The effects of Astragalus membranaceus on inflammation and apoptosis in rats with preeclampisa

BACKGROUND: Preeclampsia, an idiopathic multifactorial hypertensive disorder associated with pregnancy, is characterized by systemic immune regularization, inflammatory, excessive placental apoptosis, and widespread vasoconstriction, among other pathological features. Astragalus membranaceus (AMS) exhibits diverse biological activities, including immunomodulation, antiapoptosis, antioxidation, antiinflammatory and anticancer effects. Numerous studies have demonstrated its therapeutic potential in mitigating endothelial injury, reducing blood pressure, and improving renal function. In this systematic in-vivo investigation, we elucidated the biological activity and mechanistic underpinnings of AMS in ameliorating preeclampsia development. METHODS: The optimal dosage of AMS was determined through preliminary experiments. Pregnant Sprague-Dawley rats (n = 40) were randomly allocated into four experimental groups: control, control+AMS, L-NAME-treated, and L-NAME + AMS-treated. Inflammatory and placental apoptosis-related markers were analyzed using real-time quantitative PCR (RT-qPCR), Western blotting, and immunohistochemistry. Additionally, ELISA was conducted to quantify the expression of inflammation-related genes. RESULTS: AMS significantly ameliorated hypertension, proteinuria, and abortion rates of rats with preeclampsia with l-NAME-induced. It effectively inhibited the placental and serum expression of TNF-α at both mRNA and protein levels, while simultaneously increasing placental and serum levels of IL-10 and mitigating serum IL-6 expression, mitigating inflammation in rats with preeclampisa. Furthermore, AMS reduced FAS in the extrinsic apoptosis pathway and regulated BCL-2/BAX/BAK/AIF in the mitochondrial apoptosis pathway in rats with preeclampsia. CONCLUSION: Our study demonstrates that AMS significantly reduced the hypertension and proteinuria in rats with preeclampsia. AMS alleviates inflammation and apoptosis in rats with preeclampsia by regulating inflammatory factors and mitochondrial outer membrane permeability (MOMP). Additional AMS reduced FAS (CD95/APO-1), in the extrinsic apoptosis pathway. AMS offers a potential therapeutic strategy for preeclampsia.