Objective      To investigate the effect of ischemic preconditioning on CO

2

pneumoperitoneum-induced kidney ischemia/reperfusion injury in rats and related mechanism.       Methods      Thirty mal

e SD rats were divided into 5 groups (n=6): sham group

pneumoperitoneum (Pp) group

ischemic preconditioning group for 1 cycle (IP1)

ischemia preconditioning group for 3 cycles (IP3)

and ischemic preconditioning group for 5 cycles (IP5). The sham group was subjected to sham operation

and the other groups were subjected to CO

2

Pp for 60 min under 10 mmHg intra-abdominal pressure. IP1

IP3 and IP5 groups were subjected to preconditioning prior to Pp/deflation through 5 min of Pp

immediately followed by 5 min of deflation

for 1

3

and 5 cycles

respectively. After deflation for 60 min

the kidney pathological changes were observed with light microscopy. Kidney tissue samples were taken for measuring malondialdehyde (MDA)

superoxide dismutase (SOD) and total antioxidant capacity (T-AOC). The expression of Bcl-2 protein and Bax protein was determined by immunohistochemistry and Western blotting.       Results      Microscopic examination showed the edema

degeneration and necrosis of renal tubule endothelial cells

tubular ectasia

congestion

and infiltration of neutrophils in the Pp group. Histological damage of renal tubules in the IP1

IP3

and IP5 groups was much milder than that in the Pp group (P0.05). Compared with the Pp group

the kidney MDA levels were remarkably decreased in the IP1

IP3 and IP5 groups

whereas the kidney SOD and T-AOC contents were increased significantly (P0.05). Immunohistochemical staining and Western blotting results showed that

compared with the Pp group

the expression of Bcl-2 protein was increased and that of Bax protein was decreased in the IP3 group (P0.05).       Conclusion      Ischemic preconditioning may decrease renal ischemia/reperfusion injury induced by CO

2

Pp in the rats

and ischemic preconditioning for 3 cycles is most effective. The mechanism may be associated with the decrease of oxygen free radicals

up-regulated expression of Bc1-2 protein and down-regulated expression of Bax protein.