Hepatoprotective Effects of Against Carbon Tetrachloride-Induced Acute Liver Injury in Rats
Jie Li,
Dan Song,
Bintao Zhang,
Jinwei Guo,
Wenping Li,
Xiaoying Zhang,
Qin Zhao
Affiliations
Jie Li
Engineering Research Center of Tibetan Medicine Detection Technology, Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Dan Song
Engineering Research Center of Tibetan Medicine Detection Technology, Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Bintao Zhang
Xianyang Central Hospital, Xianyang, Shaanxi, China
Jinwei Guo
Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Wenping Li
Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Xiaoying Zhang
Engineering Research Center of Tibetan Medicine Detection Technology, Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Qin Zhao
Engineering Research Center of Tibetan Medicine Detection Technology, Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China
Purpose: To determine the hepatoprotective mechanisms of Heracleum candicans in rats with acute liver injury induced by carbon tetrachloride (CCl 4 ). Methods: Rats were intragastrically administered H candicans twice a day for 14 consecutive days and were intraperitoneally challenged with CCl 4 . Alanine aminotransferase and aspartate aminotransferase were measured to indicate liver injury. Malondialdehyde antioxidant enzyme activity and tumor necrosis factor-alpha and interleukin 6 secretion were measured as liver injury indicators. Histopathological tests were conducted to determine whether H candicans ameliorated liver injury. Results: CCl 4 -induced liver injury led to significant increases in liver injury biochemical indicators transaminase and malondialdehyde activities. H candicans pretreatments inhibited these increases. Pathological sections in pretreated samples exhibited reduced vacuole formation, neutrophil infiltration, and necrosis. Conclusion: H candicans increases the antioxidant capacity of the liver and maintains hepatocyte function in the face of CCl 4 -induced injury.
