TNF-α induces the release of high mobility group protein B1 through p38 mitogen-activated protein kinase pathway in microglia.
10.11817/j.issn.1672-7347.2015.09.004
- Author:
Ruike WANG
1
;
Qinqin ZHANG
1
;
Shenghui YANG
1
;
Qulian GUO
1
Author Information
1. Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Blotting, Western;
HMGB1 Protein;
metabolism;
Humans;
Imidazoles;
pharmacology;
MAP Kinase Signaling System;
Microglia;
drug effects;
metabolism;
Pyridines;
pharmacology;
Tumor Necrosis Factor-alpha;
pharmacology;
Up-Regulation;
p38 Mitogen-Activated Protein Kinases;
antagonists & inhibitors;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2015;40(9):967-972
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the effect of p38 MAPK inhibitor (SB203580) on TNF-α -induced high mobility group protein B1 (HMGB1) expression in microglial cells.
METHODS:Microglial cells were treated with TNF-α (25 ng/mL, TNF-α group), TNF-α plus SB203580 (10 μmol/L, TNF-α+SB203580 group), SB203580 (SB203580 group) or serum-free medium (control group). After 16 h of incubation, the protein levels of p-p38 MAPK and HMGB1, and mRNA levels of HMGB1 were examined by ELISA, Western Blot and RT-PCR, respectively.
RESULTS:There was a significant increase in p-p38 MAPK and HMGB1 levels in TNF-α-treated microglia cells (P<0.01). The TNF-α-induced HMGB1 protein and mRNA expression was suppressed by SB203580.
CONCLUSION:TNF-α up-regulates HMGB1 expression in microglial cells through activation of the p38 MAPK pathway.
