Baek Eun-Bok, Hwang Youn-Hwan, Hong Eun-Ju, Won Young-Suk, Kwun Hyo-Jung
Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea.
Herbal Medicine Research Division, Korean Institute of Oriental Medicine, Daejeon 34054, Republic of Korea.
Pharmaceuticals (Basel). 2024 Aug 5;17(8):1032. doi: 10.3390/ph17081032.
Benign prostatic hyperplasia (BPH) is a urogenital disorder that is common in aging men. (IP) is used in traditional medicine and contains pharmacologically active compounds. However, the effect for BPH progression has not been elucidated. We herein examined the protective potential of IP extract on a testosterone-induced model of BPH in rats. To generate the BPH model, daily subcutaneous administration of testosterone was applied for 4 weeks. During this period, the rats were also administered a daily oral gavage of IP (150 mg/kg), finasteride (positive control), or vehicle. Testosterone treatment was associated with a significantly higher prostate-to-body weight ratio, serum dihydrotestosterone (DHT) level, and prostatic gene expression of 5α-reductase compared to untreated controls. Notably, IP plus testosterone co-treatment was associated with decreased epithelial thickness, down-regulation of proliferating cell nuclear antigen (PCNA) and cyclin D1, and upregulation of pro-apoptotic signaling molecules. IP co-treatment also down-regulated pro-inflammatory cytokines, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) and decreased inflammatory cell infiltration compared to the levels seen in the testosterone-induced BPH. IP appears to protect rats against the progression of testosterone-induced BPH by alleviating prostate cell growth and inflammatory responses, and thus may have potential for clinical use against BPH progression.
良性前列腺增生(BPH)是一种在老年男性中常见的泌尿生殖系统疾病。印度榅桲(IP)在传统医学中使用,并且含有药理活性化合物。然而,其对BPH进展的影响尚未阐明。我们在此研究了IP提取物对睾酮诱导的大鼠BPH模型的保护潜力。为了建立BPH模型,每天皮下注射睾酮,持续4周。在此期间,大鼠还每天经口灌胃给予IP(150 mg/kg)、非那雄胺(阳性对照)或赋形剂。与未处理的对照组相比,睾酮治疗导致前列腺与体重之比、血清双氢睾酮(DHT)水平以及前列腺5α-还原酶基因表达显著升高。值得注意的是,IP与睾酮联合治疗导致上皮厚度降低、增殖细胞核抗原(PCNA)和细胞周期蛋白D1下调以及促凋亡信号分子上调。与睾酮诱导的BPH相比,IP联合治疗还下调了促炎细胞因子、环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS),并减少了炎症细胞浸润。IP似乎通过减轻前列腺细胞生长和炎症反应来保护大鼠免受睾酮诱导的BPH进展的影响,因此可能具有临床用于对抗BPH进展的潜力。