Huang Xiaoli, Sun Wen, Sun Chang, Tan Jiajun, Wu Liang, Yang Fumeng
Medical Laboratory Department, Sihong Hospital, Sihong, China.
Department of Critical Care Medicine, Jurong Hospital, Affiliated to Jiangsu University, Zhenjiang, China.
Endocr Metab Immune Disord Drug Targets. 2025;25(9):695-709. doi: 10.2174/0118715303325372241014152811.
Senna leaf is a commonly used medication for treating constipation, and long-term use can cause damage to the intestinal mucosa and lead to drug dependence. But the exact mechanism remains unclear.
Using non-targeted metabolomics technology to study the mechanism of senna leaf ethanol extract (EESL) inducing inflammation and oxidative stress in mice and causing side effects.
EESL was administered to mice by gavage to detect inflammation and oxidative stressrelated factors in mice, and the EESL components and differential metabolites in mouse plasma were analyzed using non-targeted metabolome techniques.
23 anthraquinone compounds were identified in the EESL, including sennoside and their derivatives. Administration of EESL to mice resulted in a significant increase in pro-inflammatory factors, IL-1β, and IL-6 in the plasma, while the levels of IgA significantly decreased. The levels of oxidative stress significantly increased, and the intestinal mucosal integrity was impaired. 21 endogenous in plasma metabolites were identified as differential metabolites related with taurine and taurine metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, tryptophan metabolism, and sphingolipid metabolism. These metabolic pathways are related to oxidative stress and inflammation.
Senna leaf can inhibit the expression of tight junction proteins in the intestinal mucosa and disrupt intestinal mucosal barrier integrity, exacerbating oxidative stress and inflammation induced by bacterial LPS entering the bloodstream. In addition, the impact of Senna leaf on tryptophan metabolism may be linked to the occurrence of drug dependence.
番泻叶是治疗便秘的常用药物,长期使用会对肠黏膜造成损害并导致药物依赖。但其确切机制尚不清楚。
采用非靶向代谢组学技术研究番泻叶乙醇提取物(EESL)诱导小鼠炎症和氧化应激并产生副作用的机制。
通过灌胃给予小鼠EESL,检测小鼠体内炎症和氧化应激相关因子,并采用非靶向代谢组学技术分析小鼠血浆中的EESL成分和差异代谢物。
在EESL中鉴定出23种蒽醌类化合物,包括番泻苷及其衍生物。给小鼠灌胃EESL后,血浆中促炎因子IL-1β和IL-6显著升高,而IgA水平显著降低。氧化应激水平显著升高,肠黏膜完整性受损。血浆中的21种内源性代谢物被鉴定为与牛磺酸及牛磺酸代谢、甘油磷脂代谢、花生四烯酸代谢、色氨酸代谢和鞘脂代谢相关的差异代谢物。这些代谢途径与氧化应激和炎症有关。
番泻叶可抑制肠黏膜紧密连接蛋白的表达,破坏肠黏膜屏障完整性,加剧细菌脂多糖进入血液所诱导的氧化应激和炎症。此外,番泻叶对色氨酸代谢的影响可能与药物依赖的发生有关。