Protective Effects And Mechanisms Of Renal Ischemic Preconditioning On Intracellular Calcium Overload And Lipid Peroxidation Injury

Objective To observe the changes of renal tubular epithelial intracellar inonized calcium level([Ca²⁺]i) and serum superoxide dismutase(SOD) and malondialdehyde(MDA),and investigate the relationship between lipid peroxidation injury and intracellular calcium overload during renal ischemia/reperfusion(I/R) injury and ischemic preconditioning(IPC) in order to explore the protective mechanisms of renal IPC.Methods Eighty-eight male SD rats were divided into 11 groups at random.Left renal arteries of I/R groups(â… _a～Ⅴ_a) were clamping for 45min repeatedly after right kidneys were deprived,and the left kidneys were removed at 0,1,24,48,72h after reperfusion.Rats in IPC-I/R groups(â… _b～Ⅴ_b)were preconditioning with renal ischemia by repeatedly clamping and unclamping the left arteries before the operation.Sham operation was performed as controls. Serum Scr,BUN,SOD and MDA levels were measured;Intracellular[Ca²⁺]i were assayed by a flow cytometry;Tubular cell apoptosis was detected by terminal deoxynucleotidyl transferase(TdT) mediated dUTP-biotin nick-end labeling(TUNEL).Results Serum MDA(P＜0.01),and intracellular[Ca²⁺]i(P＜0.01),significantly increased after renal I/R injury,while SOD level(P＜0.01) markedly decreased after the injury. Renal I/R injury significantly increased apoptotic tubular cells with the peak at 24h after reperfusion.IPC reduced serum MDA and intracellular[Ca²⁺]i and increased SOD level.Also, IPC significantly inhibited tubular cell apoptosis.Conclusion IPC can reduce the lipid peroxidation and attenuate intracellular calcium overload thus relieve renal injury during renal I/R;Lipid peroxidation and intracellular calcium overload functions each other to prevent the kidney from injuring.This maybe,at least partly, the mechanisms of IPC's protective effects.