Abstract
The protective effects of oxymatrine (OMT) on apoptosis and heat shock protein 90a (Hsp90a) expression in a rabbit model of lung ischemia-reperfusion injury (LIRI) were investigated. The model of LIRI was established in rabbits and they were randomly divided into two groups: The control group (group C, n=10), and experimental group (further divided into groups E1, n=10; and group E2, n=10), to measure the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissue homogenates at several time points (T(0), 0 min; T(1), 60 min; T(2), 120 min; T(3), 180 min; and T(4), 240 min), and to measures changes in lung tissue wet/dry weight ratio (W/D), apoptosis index (AI), and Hsp90a expression and organization at T(2), T(3) and T(4). Comparing group C with groups E1 and E2, the levels of SOD activity and MDA were not significantly different at T(0) and T(1) (P>0.05); W/D ratio and AI were significantly higher than in groups E1 and E2 (P<0.05, P<0.01); 120 min after LIR, MDA, W/D ratio, and AI were lower than in groups E1 and E2 (P<0.05, P<0.01). MDA, W/D ratio and AI were lower in E2 than in E1 (P<0.05), and SOD and Hsp90a expression increased (P<0.05). The ultrastructure in group E showed less injury compared with group C. In conclusion, by scavenging oxygen free radicals, OMT can inhibit apoptosis, increase Hsp90a expression, and reduce the injury caused by lung ischemia reperfusion.