Qianliening capsule treats benign prostatic hyperplasia via induction of prostatic cell apoptosis.
Qianliening capsule treats benign prostatic hyperplasia via induction of prostatic cell apoptosis.
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DOI：
10.3892/mmr.2013.1265
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发表时间：
2013-03
影响因子：
3.4
通讯作者：
Haiyin Zheng;W. Xu;Jiumao Lin;Jun Peng;Z. Hong
中科院分区：
文献类型：
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作者：
Haiyin Zheng;W. Xu;Jiumao Lin;Jun Peng;Z. Hong
本研究旨在观察前列宁胶囊（QC）对良性前列腺增生（BPH）大鼠的治疗作用，并探讨其对前列腺细胞凋亡的影响及其可能的分子机制。将50只雄性SD大鼠随机分为5组。将4组大鼠去势后皮下注射丙酸睾丸酮，建立BPH模型。造模后1周，每天灌胃不同剂量的QC，连续28天。取BPH大鼠前列腺组织，测定前列腺指数（PI）。苏木精-伊红染色观察前列腺组织学变化。TUNEL法检测细胞凋亡。采用逆转录-聚合酶链反应（RT-PCR）检测前列腺组织中Bcl-2和Bax mRNA的表达。免疫组化法检测Bcl-2、Bax和Caspase 3蛋白表达。结果表明，QC能剂量依赖性地降低BPH大鼠的PI（P<0.05或P<0.01），并能改善BPH大鼠的前列腺增生。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以剂量依赖性方式促进caspase 3的切割，caspase 3是细胞凋亡的指标。此外，QC处理后，前列腺组织中促凋亡Bax与抗凋亡Bcl-2的表达比例以剂量依赖性方式增加。结果表明，QC对大鼠BPH的治疗有效。因此，促进前列腺细胞凋亡可能是QC治疗BPH的机制之一。
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.