Abstract
Objective To investigate the protective effect and mechanism of berberine hydrochloride (BBR) on liver after acute hypoxic exposure. Methods C57BL/6 mice were divided into three groups consisting of normoxic group, hypoxic exposure group, and hypoxic exposure combined with BBR group. On the 7th day of the experiment, mice were sacrificed and liver tissue was collected. The pathological changes of liver tissue were observed by HE staining. The mRNA levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS) in liver tissue were detected by real time quantitative PCR. The protein levels of TNF-α, cleaved-caspase-3 (c-caspase-3), and caspase-8 in liver tissue were detected by Western blotting. The apoptosis of mouse liver tissue was detected by TUNEL. Results After 7 days of hypoxic exposure, the body mass and liver mass of mice decreased significantly, and the liver tissue damage was obvious; the mRNA levels of TNF-α and IL-1β and the protein levels of caspase-8 and c-caspase-3 in liver tissue cells significantly increased, and the apoptosis level of liver tissue cells markedly increased as well. BBR treatment significantly increased the body mass and liver mass of mice exposed to hypoxia for 7 days, decreased the mRNA level of TNF-α and the protein expressions of caspase-8 and c-caspase-3, and reduced the apoptosis of liver tissue cells. Conclusion BBR may attenuate liver injury induced by hypoxic exposure by inhibiting TNF-α/caspase-8/caspase-3 signaling pathway.
