1.Effects of Oligo-peptide I-C-F-6 in Carapax Trionycis on Rats with Liver Fibrosis Induced by CCl4
Mina WANG ; Jinxuan LIN ; Ying YANG ; Shixun XU ; Huazheng ZHANG ; Liwei REN ; Haimin LEI ; Yuzhong ZHANG
Chinese Journal of Information on Traditional Chinese Medicine 2014;(8):42-45
Objective To study effects of oligo-peptide I-C-F-6 in carapax trionycis on rats with liver fibrosis induced by CCl4;To discuss its anti-liver fibrosis effects and possible mechanisms. Methods Forty-eight SD male rats were randomly divided into normal control group, model group, bifendate group, and oligo-peptide I-C-F-6 group, 12 in each group.CCl4 was injected intraperitoneally to build rat liver fibrosis model.Oligo-peptide I-C-F-6 group and bifendate group were given subcutaneous injection of oligo-peptide I-C-F-6 (0.12μg/g) or bifendate (0.12μg/g). At the same time, normal control group and model group were giventhe same volume of saline for seven weeks. The levels ofALT, AST,MDA, SOD, IL-4, IL-10 and TNF-α were tested.The histomorphology changes were observed under optical microscopeby HE, and the expressions of transforming growth TGF-β1 were determined by immunohistochemistry.Results Compared with model group, serum levels of ALT and AST were reduced evidently in oligo-peptide I-C-F-6 group. Hepatic content of MDA, IL-4 and TNF-α decreased, while SOD activity and IL-10 were found significantly increased. Liver fibrosis was ameliorated significantly. Hepatic expressions of TGF-β1 were weakly positive.Conclusion Oligo-peptide I-C-F-6 can ameliorate hepatocyte damage of model rats, thus it has anti-oxidative and anti-liver fibrosis effects on liver fibrosis in rats.
2.The effects of HBx on the proliferation and invasion of hepatocellular carcinoma and sorafenib resistance
Luzheng LIU ; Jiacheng CHEN ; Liang CHEN ; Cheng CHEN ; Dafeng XU ; Shixun LIN ; Xiangxiang LUO ; Jincai WU
Chinese Journal of Hepatobiliary Surgery 2021;27(11):842-846
Objective:To investigate the effects of hepatitis B virus X (HBx) on hepatocellular carcinoma (HCC) proliferation, invasion, and sorafenib resistance.Methods:HepG2 cell line infected with HBx ORF lentivirus was set as the HBx high expression group and infected with empty vector was set as the negative control group. The interference group was infected with the HBx siRNA virus based on the HBx high expression group to reduce HBx expression. Interference control group as interference group but with infected empty vector virus. Western blotting was used to measure the protein level of HBx. Cell proliferation, invasion ability, and sorafenib semi-inhibitory concentration (IC50) of HCC cells under different HBx expression levels were respectively detected by cell proliferation assay kit, Transwell invasion assay, and cell titer-glo kit.Results:Western blotting showed that the stable cell lines were successfully established. Cell proliferation of the HBx high expression group was better than that of the blank control and negative control groups, and the cell proliferation of the interference group was lower than that of the interference control and HBx high expression groups, and the differences were all statistically significant ( P<0.05). The number of cells crossing Matrigel gel was (46.2±4.1), (50.7±5.1) and (48.2±5.2) in the blank control group, negative control group, and interference group, respectively. The number of cells crossing Matrigel gel in the HBx high expression group (124.2±8.3) and the interference control group (117.2±7.5) were higher than the above three groups, respectively, and the differences were all statistically significant ( P<0.05). The IC50 of cells in the HBx high expression group and the interference control group were (5.36±0.31) μmol/L and (5.48±0.20) μmol/L, respectively, which were higher than those in the blank control group, the negative control group, and the interference group (4.75±0.22) μmol/L, (4.60±0.14) μmol/L and (3.98±0.03) μmol/L. The differences were all statistically significant ( P<0.05). Conclusion:HBx promoted the tumor proliferation and invasion of HepG2 HCC cells, enhanced the ability to sorafenib resistance, and inhibited apoptosis.