Abstract

Qianlie Tongqiao Capsule (QTC) is clinically confirmed to be efficacious and safe in treating lower urinary tract syndromes and bladder dysfunction that are induced by benign prostatic hyperplasia (BPH). However, the functional mechanisms of QTC remain unclear. We aim to investigate the effects of QTC on both bladder weight and several growth factors in the bladder tissue of rats with testosterone-induced BPH. BPH in the rats was established through bilateral orchiectomy and subcutaneous administration of testosterone propionate (5 mg/kg) dissolved in corn oil. At the end of the study, all bladder tissues were collected and weighed, and a histological examination was conducted using H&E staining. Immunohistochemistry and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) were applied to detect the expression of nerve growth factor (NGF), basic fibroblast growth factor (bFGF), and transformation growth factor-β1 (TGF-β1) in the bladder tissue. The expression of Bcl-2 and Bax in the bladder tissue was tested by Western Blot and qRT-PCR. We found that QTC, especially when administered in high-dosages, had a significant inhibitory effect on bladder weight gain and overexpression of NGF, bFGF, and TGF-β1 in rats with BPH. In addition, QTC downregulated and upregulated protein and mRNA expression of Bcl-2 and Bax in the bladder after prostatic obstruction, respectively. Furthermore, QTC balanced the Bcl-2/Bax ratio. Overall, these results reveal possible functional mechanisms of QTC in treating BPH-caused bladder dysfunction, and further studies are needed.

Highlights

  • Benign prostatic hyperplasia (BPH), which causes bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTs), is increasingly prevalent among aging males [1]

  • This study aims to investigate the effects of Qianlie Tongqiao Capsule (QTC) on the bladder weigh, expression of nerve growth factor (NGF), basic fibroblast growth factor (bFGF), transformation growth factor-β1 (TGF-β1), and apoptosis-associated factors in the bladder tissue of rats with testosterone-induced BPH

  • Following a 4-week BPH-inducement phase, different dosages of QTC were orally administered to the rats once daily for 4 weeks and the sham and model groups were deemed the negative and positive control, respectively

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Summary

Introduction

Benign prostatic hyperplasia (BPH), which causes bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTs), is increasingly prevalent among aging males [1]. The pathophysiological mechanisms by which BPH leads to LUTs are still vague, but it is known that an enlarged prostate plays a role in BPH-induced BOO/LUTs. even after undergoing obstruction relief surgery such as prostatectomy, many patients still report persistent storage symptoms [3,4,5,6]. Mirone V. et al called the detrusor an “innocent victim” of BOO [7]. Mechanical obstruction originated from benign prostatic enlargement leads to a series of structural and functional changes in bladder detrusor [1, 7]

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