Abstract:【Abstract】 Objective To explore whether emodin could attenuate LPSinduced in ammation in RAW2647 cells, and its involved potential mechanism. Methods RAW2647 cells were divided into Control group, LPS group, Emodin group, LPS+Emodin group, LPS+Emodin+siRNAPPARγ and LPS+Emodin+siRNAscrambled group. The mRNA and protein expression of ICAM1, MCP1 and PPARγ were measured by qRCR and western blot. The level of TNFα was evaluated by ELISA. Then, the phosphorylation of NFκB p65 was also detected by western blot. Meanwhile, siRNAPPARγ transfection was performed to knockdown PPARγ expression in cells. Results After 6 hours LPS stimulation, LPSenhanced ICAM1, MCP1 and TNFα expression, LPSreduced PPARγ expression, and LPSpromoted NFκB p65 activation were substantially compromised by emdoin in RAW2647 cells. However, these effects of emodin was noticeably blocked by siRNAPPARγ in cells. Conclusion Our results indicate that LPSinduced in ammation is potently compromised by emodin very likely through the PPARγdependent inactivation of NFκB in RAW2647cells.