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通过抑制5α-还原酶活性和雄激素受体信号通路来缓解睾酮诱导的良性前列腺增生。

alleviates testosterone-induced benign prostatic hyperplasia by inhibiting 5α-reductase activity and androgen receptor signaling pathway.

作者信息

Hwangbo Hyun, Cha Hee-Jae, Kim Min Yeong, Ji Seon Yeong, Kim Da Hye, Noh Jeong Sook, Kim Tae Hee, Kim Heui-Soo, Moon Sung-Kwon, Kim Gi-Young, Choi Yung Hyun

机构信息

Department of Biochemistry, Dong-eui University College of Korean Medicine, Busan 47227, Korea.

Basic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47227, Korea.

出版信息

Nutr Res Pract. 2024 Dec;18(6):793-805. doi: 10.4162/nrp.2024.18.6.793. Epub 2024 Aug 19.

Abstract

BACKGROUND/OBJECTIVES: Recently, herbal medicines have gained attention for the treatment of benign prostatic hyperplasia (BPH), a common disease in elderly men. In this study, we aimed to determine the effect of ethanol extract of (EAR), which is traditionally used to treat various diseases, on BPH development using a testosterone-induced BPH model.

MATERIALS/METHODS: Testosterone propionate (TP)-treated Sprague-Dawley rats were used to establish a BPH model . EAR was orally administered along with TP, and finasteride was used as a positive control. All rats were sacrificed at the end of the experiment, and pathological changes in the prostate tissue and levels of key biomarkers associated with BPH pathogenesis were assessed.

RESULTS

Oral administration of EAR significantly inhibited TP-induced BPH by reducing the prostate weight, lumen size, and epithelial thickness in a concentration-dependent manner. EAR also significantly abrogated the expression of 5α-reductase type 2 (SRD5A2), proliferating cell nuclear antigen, and prostate-specific antigen (PSA) induced by TP. Additionally, serum levels of testosterone, dihydrotestosterone, and PSA were elevated in the TP-induced group but decreased in the EAR-treated group. EAR also decreased the expression levels of the androgen receptor (AR) and its coactivators in TP-induced BPH model rats.

CONCLUSION

Our findings revealed that EAR protected against BPH by inhibiting 5α-reductase activity and AR signaling pathway, suggesting its potential for BPH treatment.

摘要

背景/目的:近年来,草药在治疗良性前列腺增生(BPH)方面受到关注,BPH是老年男性的常见疾病。在本研究中,我们旨在使用睾酮诱导的BPH模型,确定传统上用于治疗各种疾病的[植物名称未给出]乙醇提取物(EAR)对BPH发展的影响。

材料/方法:使用丙酸睾酮(TP)处理的Sprague-Dawley大鼠建立BPH模型。EAR与TP一起口服给药,非那雄胺用作阳性对照。在实验结束时处死所有大鼠,评估前列腺组织的病理变化以及与BPH发病机制相关的关键生物标志物水平。

结果

口服EAR通过以浓度依赖的方式降低前列腺重量、管腔大小和上皮厚度,显著抑制TP诱导的BPH。EAR还显著消除了TP诱导的2型5α-还原酶(SRD5A2)、增殖细胞核抗原和前列腺特异性抗原(PSA)的表达。此外,TP诱导组中睾酮、双氢睾酮和PSA的血清水平升高,但EAR治疗组中降低。EAR还降低了TP诱导的BPH模型大鼠中雄激素受体(AR)及其共激活因子的表达水平。

结论

我们的研究结果表明,EAR通过抑制5α-还原酶活性和AR信号通路预防BPH,表明其在BPH治疗中的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c030/11621438/c9386567f539/nrp-18-793-g001.jpg

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