Abstract: Objective:To explore the effect and mechanism of hypoxia inducible factor-1α (HIF-1α) on energy metabolism in human ovarian granulosa cells KGN.Methods:KGN cells were randomly divided into KGN group (cells without any treatment), si-NC group (transfected with negative control si-NC) and si-HIF-1α group(transfected with siRNA si-HIF-1α).Subsequently, the mRNA expressions of HIF-1α, mitochondrial DNA(mtDNA)and hexokinase 2(HK2)were detected by real-time fluorescence quantitative polymerase chain reaction(RTqPCR).The protein expression of HIF-1α was detected by western blotting.The proliferation ability of KGN cells in each group was detected by cell counting kit-8(CCK-8)assay.Cell apoptosis in each group was detected by flow cytometry.The extracellular acidification rate was measured by extracellular flux analyzer.Mitochondrial reactive oxygen species (ROS) in each group was detected by mitochondrial superoxide (MitSOX) fluorescence staining.The cell membrane potential in each group was detected by 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetraethylbenzimidazolyl-carbocyanine iodide (JC-1) fluorescence staining.The content of intracellular ATP in each group was detected by adenosine triphosphate (ATP) detection kit.Results:Low expression of HIF-1α could reduce the proliferation activity of KGN cells (P< 0.01) and increase the apoptosis rate (P< 0.01).At the same time, the extracellular acidification rate increased significantly(P< 0.01), while the expression of HK2 decreased significantly (P< 0.01).The content of ROS in mitochondria increased significantly(P< 0.01).The relative membrane potential and ATP content decreased significantly(P< 0.01).Conclusion:Low expression of HIF-1α reduces the glycolysis ability of KGN cells and up-regulates mitochondrial ROS content to cause mitochondrial damage, which ultimately affects the growth of KGN cells.