Recombinant human erythropoietin promotes expression of HO-1 mRNA after renal ischemia reperfusion injury in mice
10.3724/SP.J.1008.2011.00155
- Author:
Shun ZHANG
1
Author Information
1. Transplantation Center
- Publication Type:Journal Article
- Keywords:
Erythropoietin;
Heme oxygenase-1;
Ischemia;
Kidney;
Reperfusion injury
- From:
Academic Journal of Second Military Medical University
2011;32(2):155-159
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of recombinant human erythropoietin (rhEPO) on the expression of heme oxygenase-1(HO-1) mRNA after renal ischemia/reperfusion (IR) in mice. Methods: Ninety male C57BL/6 mice were randomly divided into three groups, namely, the sham operation group (n = 30), renal IR group (n = 30), and rhEPO treatment group (n=30). Mice were sacrificed at 1, 2, 3, 6, 24, and 48 h after renal reperfusion, and the renal function was evaluated by determining blood creatinine. Histological damages were observed using a semi-quantitative histomorphological scoring system from 0 to 4. Cell apoptosis was analyzed by TUNEL staining in each group. HO-1 and IL-6 mRNA expression was examined by real-time PCR. Results: Compared with renal IR group, the expression of HO-1 mRNA was significantly higher in rhEPO treatment group at 3 , 6, and 24 h after reperfusion(P<0.05). The expression of IL-6 mRNA was significantly lower in the rhEPO treatment group at 6, 24, and 48 h after reperfusion(P<0.05). Serum creatinine level in the rhEPO treatment group was significantly lower than that in the renal IR group at 24 h after reperfusion(P<0.05). Compared with the renal IR group, renal histology injury was greatly attenuated by rhEPO in rhEPO treatment group. TUNEL staining analysis indicated that the apoptotic cells in the IR group were significantly more than those in the sham operation group(P<0.05), and those in the rhEPO treatment group was significantly less than those in the IR group(P<0.05). Conclusion: rhEPO can attenuate renal ischemia/reperfusion injury in mice, probably through promoting the renal expression of HO-1 mRNA.
