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.