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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&gt;0.05); W/D ratio and AI were significantly higher than in groups E1 and E2 (P&lt;0.05, P&lt;0.01); 120 min after LIR, MDA, W/D ratio, and AI were lower than in groups E1 and E2 (P&lt;0.05, P&lt;0.01). MDA, W/D ratio and AI were lower in E2 than in E1 (P&lt;0.05), and SOD and Hsp90a expression increased (P&lt;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.

Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury