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前列宁胶囊通过诱导前列腺细胞凋亡治疗良性前列腺增生。

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

机构信息

Department of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, PR China.

出版信息

Mol Med Rep. 2013 Mar;7(3):848-54. doi: 10.3892/mmr.2013.1265. Epub 2013 Jan 7.

DOI:10.3892/mmr.2013.1265
PMID:23314795
Abstract

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.

摘要

本研究旨在评估前列宁胶囊(QC)在体内对良性前列腺增生(BPH)大鼠模型的治疗效果,并探讨 QC 对前列腺细胞凋亡的影响及其可能的抗 BPH 活性的分子机制。50 只雄性 Sprague-Dawley(SD)大鼠被随机分为五组。四组大鼠去势并皮下注射丙酸睾酮生成 BPH。造模 1 周后,BPH 大鼠每日口服给予不同剂量的 QC 连续 28 天。收集 BPH 大鼠的前列腺组织,评估前列腺指数(PI)。通过苏木精和伊红染色观察前列腺组织的组织学变化。通过 TUNEL 分析检测细胞凋亡。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。通过免疫组化检测 Bcl-2、Bax 和 cleaved caspase 3 的蛋白表达。QC 给药显著降低 PI 呈剂量依赖性(P<0.05 或 P<0.01),改善 BPH 大鼠前列腺增生。此外,QC 处理以剂量依赖性方式诱导前列腺细胞凋亡。此外,QC 处理以剂量依赖性方式促进 caspase 3 的切割,这是凋亡的一个指标。进一步的,经 QC 处理后,前列腺组织中促凋亡 Bax 与抗凋亡 Bcl-2 的表达比值呈剂量依赖性增加。因此,QC 对大鼠 BPH 有效。促进前列腺细胞凋亡可能是 QC 治疗 BPH 的机制之一。

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