Total ginsenosides promotes intestinal epithelial proliferation via affecting polyamine-mediated HuR on post-transcriptional control

Ginseng, as a functional food, is widely used worldwide because of its various benefits. This study aims to elucidate the potential effects of total ginsenosides (TG) in intestinal mucosal restitution. Establishing IEC-6 cell proliferation inhibition model by culturing with 5 mmol/L DL-& alpha;-difluoromethylornithine (DFMO, a polyamine inhibitor) for 48 h. The intestinal injury mice model was induced by 3% Dextran sodium sulfate (DSS) for 7 d. TG reversed the cell growth inhibition, regulated cell cycle and the decrease in c-Myc protein expression caused by DFMO, without affecting mRNA expression; TG increased translation efficiency and half-life of c-Myc mRNA, suggesting that TG promoted cell proliferation through affecting translation of c-Myc. Furthermore, TG could prevent the decrease of human antigen R (HuR)/c-Myc mRNA, p-HuR andp-Chk2 expression caused by DFMO, as well as reduce the expression of HuR in cytoplasm while increasing the expression in nucleus, indicating that TG influenced post-transcriptional control of c-Myc through polyamine-mediated HuR pathway for intestinal mucosal restitution. Panax ginseng aqueous extract (PGE) prevented intestinal mucosal injury induced by DSS (improved clinical symptoms and restored colon integrity) through enhancing HuR and c-Myc levels. Our results may provide a scientific basis for ginseng as a potential functional food ingredient and assistance therapeutic agent to prevent intestinal injury.

Automated summary

The study investigated the potential effects of total ginsenosides (TG) in intestinal mucosal restitution. TG reversed cell growth inhibition caused by DFMO and promoted cell proliferation by affecting the translation of c-Myc. Furthermore, Panax ginseng aqueous extract (PGE) prevented intestinal mucosal injury and promoted mucosal restitution through enhancing HuR and c-Myc levels.