Investigation on improvement effects and mechanism of 7-hydroxyethyl chrysin on PC12 cell injury induced by hypobaric hypoxia / 中国药房

ABSTRACT

OBJECTIVE To investigate the improvement effects and possible mechanism of 7-hydroxyethyl chrysin （7-HEC） on PC12 cell injury induced by hypobaric hypoxia. METHODS The rat adrenal pheochromocytoma cell line PC12 was cultured under low-pressure hypoxia （5%CO2， 94%N2， 1%O2， 54 004 Pa） to investigate the different concentrations of 7-HEC （100， 10， 1， 0.1， 0.01 μmol/L） on the survival rate of hypoxic cells； the effects of 7-HEC（1 μmol/L） on the contents of lactate dehydrogenase （LDH） and malondialdehyde （MDA）， superoxide dismutase （SOD） activity， apoptotic rate， cell cycle， and the expressions of cleaved caspase-3， Bcl-2 and Bax were detected. RESULTS Compared with control group， the survival rate of cells in hypobaric hypoxia group was decreased significantly （P＜0.01）； 10， 1， 0.1 μmol/L 7-HEC could reverse the decrease of cell survival rate caused by hypobaric hypoxia （P＜0.05 or P＜0.01）. Compared with control group， LDH content in supernatant， MDA content in cells， apoptotic rate， the proportion of cells at G1 stage and the protein expression of cleaved caspase-3 were increased significantly in hypobaric hypoxia group， while SOD activity in cells， the proportion of cells at S stage and G2 stage and Bcl-2/Bax ratio were decreased significantly （P＜0.05 or P＜0.01）. Compared with hypobaric hypoxia group， the contents of LDH and MDA， apoptotic rate， the proportion of cells at G1 stage and the expression of cleaved caspase-3 in 7-HEC group were decreased significantly， while SOD activity， the proportion of cells at G2 stage and Bcl-2/Bax ratio were increased significantly （P＜ 0.01）. CONCLUSIONS 7-HEC can significantly increase the survival rate of hypobaric hypoxia cells， reduce the LDH content in supernatant， improve cell cycle arrest， and reduce the rate of apoptosis. Its improvement effects on hypobaric hypoxia cell injury may be related to the inhibition of caspase-3/Bax/Bcl-2 pathway activation.