Abstract

Objective To investigate the effects of human placenta mesenchymal stem cell (hPMSC) transplantation on superoxide dismutase 1 (SOD1) and uncoupling protein-2 (UCP-2) in the treatment of premature ovarian failure in rats. Methods Sixty SD female rats with normal estrous cycle were randomly divided into four groups (n=15): blank control group, POF model group, treatment control group, and hPMSC transplantation group. It was determinated the ROS levels and 8-OHdG of serum by ELISA method. The ovarian tissue fibrosis was detected by VG staining method; The expression of SOD1 and UCP-2 protein was detected by Western blotting and immunohistochemical staining. Results Serum FSH level in the model group [(10.60±1.0) IU/L] was significantly higher than that in blank control group [(5.83±0.92) IU/L] (P<0.01), while E2 and AMH levels in the model group [(35.52±10.27) ng/L, (2 090.6±397.5) ng/L] were significantly lower than those in blank control group [(65.62±3.76) ng/L, (3 636.39±204.46) ng/L] (P<0.01). The count of the atretic follicle in hPMSC transplantation group (5.36±1.11) was lower than that in treatment control group (8.01±2.22) and POF model group (11.21±1.69) (P<0.05). Compared with the blank control group, the serum ROS was increased in the model group and the treatment control group (P<0.05); compared with the treatment control group, there was a significant change in ROS and 8-OHdG in the hPMSC transplantation group (P<0.05). VG staining showed that the ovarian tissue fibrosis in the model group was obvious, and after hPMSC transplantation there was a significant reduction compared with that in the treatment control group. The expression of SOD1 and UCP-2 protein has a statistical decrease in the hPMSC transplantation group compared with the treatment control group (P<0.05). Conclusion hPMSC transplantation may regulate the mitochondrial ROS synthesis and decrease oxidative stress by decreasing the expression of SOD1 and UCP-2 in rats. Key words: Human placenta mesenchymal stem cell (hPMSC); Premature ovarian failure (POF); Superoxide dismutase 1 (SOD1)/uncoupling protein 2 (UCP-2); Rats

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