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

ABSTRACT

<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>