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摘要
Objective To investigate the preventive effect and mechanism of baicalein 6,7-diacetate (BD) on thioacetamide-induced hepatic encephalopathy in rats. Methods Tatolly sixty male Wistar rats were randomly divided into control group, model group, lactulose (positive drug, 6 g/kg) group and 6,7-diacetyl baicalein low, medium and high dose (6.25, 12.50 and 25.00 mg/kg) groups, ig once a day for seven days. A rat model of actue hepatic encephalopathy was established by continuous ip injection of thioacetamide for two days. To observe the status of rats and investigate the stage of hepatic encephalopathy and mortality in rats. The levels of ammonia, AST, ALT, ALP and TBIL in serum and colonic pH of rats in each group were measured. HE staining was used to evaluate the pathological changes of liver in rats.The level of GABA and glutamic acid (Glu) in rat brain, and the level of serotonin (5-HT) and norepinephrine (NE) in plasma were determined by ELISA. The expression of GABA-α1 in brain tissue was determined by Western Blotting. Results 48 hours after modeling, compared with the model group, BD high-dose group significantly increased body weight (P < 0.05), hepatic encephalopathy score decreased significantly (P < 0.05), mortality of each dose group was reduced, serum ALT, AST, ALP and TBIL levels were significantly decreased in middle and high dose groups (P < 0.05); blood ammonia level in low, medium and high dose groups was significantly decreased (P < 0.05, 0.01); colon pH was significantly decreased in middle and high dose groups. Compared with model group, the level of GABA in brain tissue was significantly decreased (P < 0.01); The level of 5-HT in the middle and high-dose groups was significantly decreased (P < 0.01); the plasma NE level in the high-dose group was significantly decreased (P < 0.01); the Glu content in the brain tissue of the high-dose group was significantly increased (P < 0.01); the expression of GABA - α1 protein in the high-dose group was significantly decreased (P < 0.05). Conclusion BD has a protective effect on the liver and a preventive effect on acute hepatic encephalopathy in rats. The mechanism may be related to reducing blood ammonia and colon pH, regulating neurotransmitter level, and inhibiting the expression of related neurotransmitter receptors.
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