Objective To observe the effects of schisandrin B（ SchB） on acute kidney injury induced by renal ischemia-reperfusion（ I/R） in mice

and to explore its possible mechanism. Methods A total of 45 C57 BL/6 mice were randomly divided into sham operation group

model group and SchB group

with 15 mice in each group.The model group and SchB group were treated with clamping bilateral renal pedicles for 40 min to establish I/R model. Before modeling

SchB group was pretreated with 80 mg/（ kg·d） of SchB by gavage for 7 days. The levels of serum creatinine（ Scr） and urea nitrogen（ BUN） of each group were detected on the 1 st

2 nd and 7 th day after modeling. The expression of kidney injury molecule 1（ Kim-1） and neutrophil gelatinase-associated lipocalin（ NGAL）mRNA in kidney tissues were detected by PCR. The expression of cysteine-containing aspartate-specific proteases 3（ caspase-3）

B cell lymphoma/promyelocytic leukemia（ Bcl-2） and Bcl-2 related protein were detected by Western blot. HE staining was used to observe the pathological changes of kidney tissues. Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling（ TUNEL） was used to detect the apoptosis of renal tubular cell. Results On the1 st and 2 nd day

compared with sham operation group

renal tissue apoptosis index

Caspase-3 protein expression

blood Scr and BUN levels

and expression of Kim-1 and NGAL mRNA in renal tissue were significantly increased in the model group（ P < 0. 05 or P < 0. 01）. The pathological damage of renal tissue was obviously aggravated. The Bcl-2/Bax value decreased（ P < 0. 01）. Compared with the model group

the apoptotic index

Bcl-2/Bax value

Caspase-3 protein expression

blood Scr and BUN levels and the expression of Kim-1 and NGAL mRNA in renal tissue were decreased in SchB group（ P < 0. 05 or P < 0. 01）

and the pathological damage of renal tissue was significantly alleviated. On the 7 th day

there was no significant difference between the model group and the SchB group（ P >0. 05）. Conclusion SchB can improve the renal function

pathological damage and apoptosis of acute kidney injury induced by ischemia-reperfusion. It may be related to down-regulation of caspase-3 and up-regulation of Bcl-2/Bax ratio.