In vitro and in vivo protective effect of Lotus seedpod extract against acetaminophen-induced liver injury

• Main Authors: Xiao-Yin Huang, 黃筱尹
• Other Authors: Jing-Hsien Chen
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/x7r4ff

碩士 === 中山醫學大學 === 營養學系碩士班 === 104 === Acetaminophen (APAP) is one of the most widely used analgesic and antipyretic drug in the world. APAP overdose will lead to severe liver injury and have potential to result in acute liver failure. Lotus seedpod, a traditional herbal, is rich in polyphenol and has been shown to possess antioxidant, radioprotective and anti-cancer activities. However, there were no significant reports on the hepatoprotective effect of LSE. In this study, we examined the hepatoprotective role of lotus seedpod extracts (LSE) in vitro and in vivo. Firstly, LSE or its main compound epigallocatechin (EGC) dose-dependently improved the survival of human hepatocyte HepG2 cells from APAP-induced loss of viability. LSE or EGC showed potential in reducing APAP-induced occurrence of apoptosis confirmed by morphological and biochemical features, including an increase in the distribution of hypodiploid phase, apoptotic bodies formation and caspases activation. Molecular data showed that antiapoptotic effects of LSE or EGC might be mediated via intrinsic, extrinsic and ASK 1/JNK apoptotic signaling pathways. Further data showed that LSE inhibited the APAP-induced the protein expression of iNOS. In vivo study, the BALB/c mice were supplemented with or without LSE (1% and 2%) during the 9-week treatment period in the presence or absence of APAP (i.p.; 400 mg/kg) twice per week. Our investigation demonstrated that LSE treatments significantly decreased the serum levels of the hepatic enzyme markers GOT and GPT, and triglyceride (TG) induced by APAP. LSE also inhibited the serum levels of inflammatory cytokines (IL-6 and IL-1β) during APAP treatment. LSE at 1% significantly restored the decrease in glutathione (GSH) content and elevated the levels of antioxidant enzymes, including catalase and glutathione reductase (GRd), in the liver. Western blotting data demonstrated that LSE and N-acetylcysteine (NAC) inhibited the expression of caspase -3, -8, -9 in APAP-induced liver injury. Our data imply that LSE reduced APAP-induced hepatocytes apoptosis, and these findings may open interesting perspectives to the strategy in treatment of liver injury.