Bushen Tongluo formula ameliorated testosterone propionate-induced benign prostatic hyperplasia in rats
- Phytomedicine. 2023 Nov:120:155048. doi: 10.1016/j.phymed.2023.155048.
- 1. Department of Traditional Chinese Medicine, School of Medicine, Xiamen University, No. 4221-122, Xiang'an South Road, Xiamen, Fujian 361102, China.
- 2. Department of Traditional Chinese Medicine, School of Medicine, Xiamen University, No. 4221-122, Xiang'an South Road, Xiamen, Fujian 361102, China; Department of Traditional Chinese Medicine, Xiang'an Hospital of Xiamen University, No. 2000, Xiang'an East Road, Xiamen, Fujian 361101, China. Electronic address: [email protected].
- 3. The Third Affiliated Hospital, Beijing University of Chinese Medicine, No. 51, Anwai Xiaoguan Street, Beijing 100029, China.
- 4. Department of Geriatrics, Xiamen Hospital of Traditional Chinese Medicine, No. 1739, Xianyue Road, Xiamen, Fujian 361015, China. Electronic address: [email protected].
Background: Benign prostatic hyperplasia (BPH) is a common disease in older men worldwide. However, there is currently no effective treatment for BPH. Bushen Tongluo Formula (Kidney-supplementing and collaterals-unblocking formula [KCF]) is a traditional Chinese medicine formula commonly used to ameliorate the symptoms of BPH, although the specific molecular mechanisms remain unclear.
Purpose: We aimed to discover the effects and potential mechanisms of KCF against BPH.
Methods: Sixty male SD rats were randomly assigned to one of six group (n = 10): control, low-dosage KCF, medium-dosage KCF, high-dosage KCF, BPH model, and finasteride. A rat model of BPH was established by surgical castration followed by subcutaneous injection of testosterone propionate (TP) for 4 weeks. After treatment, the prostate index, histopathological staining, serum levels of estradiol (E2) and dihydrotestosterone (DHT), protein/mRNA levels of E-cadherin, TGF-β1, Caspase-3, Ki67, and vimentin, abundances of serum metabolites, and the proliferation, cell cycle, and Apoptosis of BPH-1 cells were documented.
Results: KCF treatment for 4 weeks reduced the prostate volume and prostate index, alleviated histopathological changes to the prostate of rats with TP-induced BPH, decreased serum levels of E2 and DHT, reduced protein/mRNA levels of TGF-β1 and vimentin, and increased E-cadherin levels. Moreover, KCF-spiked serum inhibited proliferation of BPH-1 cells, blocked the cell cycle, and promoted Apoptosis. KCF was also found to regulate the contents of three metabolites (D-maltose, citric acid, and fumaric acid).
Conclusion: The present study was the first to report that KCF exhibited therapeutic effects against BPH by regulating energy metabolism and inhibiting epithelial-mesenchymal transition in prostate tissues. Hence, KCF presents a viable treatment option for BPH.
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Research Areas: Cancer