雪菊乙醇提取物对丙烯酰胺所致肝损伤的保护作用

Protective Effect of Coreopsis tinctoria Nutt. Ethanol Extract against Acrylamide-induced Liver Injury

该研究探讨雪菊乙醇提取物对ACR所致人肝癌HepG_(2)细胞损伤及小鼠肝损伤的保护作用。以细胞存活率评价雪菊乙醇提取物对HepG_(2)细胞损伤的保护作用,以小鼠体重变化、肝功能和肝脏病理切片结果评价雪菊乙醇提取物对小鼠肝损伤的保护作用,并测定氧化指标探讨保护作用机制。结果显示,雪菊乙醇提取物(2.00 mg/mL)预孵育可使ACR致毒的HepG_(2)细胞存活率增加12.81%,细胞内活性氧(ROS)和丙二醛(MDA)分别降低了57.67%、4.68nmol/mg,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性分别提高了4.68、10.48、13.81 U/mg。雪菊乙醇提取物低(0.25 g/kg)、中(0.5 g/kg)、高剂量(1.0g/kg)组小鼠体重增长率是ACR组的2.2-2.5倍。高剂量组小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)分别降低了27.76、46.79U/L,MDA降低了1.86 nmol/mg,SOD、GSH-Px分别提高了56.73、330.44 U/mg;肝组织HE染色结果显示,雪菊乙醇提取物可改善肝小叶结构和肝细胞形态,减轻小鼠肝组织损伤。综上所述,雪菊乙醇提取物能够阻止ACR对HepG_(2)细胞和小鼠肝组织的损伤,其作用机制与抗氧化能力有关。

The ethanol extract of Coreopsis tinctoria Nutt. was applied to human hepatocellular carcinoma HepG_(2) cells and mouse liver to evaluate its protective effect against acrylamide(ACR)-induced injury. Cell survival rate was used to evaluate the protective effect of C. tinctoria ethanol extract against HepG_(2)cell injury, whereas body weight change, liver function, and liver pathological sections were used to evaluate the protective effect of C. tinctoria ethanol extract against mouse liver injury. Antioxidant indices were also determined to evaluate the underlying protective mechanisms. The results indicated that after preincubation with C. tinctoria ethanol extract(2.00 mg/m L), the survival rate of ACR-injured HepG_(2)cells increased by 12.81%;intracellular reactive oxygen species(ROS) and malondialdehyde(MDA) decreased by 57.67%and 4.68 nmol/mg, respectively;and superoxide dismutase(SOD), catalase(CAT), and glutathione peroxidase(GSH-Px) levels increased by 4.68, 10.48, and 13.81 U/mg, respectively. The weight gain of mice in the low-dose(0.25 g/kg), medium-dose(0.25 g/kg), and high-dose(0.25g/kg) groups of C. tinctoria ethanol extract were 2.2-2.5 times that of the ACR group. In the high-dose group(1.0 g/kg), serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) decreased by 27.76 and 46.79 U/L, respectively;MDA decreased by 1.86nmol/mg, whereas SOD and GSH-Px increased by 56.73 and 330.44 U/mg, respectively. Hematoxylin and eosin staining results of liver tissue showed that the hepatic lobule structure and hepatocyte morphology of mice had improved to varying degrees with low, medium, and high doses of C. tinctoria ethanol extract, with significant alleviation of the injury to liver tissue. In conclusion, C. tinctoria ethanol extract could prevent the ACR-induced injury of HepG_(2)cells and mouse liver tissue, and the underlying mechanism was related to its antioxidant capacity.