Reproductive biomedicine online · 2025
Pyrroloquinoline quinone activates lactate and inhibits NLRP3 to improve ovarian reserve in premature ovarian insufficiency.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Liu Ke, Lei SiYuan, Li BaoXiang, Huo Peng, Ma Yue, Zhong Ou, Li Wanhan, Zhang Shun, Chen Xi, Hu Linlin, Lei Xiaocan
Аннотация
RESEARCH QUESTION: Can the use of pyrroloquinoline quinone (PQQ) to treat premature ovarian insufficiency (POI) induced by cyclophosphamide (CTX) in rats restore ovarian function?
DESIGN: Thirty female Sprague-Dawley rats were divided at random into three groups: control group (n = 10), POI group (n = 10), and POI-PQQ group (n = 10). An ovarian aging model was induced by CTX and treated with PQQ. The body weight of the rats was monitored throughout the process, and serum samples were collected to determine hormone concentrations. Biochemical, histopathological, TUNEL, immunohistochemical, transcriptomic, metabolomic, glycolytic pathway, and inflammatory pathway analyses were undertaken for each ovarian tissue sample. To explore the mechanisms further, KGN cells were treated with lipopolysaccharides (LPS) to mimic the inflammatory environment, alongside PQQ. Each group underwent investigation of the inflammatory and glycolytic pathways.
RESULTS: PQQ increased the body weight and ovarian index of rats with POI, partially restored the interrupted oestrous cycle, prevented follicle loss, restored ovarian reserve, decreased serum FSH concentration significantly (P = 0.0002), increased oestradiol concentration (P = 0.0306), and reduced granulosa cell apoptosis. PQQ treatment also up-regulated the lactate concentration and expression of key rate-limiting enzymes of glycolysis, and down-regulated the expression of inflammatory factors in rats with POI. Further experiments showed that the inflammatory response, abnormal glycolysis and apoptosis in KGN cells caused by LPS could be recovered through PQQ intervention.
CONCLUSIONS: Ovarian reserve in rats with POI can be restored by PQQ treatment by reducing inflammation by the glycolytic pathway.
DESIGN: Thirty female Sprague-Dawley rats were divided at random into three groups: control group (n = 10), POI group (n = 10), and POI-PQQ group (n = 10). An ovarian aging model was induced by CTX and treated with PQQ. The body weight of the rats was monitored throughout the process, and serum samples were collected to determine hormone concentrations. Biochemical, histopathological, TUNEL, immunohistochemical, transcriptomic, metabolomic, glycolytic pathway, and inflammatory pathway analyses were undertaken for each ovarian tissue sample. To explore the mechanisms further, KGN cells were treated with lipopolysaccharides (LPS) to mimic the inflammatory environment, alongside PQQ. Each group underwent investigation of the inflammatory and glycolytic pathways.
RESULTS: PQQ increased the body weight and ovarian index of rats with POI, partially restored the interrupted oestrous cycle, prevented follicle loss, restored ovarian reserve, decreased serum FSH concentration significantly (P = 0.0002), increased oestradiol concentration (P = 0.0306), and reduced granulosa cell apoptosis. PQQ treatment also up-regulated the lactate concentration and expression of key rate-limiting enzymes of glycolysis, and down-regulated the expression of inflammatory factors in rats with POI. Further experiments showed that the inflammatory response, abnormal glycolysis and apoptosis in KGN cells caused by LPS could be recovered through PQQ intervention.
CONCLUSIONS: Ovarian reserve in rats with POI can be restored by PQQ treatment by reducing inflammation by the glycolytic pathway.