Effects of hot shock protein 70 inhibitor PFTµ on inflammatory response in lipopolysaccharide-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion injury / 中华心血管病杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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 inflammatory responses.</p>

The protective role of transient receptor potential vanilloid subtype 1 in post-myocardial infarction inflammation process / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the protective role of transient receptor potential vanilloid subtype 1 (TRPV1) in inflammatory process after myocardial infarction.</p><p><b>METHODS</b>The survival rate, infarct size, the levels of plasma cardiac troponin I, infiltration of inflammatory cells, the levels of cytokines and chemokines, and cardiac function were monitored 3 and 7 days post-myocardial infarction in TRPV1 gene knockout (TRPV1(-/-)) and wild type (WT) mice.</p><p><b>RESULTS</b>The survival rate was significantly lower in TRPV1(-/-) mice than that in WT mice (62.5% vs. 82.1%, P < 0.05). The infarct size on day 3 after MI was significantly larger in TRPV1(-/-) mice than that in WT mice (INF/AAR: 69.5% +/- 3.1% vs. 40.1% +/- 2.6%, P < 0.05). Plasma cardiac troponin I level, number of infiltrated inflammatory cells including neutrophils and macrophages were significant increased in TRPV1(-/-) mice compared to WT mice. Expressions of cytokines including TNF-alpha, IL-1beta, and IL-6, chemokines including MCP-1 and MIP-2 in the infarct area at 3 and 7 days after MI were significantly higher in TRPV1(-/-) mice than those in WT mice (all P < 0.05). Furthermore, end-systolic and -diastolic diameters were significantly increased and contractile function of the heart significantly reduced in TRPV1(-/-) mice compared to WT mice.</p><p><b>CONCLUSION</b>TRPV1 gene deletion results in reduced survival rate, excessive inflammation, deteriorated cardiac function and aggravated left ventricular remodelling after MI, indicating that TRPV1 may prevent infarct expansion and cardiac injury by inhibiting inflammation and reservation cardiac function.</p>