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

Zheng,Haiyin; Xu,Wei; Lin,Jiumao; Peng,Jun; Hong,Zhenfeng

doi:10.3892/mmr.2013.1265

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

Authors:
- Haiyin Zheng
- Wei Xu
- Jiumao Lin
- Jun Peng
- Zhenfeng Hong
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Affiliations: Department of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, Department of Pharmacology, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, Department of Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China
Published online on: January 7, 2013 https://doi.org/10.3892/mmr.2013.1265
Pages: 848-854

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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.

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