作者: Lingying Liu , Huifeng Song , Hongjie Duan , Jiake Chai , Jing Yang
DOI: 10.1038/SREP30121
关键词: Phosphorylation 、 TSG-6 、 Mesenchymal stem cell 、 p38 mitogen-activated protein kinases 、 MAPK/ERK pathway 、 Medicine 、 Pharmacology 、 Gene knockdown 、 Inflammation 、 Signal transduction 、 Immunology
摘要: The hMSCs have become a promising approach for inflammation treatment in acute phase. Our previous study has demonstrated that human umbilical cord-MSCs could alleviate the inflammatory reaction of severely burned wound. In this study, we further investigated potential role and mechanism MSCs on severe burn-induced excessive inflammation. Wistar rats were randomly divided into following groups: Sham, Burn, Burn+MSCs, Burn+MAPKs inhibitors, Burn+Vehicle, Burn+siTSG-6, Burn+rhTSG-6 both experiments. It was found only down-regulate P38 JNK signaling, but had no effect ERK peritoneal macrophages burn rats. Furthermore, suppression activations significantly reduced induced by burn. TSG-6 secreted using different mediators. from recombinant (rh)TSG-6 all signaling then attenuated inflammations. On contrary, knockdown cells increased phosphorylation therapeutic Taken together, suggested via inhibiting activation signaling.