cardiomyocyte were detected by flow cytometry. The expression of ERK1 / 2,Bcl - 2 and Bax were tested by western blotting. Results Propofol suppressed the cardiomyocyte death induce by H2 O2(P < 0. 01),and decreased the production of MDA(P < 0. 01),promoted the ability of SOD(P < 0. 01). The ap-optosis rates of propofol group significant different from that of H2 O2 group(P < 0. 05). Propofol activated the phosphorated ERK1 / 2. The expression of Bcl - 2 was increased while that of Bax was suppressed. Conclusion Propofol protected on cul-tured rat cardiomyocytes damaged by H2 O2 via ERK1 / 2 signal pathway.
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