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首页> 外文期刊>Life sciences >Ischemia/reperfusion in rat heart induces leptin and leptin receptor gene expression
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Ischemia/reperfusion in rat heart induces leptin and leptin receptor gene expression

机译：大鼠心脏缺血/再灌注诱导瘦素和瘦素受体基因表达

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Concentrations of leptin, an adipocyte-derived hormone, are elevated in obesity. Recently, leptin has been shown to participate in multiple biological actions including inflammation, reproduction, and angiogenesis. Leptin has also been documented as a critical component in the process of wound healing; however, leptin involvement in cardiovascular disease is poorly understood. We examined the expression of leptin (ob) and leptin receptor (ob-R) genes in the rat heart following ischemia/reperftision, which was induced by coronary artery ligation, and mRNA was obtained from hearts 0.5 to 36 h after initiating reperfusion. Expressions of ob and ob-R mRNA were examined by real-time quantitative RT-PCR and immunohistochemistry. The ob and ob-Ra mRNA and protein expressions were significantly increased (p<0.01) and ob-Rb mRNA was significantly decreased (p<0.01) in hearts after 8 h of reperfusion. Furthermore, ob and ob-R proteins were expressed in injured myocytes where inflammatory cells infiltrated. In contrast, those expressions were not influenced in hearts after 8 h of ischemia stress only. To determine the functional effects of leptin on the ischemic/reperfused heart, rats were treated with anti-leptin antibodies prior to ischemia/reperfusion; however, this treatment did not affect the elevation of mRNA expression levels of inflammatory markers such as TNF-a andlL-lfi in ischemic hearts. Our results demonstrated for the first time mat ischemia/reperfusion induced leptin and leptin receptor gene expression in the rat heart. This study helps to elucidate the mechanisms behind the onset and development of ischemic heart disease concomitant with obesity. 500Leptin; Obesity; Ischemia; Reperfusion; Inflammation
机译：在肥胖症中，瘦素（一种来自脂肪细胞的激素）的浓度升高。最近，瘦蛋白已显示出参与多种生物作用，包括炎症，繁殖和血管生成。瘦素也被证明是伤口愈合过程中的关键成分。然而，瘦素参与心血管疾病的了解很少。我们检查了缺血/再灌注后大鼠心脏中瘦素（ob）和瘦素受体（ob-R）基因的表达，该基因是由冠状动脉结扎诱导的，并且在开始再灌注后0.5至36 h从心脏获得了mRNA。通过实时定量RT-PCR和免疫组织化学检查ob和ob-R mRNA的表达。再灌注8 h后，ob和ob-Ra mRNA和蛋白质表达显着升高（p <0.01），ob-Rb mRNA显着降低（p <0.01）。此外，ob和ob-R蛋白在炎性细胞浸润的受损心肌细胞中表达。相反，仅在局部缺血应激8小时后，心脏中的这些表达才受到影响。为了确定瘦素对缺血/再灌注心脏的功能作用，在缺血/再灌注之前用抗瘦素抗体对大鼠进行治疗。然而，这种治疗并没有影响缺血性心脏中炎性标志物如TNF-α和IL-lfi的mRNA表达水平的升高。我们的结果首次证明了缺血/再灌注诱导的大鼠心脏中的瘦素和瘦素受体基因表达。这项研究有助于阐明与肥胖相关的缺血性心脏病的发作和发展背后的机制。 500瘦素;肥胖;缺血;再灌注炎

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