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Increased chromogranin A and neuron-specific enolase in rats with chronic nonbacterial prostatitis induced by 17-beta estradiol combined with castration

机译:17-β-雌二醇联合去势导致慢性非细菌性前列腺炎大鼠嗜铬粒蛋白A和神经元特异性烯醇化酶增加

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摘要

Although chronic nonbacterial prostatitis (CNBP) is a common diagnosis in middle-aged men, the etiology of this disease remains poorly understood. Neuroendocrine cells play an important role in the neuroendocrine regulation of the prostate, and chromogranin A (CgA) and neuron-specific enolase (NSE) are regarded as classic markers of neuroendocrine cells. This study aimed to determine CgA and NSE levels in a CNBP rat model to evaluate the role of neuroendocrine cells in the pathogenesis of CNBP. For developing a CNBP rat model, we examined the ability of 17-beta estradiol and surgical castration alone or in combination to induce CNBP. Histologic inflammation of the prostate was assessed in CNBP-induced rats by hematoxylin-eosin staining, whereas CgA and NSE protein levels were assessed by immunohistochemistry, Western blot analysis, and enzyme-linked immunosorbent assays. Our results showed that 17-beta estradiol combined with castration successfully induced CNBP and that CgA and NSE levels were increased in the prostate of CNBP rats as compared to those without CNBP. These findings indicate that the neuroendocrine regulation mediated by neuroendocrine cells may be involved in the pathogenesis of CNBP.
机译:尽管慢性非细菌性前列腺炎(CNBP)是中年男性的常见诊断,但对该病的病因学知之甚少。神经内分泌细胞在前列腺的神经内分泌调节中起着重要作用,嗜铬粒蛋白A(CgA)和神经元特异性烯醇化酶(NSE)被视为神经内分泌细胞的经典标志物。这项研究旨在确定CNBP大鼠模型中的CgA和NSE水平,以评估神经内分泌细胞在CNBP发病机理中的作用。为了建立CNBP大鼠模型,我们研究了17-β雌二醇和单独或联合手术去势诱导CNBP的能力。用苏木精-曙红染色在CNBP诱导的大鼠中评估前列腺的组织学炎症,而通过免疫组化,Western印迹分析和酶联免疫吸附法评估CgA和NSE蛋白水平。我们的研究结果表明,与无CNBP的大鼠相比,与去势结合的17-β雌二醇可成功诱导CNBP,并且CNBP大鼠的前列腺中CgA和NSE水平升高。这些发现表明,由神经内分泌细胞介导的神经内分泌调节可能与CNBP的发病有关。

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