Mechanism of Thymopentin Alleviating Cisplatin-Induced Premature Ovarian Failure by Reducing Endoplasmic Reticulum Stress in Granulosa Cells

Abstract

The paper aimed to investigate the mechanism of thymopentin alleviating cisplatin-induced premature ovarian failure by reducing endoplasmic reticulum pressure in granulosa cells. Mice at 2 mo of age were intraperitoneally injected with cisplatin to establish premature ovarian failure model. Ovarian premature failure model was induced by granulosa cells treated with cisplatin (10 μm) for 24 h. The mice were getting into the following groups; control group, premature ovarian failure group, thymopentin+premature ovarian failure group. Isolated and cultured granulosa cells were divided into granulosa cells group, cisplatin induced group and thymopentin group. Cisplatin induces mitochondrial integrity but mitochondrial damage, membrane swelling and rupture. The mitochondrial damage rate in cisplatin induced group was higher than control group (p<0.05), and thymopentin significantly improved the mitochondrial damage induced by cisplatin. Follicle stimulating hormone receptor and estradiol expression horizontals in premature ovarian failure were reduced than control group, the expression horizontals of follicle stimulating hormone receptor and estradiol in thymopentin+premature ovarian failure group were raised than premature ovarian failure group (p<0.05), and the horizontal of follicle stimulating hormone in premature ovarian failure group was raised than control group (p<0.05). The horizontal of follicle stimulating hormone in thymopentin+premature ovarian failure group was lower than that in premature ovarian failure. Premature ovarian failure atretic follicle rate was higher than control group, atretic follicle rate in thymopentin+premature ovarian failure was lower than premature ovarian failure, and the ratio of original follicle to total follicle number in premature ovarian failure group was lower than control group. Thymopentin can reduce endoplasmic reticulum stress and apoptosis of granulosa cells induced by cisplatin, increase the number of follicles, prevent follicle atretic, and participate in the protection of cisplatin induced premature ovarian failure, which provides the basis for clinical drug treatment of premature ovarian failure002E