Growth hormone (GH) is a polypeptide hormone that could reduce the mitochondria-mediated oxidative stress and improve the mitochondrial function. However, the mechanisms of GH on granulosa cell apoptosis and mitochondrial function is still unclear. The aim of this study is to determine the effects of GH on granulosa cells apoptosis and the underlying mechanisms. In this study, we exposed the ovarian granulosa cell line (KGN cell) with cisplatin to establish an ovarian granulosa cell apoptosis and mitochondrial dysfunction model in vitro. To examine the benefit of GH in restoration of granulosa cell, we determined cell proliferation, cell apoptosis, reactive oxygen species (ROS) level, the expression of antioxidant components Sod2, Sirt3, as well as the mitochondrial membrane potential and mitochondrial DNA (mtDNA) copy number after GH treatment. We found that the cisplatin exposure significantly inhibited cell proliferation and elevated the apoptotic rate by student's t-test (p < 0.05). Whereas, the GH treatment could rescue the cell proliferation and decrease the apoptotic rate, as well as reduce the Bax/Bcl-2 ratio (p < 0.05). Additionally, GH significantly reduced abnormal ROS levels and increased the level of Sirt3 and Sod2 thus alleviating the oxidative stress. We also found that GH facilitated the recovery of mitochondrial membrane potential and mitochondrial DNA (mtDNA) copy number in granulosa cells. Our results indicated that GH exerted protective effects in cisplatin-induced ovarian granulosa cell apoptosis by alleviating oxidative stress and enhancing mitochondrial function via Sirt3-Sod2 pathway.
Keywords: Cell apoptosis; Growth hormone; Mitochondrial function; Ovarian granulosa; Oxidative stress.
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