Objective: To study the effect of ginseng polysaccharides (GSP) on ethanol-induced behavioral sensitization and its possible mechanism.
Method: 80 KM mice were randomly divided into five groups, blank group, model group, GSP low-dose group (100mg/kg), GSP medium-dose group (200mg/kg) and GSP high-dose group (400mg/kg). Except for the blank group, the other groups can freely take water or ethanol, and the ethanol concentration gradually increases with time (3%-12%, 3% every 4 days).After the 4d conversion period, the initial dose of 3% ethanol is given to challenge. This establishes a behavioral sensitization model of active alcohol intake. Ethanol consumption and autonomous activities of each group were measured every day during the experimental period; the opening experiment was conducted during the transformation period; the expression of behavioral sensitization was measured during the expression period. Enzyme-linked immunosorbent assay (ELISA) was used to detect the MDA content and SOD and CAT activity in the prefrontal cortex. Western blotting was used to detect the expression of ERK, pERK and c-fos protein in the prefrontal cortex. Real-time PCR (Real-time PCR) detects the mRNA expression of p-ERK and C-FOS in the prefrontal cortex.
Results: The three doses of GSP significantly reduced the increase in voluntary activity induced by 9% and 12% ethanol during the formation period, and significantly inhibited the increase in voluntary activity and ethanol intake induced by the initial dose of 3% alcohol challenge (day 25). The medium and high doses of GSP can significantly reduce the number of crawls and standing times in the opening experiment. GSP can significantly inhibit the ethanol-induced increase in MDA levels in the prefrontal cortex, and increase the activity of SOD and CAT. Westernblot and Real-timePCR results show that GSP can down-regulate the overexpression of p-ERK and c-fos protein and mRNA in the prefrontal cortex.
Conclusion: GSP has inhibitory effects on ethanol-induced behavioral sensitization and ethanol uptake in mice, and this effect may be through intervention in the ERK/c-fos pathway.