Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research (DIPSAR), University of Delhi, Pushp Vihar, Sector-3, M.B. Road, New Delhi 110 017, India.
Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research (DIPSAR), University of Delhi, Pushp Vihar, Sector-3, M.B. Road, New Delhi 110 017, India; Pharamcology Research Laboratory, University Institute of Pharmaceutical Sciences (UIPS), Panjab University, Sector-14, Chandigarh 160014, India.
Biomed Pharmacother. 2017 Nov;95:1040-1050. doi: 10.1016/j.biopha.2017.08.082. Epub 2017 Sep 13.
Oxidative stress and hepatic inflammatory response is primarily implicated in the pathogenesis of LPS induced acute liver injury. Stevioside, a diterpenoidal glycoside isolated from the Stevia rebaudiana leaves, exerts potent anti-oxidant, anti-inflammatory and immunomodulatory activities. The present study was aimed to investigate the hepatoprotective effect of hydroalcoholic extract of Stevia rebaudiana leaves (STE EXT) and its major phytochemical constituent, stevioside (STE) in LPS induced acute liver injury. The hepatoprotective activity of STE EXT (500mg/kg p.o) and STE (250mg/kg p.o) was investigated in lipopolysaccharide (LPS 5mg/kg i.p.) induced acute liver injury in male wistar rats. Our results revealed that both STE EXT and STE treatment ameliorated LPS induced hepatic oxidative stress, evident from altered levels of reduced SOD, Catalase, GSH, MDA, NO. Histopathological observations revealed that both STE EXT and STE attenuated LPS induced structural changes and hepatocellular apoptosis providing additional evidence for its hepatoprotective effect. Further, STE EXT and STE significantly restored the elevated serum and tissue levels of AST and ALT in LPS treated rats. Furthermore, both STE EXT and STE rescued hepatocellular dysfunctions to normal by altering the level of proinflammatory cytokines such as TNF-α, IL-1β and IL-6 exhibiting its anti-inflammatory potential. In conclusion, both STE EXT and STE demonstrated excellent hepatoprotective effects against endotoxemia induced acute liver injury possibly through suppression of hepatic inflammatory response and oxidative stress, attributing to its medicinal importance in treating various liver ailments.
氧化应激和肝脏炎症反应主要与 LPS 诱导的急性肝损伤的发病机制有关。甜菊糖苷是从甜叶菊叶子中分离出来的二萜糖苷,具有很强的抗氧化、抗炎和免疫调节作用。本研究旨在探讨甜叶菊叶水醇提取物(STE EXT)及其主要化学成分甜菊苷(STE)对 LPS 诱导的急性肝损伤的保护作用。在雄性 Wistar 大鼠中,研究了 STE EXT(500mg/kg po)和 STE(250mg/kg po)对脂多糖(LPS 5mg/kg ip)诱导的急性肝损伤的保护作用。我们的结果表明,STE EXT 和 STE 治疗均改善了 LPS 诱导的肝氧化应激,这从降低 SOD、过氧化氢酶、GSH、MDA、NO 的水平上可以看出。组织病理学观察表明,STE EXT 和 STE 均减轻了 LPS 诱导的结构变化和肝细胞凋亡,为其保肝作用提供了额外的证据。此外,STE EXT 和 STE 还显著恢复了 LPS 处理大鼠升高的血清和组织中 AST 和 ALT 水平。此外,STE EXT 和 STE 通过改变 TNF-α、IL-1β 和 IL-6 等促炎细胞因子的水平,使肝细胞功能紊乱恢复正常,表现出其抗炎潜力。总之,STE EXT 和 STE 对内毒素血症诱导的急性肝损伤均显示出良好的保护作用,可能是通过抑制肝脏炎症反应和氧化应激,这归因于其在治疗各种肝脏疾病方面的重要医学意义。