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Qianliening capsule treats benign prostatic hyperplasia via induction of prostatic cell apoptosis

机译:前列宁胶囊通过诱导前列腺细胞凋亡治疗前列腺增生症

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The aim of this study was to evaluate the therapeutic efficacy of Qianliening capsule (QC) against benign prostatic hyperplasia (BPH) in vivo in a BPH rat model, as well as to investigate the effects of QC on prostatic cell apoptosis and the possible molecular mechanisms mediating its anti-BPH activity. Fifty male Sprague-Dawley (SD) rats were randomly classified into five groups. The rats of the four groups were castrated and subcutaneously injected with testosterone propionate to generate BPH. One week after model establishment, BPH rats were orally administrated with various doses of QC daily for 28 days. The prostatic tissues from BPH rats were collected to evaluate prostatic index (PI). The histological changes of prostate were observed by hematoxylin and eosin staining. TUNEL analysis was performed to examine cell apoptosis. The mRNA expression of Bcl-2 and Bax in prostatic tissues was determined by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of Bcl-2, Bax and cleaved caspase 3 were examined by immunohistochemistry. Administration with QC significantly decreased PI in a dose-dependent manner (P<0.05 or P<0.01) and improved prostatic hyperplasia in BPH rats. Additionally, QC treatment induced prostatic cell apoptosis in a dose-dependent manner. Moreover, QC promoted the cleavage of caspase 3, an indicator of apoptosis, in a dose-dependent manner. Furthermore, following QC treatment, the expression ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2 in prostatic tissues was increased in a dose-dependent manner. As a result, QC was effective in the treatment of BPH in rats. Promoting apoptosis of prostatic cells may therefore be one of the mechanisms by which QC treats BPH.
机译:这项研究的目的是评估前列宁胶囊(QC)在BPH大鼠模型中对体内良性前列腺增生(BPH)的治疗效果,并研究QC对前列腺细胞凋亡的影响及其可能的分子机制介导其抗BPH活性。将五十只雄性Sprague-Dawley(SD)大鼠随机分为五组。将四组大鼠去势并皮下注射丙酸睾丸激素以产生BPH。建立模型后一周,每天给BPH大鼠口服28天的各种剂量的QC。收集BPH大鼠的前列腺组织以评估前列腺指数(PI)。通过苏木精和曙红染色观察前列腺的组织学变化。进行TUNEL分析以检查细胞凋亡。通过逆转录-聚合酶链反应(RT-PCR)测定前列腺组织中Bcl-2和Bax的mRNA表达。通过免疫组织化学检查Bcl-2,Bax和裂解的胱天蛋白酶3的蛋白表达。 QC的给药以剂量依赖性方式显着降低PI(P <0.05或P <0.01),并改善BPH大鼠的前列腺增生。另外,QC处理以剂量依赖性方式诱导前列腺细胞凋亡。而且,QC以剂量依赖的方式促进了caspase 3的裂解,caspase 3是凋亡的指示剂。此外,在进行QC处理后,前列腺组织中促凋亡Bax与抗凋亡Bcl-2的表达比例呈剂量依赖性。结果,QC对大鼠BPH的治疗有效。因此,促进前列腺细胞的凋亡可能是QC治疗BPH的机制之一。

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