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黄芩苷通过雄激素依赖性凋亡缓解良性前列腺增生。

Baicalin alleviates benign prostate hyperplasia through androgen-dependent apoptosis.

机构信息

Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si 26339, Gangwon-do, Republic of Korea.

出版信息

Aging (Albany NY). 2020 Feb 4;12(3):2142-2155. doi: 10.18632/aging.102731.

DOI:10.18632/aging.102731
PMID:32018227
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7041748/
Abstract

BPH is a disease prevalent among elderly men that is characterized by abnormal proliferation of prostatic epithelial and stromal tissues. No effective treatment exists for BPH owing to lack of a clear understanding of its molecular etiology. Although several studies have reported therapeutic effects of baicalin against numerous diseases, including prostate cancer, its beneficial effects on BPH have not yet been explored. The present study investigated the therapeutic effects of baicalin on the development of BPH and its mechanism of action. We established a testosterone-treated BPH animal model and DHT-stimulated prostate cell lines, including RWPE-1 and WPMY-1. Administration of baicalin ameliorated the pathological prostate enlargement, suppressed the production of DHT, and inhibited the activity of 5α- reductase Type II in the animal model. BC exerted these effects via its anti-proliferative effects by restoring the Bax/Bcl-2 ratio, activating caspase-3 and caspase-8, and inducing the phosphorylation of AMPK. studies using DHT-stimulated prostate cells demonstrated an up-regulation of BPH-related and proliferation markers, whereas baicalin clearly reduced the overexpression of AR, PSA, PCNA, and Bcl-2. These results suggested that baicalin could suppress androgen-dependent development of BPH both and by inducing apoptosis.

摘要

BPH 是一种常见于老年男性的疾病,其特征是前列腺上皮和基质组织的异常增殖。由于对其分子发病机制缺乏清晰的认识,目前尚无有效的治疗方法。尽管有几项研究报道了黄芩苷对包括前列腺癌在内的多种疾病的治疗作用,但它对 BPH 的有益作用尚未得到探索。本研究探讨了黄芩苷对 BPH 发展的治疗作用及其作用机制。我们建立了睾酮处理的 BPH 动物模型和 DHT 刺激的前列腺细胞系,包括 RWPE-1 和 WPMY-1。黄芩苷的给药改善了病理性前列腺增大,抑制了 DHT 的产生,并抑制了动物模型中 5α-还原酶 II 型的活性。BC 通过恢复 Bax/Bcl-2 比值、激活 caspase-3 和 caspase-8 以及诱导 AMPK 磷酸化来发挥这些作用。使用 DHT 刺激的前列腺细胞进行的研究表明,BPH 相关和增殖标志物的上调,而黄芩苷则明显降低了 AR、PSA、PCNA 和 Bcl-2 的过度表达。这些结果表明,黄芩苷可以通过诱导细胞凋亡来抑制雄激素依赖性 BPH 的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/0a6bc7c05c7d/aging-12-102731-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/8ee70bcc7862/aging-12-102731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/2d0f7a1e3f18/aging-12-102731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/6e7bd28fd058/aging-12-102731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/bf1ad8c07518/aging-12-102731-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/c06f6485f519/aging-12-102731-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/0a6bc7c05c7d/aging-12-102731-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/8ee70bcc7862/aging-12-102731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/2d0f7a1e3f18/aging-12-102731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/6e7bd28fd058/aging-12-102731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9f6/7041748/bf1ad8c07518/aging-12-102731-g004.jpg
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