To explore the effect of Gallic acid on liver tissue damage in autoimmune hepatitis (AIH) mice by adjusting adenosine monophosphate-activated protein kinase (AMPK) / acetyl-coa carboxylase (ACC) signaling pathway.

An AIH mouse model was established by injecting 15 mg·kg^-1 concanavalin A through the tail vein. The mice were randomly divided into model group, low-dose experimental group (50 mg·kg^-1), high-dose experimental group (100 mg·kg^-1), AMPK inhibitor group (5 μmol·L^-1), gallic acid + AMPK inhibitor group and normal mice group with the same volume of phosphate-buffered solution as control group. After the intervention, the automatic biochemical analyzer was used to analyze glutamic pyruvic transaminase (GPT), the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in liver homogenate were detected by enzyme-linked immunosorbent assay (ELISA), and the levels of interleukin (IL)-10, IL-6 and tumor necrosis factor (TNF-α) in serum supernatant were also measured. The histopathological changes were detected by the hematoxylin-eosin (HE) staining method; the apoptosis status was examined by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. The relative expression levels of phosphorylated (p-) AMPK/AMPK, Bcl-2 related X protein (Bax), B-cell lymphoma/leukemia-2 protein (Bcl-2) and ACC protein were detected by Western blotting.

The glutamic-oxalacetic transaminase (GOT) levels in control group, model group, low-dose experimental group, high-dose experimental group, AMPK inhibitor group and high-dose experimental+AMPK inhibitor group were (82.05±8.31), (210.20±21.14), (135.26±14.64), (91.02±9.21), (308.15±30.85) and (129.84±13.08) U·L^-1, respectively; the GPT levels were (50.23±5.11), (324.85±33.25), (152.34±15.48), (88.64±8.95), (482.62±50.02) and (148.85±15.02) U·L^-1, respectively; the TNF-α levels were (41.06±4.37), (149.85±15.28), (88.39±8.97), (51.06±5.21), (267.85±27.18) and (154.62±15.68) pg·mL^-1, respectively; the IL-6 levels were (48.42±4.92), (134.52±13.58), (75.42±7.61), (57.85±5.81), (215.84±21.98) and (78.62±7.98) pg·mL^-1, respectively; the IL-10 levels were (486.52±49.02), (188.72±19.08), (318.54±32.08), (445.67±45.11), (114.21±11.94) and (324.15±32.67) pg·mL^-1, respectively; the SOD levels were (48.26±4.99), (19.52±2.11), (32.25±3.44), (44.21±4.57), (11.37±1.21) and (31.24±3.22) U·mg^-1, respectively; the MDA levels were (0.28±0.03), (0.84±0.09), (0.56±0.06), (0.31±0.04), (1.31±0.15) and (0.64±0.07) nmol·mg^-1, respectively; the tissue pathological scores were 0, 2.64±0.27, 2.27±0.24, 1.22±0.14, 3.54±0.36 and 2.19±0.23, respectively; the apoptosis rates were (5.24±0.54)%, (23.62±2.44)%, (16.42±1.72)%, (8.52±0.89)%, (34.85±3.61)% and (17.06±1.75)%, respectively. The above indexes of model group were compared with those of control group; low-dose and high-dose experimental group were compared with those of model group and high-dose experimental+AMPK inhibitor group were compared with those of high-dose experimental group, there were statistically significant differences (all P<0.05).

Gallic acid can inhibit the inflammatory response and oxidative stress level in AIH mice, reduce cell apoptosis, improve liver function, alleviate liver tissue pathological damage, down-regulate Bax and ACC expression, up-regulate p-AMPK/AMPK and Bcl-2 expression; the AMPK inhibitor reverses the protective effect of high-dose gallic acid on AIH mice. Gallic acid activates the AMPK/ACC signaling pathway to alleviate liver tissue damage in AIH mice.