Abstract:

BACKGROUND: Connexin is the primary structure to compose intracellular channel, is responsible for substance transport and information exchange and can help regulate cell growth and differentiation.
OBJECTIVE: To investigate the relationship of connexin 32 expression and hepatocyte proliferation in a rat model of acute liver failure.
METHODS: Rat models of acute liver failure were established by intragastric administration of lactulose and gentamicin and intraperitoneal administration of carbon tetrachloride and olive oil. From 7 days before acute liver failure induction, phenobarbital group rats were raised with water containing 0.08% phenobarbital till sample harvesting. Acute liver failure was not induced in the control group, and only intraperitoneal administration of mixture of olive oil and physiological saline was performed. At 1, 3, 7, 10, and 14 days after modeling, samples were harvested.
RESULTS AND CONCLUSION: After liver failure, some rats died, the hepatocytes of surviving rats were degenerative and necrotic, glutamic-pyruvic transaminase was obviously increased, connexin 32 mRNA and protein expression was obviously decreased. Phenobarbital can decrease the mortality of rats with liver failure and it can also decrease glutamic-pyruvic transaminase level and connexin 32 mRNA and protein expression. These results showed that phenobarbital can downregulate connexin 32 expression in the hepatocytes, which can alleviate the liver damage of liver failure rats during the acute stage, promote the proliferation of remaining hepatocytes, improve liver function, and finally decrease the mortality of rats with acute liver failure.