Objective. Severe acute pancreatitis (SAP) is a serious and life-threatening disease associated with multiple organ failure and a high mortality rate and is accompanied by distinct oxidative stress and inflammatory responses. Saikosaponin A has strong antioxidant properties and can affect the composition of gut microbiota. We sought to determine the effects of Saikosaponin A interventions on SAP by investigating the changes of gut microbiota and related antioxidant signaling. Methods. A SAP model was established in Sprague-Dawley (SD) rats through the injection of sodium taurocholate into the biliopancreatic duct and confirmed by elevated levels of serum lipase and amylase. The model was fed a standard diet either with saline solution or with Saikosaponin A. Fecal microbiota transplantation (FMT) from Saikosaponin A-induced rats into the rat model was performed to test the effects of gut microbiota. The composition of gut microbiota was analyzed by using 16S rRNA gene sequencing. We measured apoptotic status, inflammatory biomarkers, and Keap1-Nrf2-ARE ((Kelch-like ECH-associated protein 1) nuclear factor erythroid 2-related factor 2-antioxidant response element) antioxidant signaling. Results. Saikosaponin A intervention attenuated SAP lesions and reduced the levels of serum amylase and lipase, oxidative stress, and inflammatory responses by reducing pathological scores and affecting the serum level of oxidative and inflammatory factors. Meanwhile, the expression of Keap1-Nrf2-ARE was increased. Saikosaponin A intervention improved microbiota composition by increasing the relative abundance of Lactobacillus and Prevotella species. FMT resulted in similar results as those caused by the Saikosaponin A intervention, suggesting Saikosaponin A may exert its function via the improvement of gut microbiota composition. Conclusions. Saikosaponin A-induced gut microbiota changes attenuate SAP progression in the rat model and may be a potential natural drug for adjuvant treatment of SAP. Further work is needed to clear up the points.

中文翻译：

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柴胡皂苷 A 诱导的肠道微生物群变化通过激活 Keap1/Nrf2-ARE 抗氧化信号传导来减轻严重急性胰腺炎

客观。重症急性胰腺炎 (SAP) 是一种严重且危及生命的疾病，与多器官衰竭和高死亡率相关，并伴有明显的氧化应激和炎症反应。Saikosaponin A 具有很强的抗氧化特性，可以影响肠道微生物群的组成。我们试图通过调查肠道微生物群的变化和相关的抗氧化信号来确定柴胡皂苷 A 干预对 SAP 的影响。方法. 通过将牛磺胆酸钠注射到胆胰管中，在 Sprague-Dawley (SD) 大鼠中建立了 SAP 模型，并通过血清脂肪酶和淀粉酶水平升高来证实。该模型喂食盐水溶液或柴胡皂苷 A 的标准饮食。将柴胡皂苷 A 诱导的大鼠的粪便微生物群移植 (FMT) 移植到大鼠模型中以测试肠道微生物群的影响。通过使用 16S rRNA 基因测序分析肠道微生物群的组成。我们测量了凋亡状态、炎症生物标志物和 Keap1-Nrf2-ARE（（Kelch 样 ECH 相关蛋白 1）核因子红细胞 2 相关因子 2-抗氧化反应元件）抗氧化信号。结果. Saikosaponin A 干预通过降低病理评分和影响血清氧化和炎症因子水平来减轻 SAP 病变并降低血清淀粉酶和脂肪酶、氧化应激和炎症反应的水平。同时，Keap1-Nrf2-ARE 的表达增加。Saikosaponin A 干预通过增加乳酸杆菌和普氏菌的相对丰度来改善微生物群组成。FMT 导致的结果与由 Saikosaponin A 干预引起的结果相似，表明 Saikosaponin A 可能通过改善肠道微生物群组成来发挥其功能。结论. Saikosaponin A 诱导的肠道菌群变化减弱了大鼠模型中 SAP 的进展，可能是一种潜在的用于辅助治疗 SAP 的天然药物。需要进一步的工作来澄清这些点。