Protective effects of pravastatin against P38MAPK signaling pathway-mediated inflammatory toxicity in islet micro-endothelial cells.
- Author:
Nan HU
1
;
Jia SUN
;
Yuancheng KANG
;
Jiansheng CHEN
;
Lishan LUO
;
Juchang ZHANG
;
Songyuan CHEN
;
Dehong CAI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Endothelial Cells; drug effects; metabolism; Endothelium, Vascular; cytology; Inflammation; Islets of Langerhans; blood supply; MAP Kinase Signaling System; drug effects; Mice; Nitric Oxide Synthase Type II; metabolism; Phosphorylation; Pravastatin; pharmacology; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Journal of Southern Medical University 2013;33(8):1232-1235
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the signaling pathways associated with lipopolysaccharide (LPS)-induced inflammation in islet micro-endothelial cells (IMECs) and the mechanism of pravastatin intervention.
METHODSIMECs exposed to LPS, SB203580, pravastatin, or SB203580+pravastatin were examined for cell apoptosis with Hoechst staining and flow cytometry and for expression levels of total-p38, photophosphorylation-p38 (p-p38) and iNOS with Western blotting.
RESULTSThe apoptosis rate and expression levels of total-p38, p-p38, iNOS in IMECs all increased after LPS exposure. Pravastatin, SB203580, and their combination significantly attenuated LPS-induced enhancement of cell apoptosis and total-p38, p-p38, and iNOS expressions in IMECs.
CONCLUSIONLPS-induced inflammatory toxicity in IMECs is associated with the activation of P38MAPK and iNOS/NO signaling pathways. Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve the cell inflammatory injuries.
