Abstract: Abstract： Objective To explore the protective effects of schisandrin B (Sch B) on hypoxia injury induced by cobal⁃ tous chloride (CoCl2) in human proximal renal tubular epithelial (HK-2) cells, and the possible mechanism thereof. Meth⁃ ods HK-2 cells were randomly assigned to four groups: control group (Con, cells were untreated), CoCl2 group (CoCl2, cells were treated with 600 μmol/L CoCl2 for 24 h), Sch B pretreat group (CoCl2+Sch B, cells were pretreated with 1 μmol/L and 10 μmol/L Sch B for 2 h) and Sch B group (Sch B, cells were treated with 1 μmol/L and 10 μmol/L Sch B for 2 h). CCK-8 kit was used to detect the cell viability of four groups. Flow cytometry was used to detect the apoptotic rate of four groups. The protein expression of hypoxia-inducible factor 1α (HIF-1α) was assessed by Western blot assay. The expressions of HIF-1α and inducible nitric oxide synthase (iNOS) mRNA were determined by RT-PCR. Results Compared with the control group, after treated with 600 μmol/L CoCl2, the cell viability was decreased, and the apoptosis was increased, the expressions of HIF-1α and iNOS mRNA were up-regulated in HK-2 cells. There was no significant difference in the expression of HIF- 1α mRNA between control group and CoCl2 group. Compared with the CoCl2 group, after pretreated with 1 μmol/L and 10 μmol/L Sch B, the cell viability was increased and the apoptosis was decreased, the expressions of HIF-1α and iNOS were down-regulated in HK-2 cells. There were no significant differences in the cell viability and apoptotic rate between control group and Sch B group. Conclusion Pretreatment with Sch B can reduce the apoptosis of HK-2 cells by inhibiting the ex⁃ pression of HIF-1α and iNOS mRNA, which shows protective effects on hypoxia injury.

Key words: schisandrin B, HK-2 cell, CoCl2, hypoxia injury, HIF-1α, iNOS