Effects of hot shock protein 70 inhibitor PFTµ on inflammatory response in lipopolysaccharide-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion injury.
- Author:
Xiao-Mei YUAN
1
;
Han LEI
;
Qing LIU
;
Yong XIA
;
Kang-Hua MA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Benzothiazoles; pharmacology; Cell Line; HSP70 Heat-Shock Proteins; antagonists & inhibitors; Inflammation; Lipopolysaccharides; adverse effects; Macrophages; drug effects; metabolism; Male; Mice; Mice, Inbred C57BL; Myocardial Reperfusion Injury; metabolism; pathology; Myocardium; metabolism; Nitric Oxide; metabolism; Nitric Oxide Synthase Type II; metabolism; Toluene; analogs & derivatives; pharmacology
- From: Chinese Journal of Cardiology 2011;39(6):522-525
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effects of hot shock protein 70 (HSP70) inhibitor (PFTµ) on inflammation response in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion (I/R) injury.
METHODSRAW264.7 macrophage line of mice was stimulated by LPS as an inflammatory model. These were divided into control (15 min DMSO pretreatment and LPS 2 g/L) and PFTµ treated groups (15 min PFTµ 20 µmol/L pretreatment and LPS 2 g/L). NO concentration was measured by Griess Kit. The expression of iNOS protein and mRNA were detected by Western blot and RT-PCR. Infarct size was determined on mice underwent myocardial ischemia-reperfusion (I/R) injury in the absence or presence (PFTµ 40 mg/kg, intraperitoneal injection).
RESULTSPFTµ significantly blocked the production of NO and protein and mRNA expression of iNOS (P < 0.05 vs. control). PFTµ also significantly reduced the infarct size on mice underwent I/R injury (P < 0.05 vs. control).
CONCLUSIONThese results suggest that PFTµ could be a potential therapeutic agent for the treatment of inflammatory diseases through inhibiting the production of NO and reducing inflammatory responses.
