Protective Effect of Zinc on Mouse Renal Ischemia-reperfusion Injury by Anti-apoptosis and Antioxidation

The paper discussed the protective effect of zinc pretreatment on renal ischemia-reperfusion injury (RIRI) and its mechanism. 50 male ICR mice were randomly divided into five groups: sham-operated group, model group, high-dose group with zinc sulfate pretreatment (60mg/kg body weight), medium-dose group with zinc sulfate pretreatment (30mg/kg body weight) and low-dose group with zinc sulfate pretreatment (15mg/kg body weight). The mice were administrated with zinc sulfate once a day for two weeks, subsequently the RIRI animal models were prepared by ligation of the left renal pedicle 30 minutes. 24h after reperfusion, the kidney tissue was removed and pathological results by HE staining showed that in the model group, kidney surface covered with a large number of red exudates, renal tubular dilatated, disorganized, renal tubular epithelial cell vacuolar degenerated, nuclear pyknosis and necrosis appeared; congestive and necrosis were visible in medullary junction. The pathological changes of renal ischemia- reperfusion were obviously relieved in the animals with medium and low-dose zinc pretreatment. The superoxide dismutase (SOD) activity in the lowdose zinc sulfate pretreatment group was significantly higher than that in the model and high-dose groups (P <0.05). The malondialdehyde (MDA) content of renal tissue, the apoptotic cells percentage in the medium and low dose groups were significantly lower than those in the model group (P <0.05), and MDA content in the low-dose group was significantly lower than that in the medium dose group (P <0.05). The ratio of BCL-2/BAX protein expression in the medium and low dose groups was significantly higher than that in the model group (P<0.05), the ratio in the low groups was significantly higher than that in the medium dose and high dose group by double immunofluorescence staining (P <0.05). In conclusion, zinc has a protective effect on the renal ischemia-reperfusion injury by antioxidant capacity and inhibition of apoptosis in the kidney.