Abstract: Objective To investigate the influence of acute biliary tract infection on apoptosis-related protein expression
of liver cells in rats. Methods Total of 35 rats were selected and randomly divided into five groups after adaptive
feeding for 1 week, 7 rats in each group. Rats in experimental groups were given injection of Escherichia coli into
common bile duct to make acute biliary tract infection model and sacrificed after 6 h, 12 h, 24 h and 48 h of injection,
respectively. Rats in control group were injected with normal saline into the common bile duct and sacrificed after 6
hours of injection. The number of apoptotic liver cells was counted by Tunel staining and positive expression rate of
Bcl-2 and Bax in liver were detected by immunohistochemistry method. Results The liver cells in control group had
no obvious pathological changes and the apoptotic hepatocytes were rare. The liver cells in all experimental groups
were found necrotic and deformed and occured apoptosis. The apoptosis index (AI) in control group were significantly
lower than those at 6 h, 12 h, 24 h and 48 h after infection (t = 5.921, 7.559, 8.919, 10.520; P < 0.001). The positive
expression rate of Bcl-2 in control group and 6 h infection group were 85.71% and 71.43%, respectively, the difference
had no statistical significance (χ 2 = 0.000, P = 1.000). The positive expression rate of Bcl-2 in 6 h and 12 h infection
groups were significantly higher than those of 12 h and 24 h infection group (P < 0.05). The positive expression
rate of Bax in control group, 6 h, 12 h, 24 h and 48 h infection group were 14.29%, 28.57%, 42.86%, 100.00% and
85.71%, respectively, the difference was statistically significant (F = 9.314, P < 0.001). The positive expression rate
of Bax increased with time going on, and decreased in 48 h after infection. Conclusion Acute biliary tract infection
can induce the apoptosis of liver cells in a short time, which is accompanied by decreased expression of apoptosis
related protein Bcl-2 and increased expression of Bax.
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