关键词: 酒精性肝纤维化, 甲状腺激素T3, 增殖, 凋亡

Abstract: Objective Exploring the effects of exogenous thyroid hormone T3 on liver cell proliferation and apoptosis in alcoholic liver fibrosis in mice. Methods Thirty eight healthy SPF grade C57BL/6N male rats aged 6-8W were divided into five groups: six mice in the normal control group, eight in the model group and eight in the three different doses of T3 intervention groups. The control group was fed with TP4060C liquid control diet for 8W, the model group and T3 intervention groups were fed with TP4060A alcohol diet for 8W and gavage with 31.5% alcohol from the 3rd week to establish an alcoholic liver fibrosis model. Starting from the 6th week, mice in the intervention group were injected intraperitoneally with different doses of T3 daily until the 8th week. Blood samples were taken from the eyeballs of all mice to detect serum transaminase (ALT, AST) activity. Liver samples were dissected for HE staining and Sirius red staining; Western blot was used to detect the expression levels of PCNA, Caspase-9, and a-SMA. Results The ALT activity (35.544 ± 4.039) and AST activity (78.250 ± 9.307) in the model group were higher than those in the normal group (ALT activity: 14.336±3.553; AST activity: 40.842±3.834, P<0.05), but the serum ALT activity (25.242 ± 3.469, 22.940 ± 4.566, 27.556 ± 4.609) in the T3 intervention groups was lower than that in the model group (P<0.05); At the same time, the AST activity of T3 intervention groups (52.213 ± 9.664, 40.938 ± 7.565, 48.696 ± 12.443) was also decreased in varying degrees compared with the model group (P<0.05). Immunoblotting showed that PCNA (0.475 ± 0.019, 1.001 ± 0.034, 0.876 ± 0.015, 0.618 ± 0.035, 0.906 ± 0.092), caspase-9 (0.832 ± 0.024, 1.23 ± 0.054, 1.040 ± 0.035, 0.943 ± 0.036, 1.114 ± 0.072), a-SMA (0.592 ± 0.046, 1.037 ± 0.043, 0.892 ± 0.028, 0.715±0.034、0.854±0.047) in the five groups of mice, the relative expression levels of the three factors in the model group were higher than those in the normal group (P<0.05), and the relative expression levels of the three factors in the T3 intervention group were lower than those in the model group (P<0.05). Conclusion Adequate supplementation of thyroid hormone T3 can inhibit the activation of HSC in liver fibrosis mice, thereby inhibiting liver cell apoptosis.

Key words: Alcoholic liver fibrosis, Thyroid hormone T3, Proliferation, Apoptosis