HONG Yue, CHEN Youxia, LIU Zhenzhen, et al. Protective Effect of Caffeic Acid on CCl4-Induced Injury of BRL Hepatocyte[J]. Science and Technology of Food Industry, 2021, 42(23): 356−361. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021020121.
Citation: HONG Yue, CHEN Youxia, LIU Zhenzhen, et al. Protective Effect of Caffeic Acid on CCl4-Induced Injury of BRL Hepatocyte[J]. Science and Technology of Food Industry, 2021, 42(23): 356−361. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021020121.

Protective Effect of Caffeic Acid on CCl4-Induced Injury of BRL Hepatocyte

  • This work aimed to investigate protective effect of caffeic acid on CCl4-induced BRL hepatocyte injury. The experiment was divided into control group, CCl4 model group (100 mmol/L CCl4 injury for 3 hours) and CA pretreated group (pretreated with 0.2, 0.4 and 0.8 mg/mL CA in DMEM for 4 hours, followed by CCl4 exposure for 3 hours). The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) were detected by automatic biochemical analyzer. The levels of reactive oxygen species (ROS), cytochrome C (Cyt c) and 8-hydroxydeoxyguanosine (8-OHdG) were measured by the kit. The expression levels of nuclear factor E2-related factor 2 (Nrf2), glutathione reductase (GSR), quinine oxidoreductase (NQO1) and superoxide dismutase (SOD) were detected by qRT-PCR. Significant inhibitory effects of CA were observed on the CCl4-induced elevation of AST, ALT, LDH, ROS, Cyt c and 8-OHdG in culture medium (P<0.05). Compared with the control group, no significant differences of the mRNA expression levels of Nrf2, GSR, NQO1 and SOD gene were found in the model group (P>0.05). However, the mRNA expression levels of all detected genes were significantly increased in CA-treated group compared with the control group and a dose-dependent manner was observed. In conclusion, CCl4 exposure induced oxidative stress in BRL hepatocytes and CA inhibited the CCl4-induced BRL hepatocyte damage by activating the Nrf2/ARE signaling pathway and up-regulating the mRNA levels of antioxidant genes.
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