Effects of hot shock protein 70 inhibitor PFTμ on inflammatory response in lipopolysaccharide-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion injury
10.3760/cma.j.issn.0253-3758.2011.06.010
- VernacularTitle:热休克蛋白70抑制剂PFTμ对小鼠炎症反应的影响
- Author:
Xiao-Mei YUAN
1
;
Han LEI
;
Qing LIU
;
Yong XIA
;
Kang-Hua MA
Author Information
1. 重庆医科大学附属第一医院
- Keywords:
Myocardial reperfusion injury;
Lipopolysaccharides;
Nitric oxide synthase;
PFTμ
- From:
Chinese Journal of Cardiology
2011;39(6):522-525
- CountryChina
- Language:Chinese
-
Abstract:
Objective To 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.Methods RAW264.7 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).Results PFTμ 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).Conclusion These results suggest that PFTμ could be a potential therapeutic agent for the treatment of inflammatory diseases through inhibiting the production of NO and reducing informatory responses.
