Journal of ginseng research · 2026
Ginsenoside Rb1 inhibits oxidative stress and ferroptosis to alleviate salpingitis infertility by down-regulating PTGS2 and up-regulating GPX4.
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Wang Yuhan, Kuang Jilin
Аннотация
BACKGROUND: Salpingitis infertility (SI) is a common disease among women of childbearing age, referring secondary infertility caused by acute or chronic salpingitis. Ginsenoside Rb1 (Rb1) has been confirmed to be an effective drug agent SI. Nevertheless, the underlying mechanism by which Rb1 acts on SI remains unclear.
METHODS: Female mice and FT194 cells were employed as experimental subjects to establish SI models. HE staining was performed to evaluate the morphology changes of fallopian tube tissues. ELISA assays were conducted to determine the levels of inflammatory factors. Commercial kits were performed to examine the contents of MDA, SOD and Fe2+. Western blot and IHC were used to determine protein levels. Cell viability and proliferation were assessed via CCK-8 and EdU assay, respectively.
RESULTS: Rb1 alleviated pathological lesions in fallopian tubal tissues, improved the pregnancy rate and litter size of SI mice and mitigated inflammation, oxidative stress and ferroptosis in both in vivo mouse and in vitro cell models of SI. In SI models, PTGS2 expression was upregulated while GPX4 expression was downregulated and these abnormal expression patterns were reversed by Rb1 treatment. PTGS2 knockdown inhibited ferroptosis and elevated the pregnancy rate and litter size of SI mice, whereas GPX4 knockdown abolished the above beneficial effects. Moreover, PTGS2 was found to downregulate GPX4 expression in SI models under Rb1 intervention.
CONCLUSION: Rb1 treatment decreased PTGS2 expression and increased GPX4 expression, thereby enhancing cell viability and proliferation, alleviating oxidative stress and ferroptosis, and ultimately ameliorating SI.
METHODS: Female mice and FT194 cells were employed as experimental subjects to establish SI models. HE staining was performed to evaluate the morphology changes of fallopian tube tissues. ELISA assays were conducted to determine the levels of inflammatory factors. Commercial kits were performed to examine the contents of MDA, SOD and Fe2+. Western blot and IHC were used to determine protein levels. Cell viability and proliferation were assessed via CCK-8 and EdU assay, respectively.
RESULTS: Rb1 alleviated pathological lesions in fallopian tubal tissues, improved the pregnancy rate and litter size of SI mice and mitigated inflammation, oxidative stress and ferroptosis in both in vivo mouse and in vitro cell models of SI. In SI models, PTGS2 expression was upregulated while GPX4 expression was downregulated and these abnormal expression patterns were reversed by Rb1 treatment. PTGS2 knockdown inhibited ferroptosis and elevated the pregnancy rate and litter size of SI mice, whereas GPX4 knockdown abolished the above beneficial effects. Moreover, PTGS2 was found to downregulate GPX4 expression in SI models under Rb1 intervention.
CONCLUSION: Rb1 treatment decreased PTGS2 expression and increased GPX4 expression, thereby enhancing cell viability and proliferation, alleviating oxidative stress and ferroptosis, and ultimately ameliorating SI.