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前列宁胶囊通过HIF-1α信号通路抑制良性前列腺增生血管生成。

Qianliening capsule inhibits benign prostatic hyperplasia angiogenesis via the HIF-1α signaling pathway.

作者信息

Lin Jiumao, Zhou Jianheng, Xu Wei, Hong Zhenfeng, Peng Jun

机构信息

Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China ; Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

Department of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

出版信息

Exp Ther Med. 2014 Jul;8(1):118-124. doi: 10.3892/etm.2014.1723. Epub 2014 May 19.

DOI:10.3892/etm.2014.1723
PMID:24944609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4061199/
Abstract

Angiogenesis plays an important role in the progression and development of benign prostatic hyperplasia (BPH), and has become a promising target for BPH treatment. The hypoxia-inducible factor-1α (HIF-1α) signaling pathway promotes the process of angiogenesis, contributing to the growth and progression of a number of hyperplasia diseases, including BPH. Qianliening capsule (QC) is a traditional Chinese formula that has been used clinically in China to treat BPH for a number of years. Recently, QC was demonstrated to inhibit prostatic cell growth and induce apoptosis and via regulating the epidermal growth factor/signal transducer and activator of transcription 3 signaling pathway and mitochondrion-dependent apoptosis pathway. However, the mechanisms underlying the anti-BPH effect remain largely unknown. To further elucidate the mechanism of QC activity in BPH treatment, a rat BPH model established by injecting testosterone following castration was established and the effect of QC on prostatic tissue angiogenesis was evaluated, as well as the underlying molecular mechanisms. QC was shown to reduce the prostatic index in BPH rats, but without affecting the body weight, demonstrating that QC is effective in the treatment of BPH and without apparent toxicity. In addition, QC treatment significantly reduced the intraprostatic microvessel density, indicating antiangiogenesis activity . In addition, treatment with QC inhibited the expression of HIF-1α in BPH rats, as well as the expression of vascular endothelial growth factor and basic fibroblast growth factor. Therefore, for the first time, the present study hypothesized that QC inhibits angiogenesis in prostatic tissue of BPH rats via the inhibition of the HIF-1α signaling pathway, which may be one of the mechanisms in which QC treats BPH.

摘要

血管生成在良性前列腺增生(BPH)的进展和发展中起重要作用,并且已成为BPH治疗的一个有前景的靶点。缺氧诱导因子-1α(HIF-1α)信号通路促进血管生成过程,促成包括BPH在内的多种增生性疾病的生长和进展。前列宁胶囊(QC)是一种中药配方,在中国临床上已用于治疗BPH多年。最近,已证明QC通过调节表皮生长因子/信号转导和转录激活因子3信号通路以及线粒体依赖性凋亡通路来抑制前列腺细胞生长并诱导凋亡。然而,其抗BPH作用的潜在机制在很大程度上仍然未知。为了进一步阐明QC在BPH治疗中的活性机制,建立了去势后注射睾酮建立的大鼠BPH模型,并评估了QC对前列腺组织血管生成的影响以及潜在的分子机制。结果显示,QC可降低BPH大鼠的前列腺指数,但不影响体重,表明QC对BPH治疗有效且无明显毒性。此外,QC治疗显著降低前列腺内微血管密度,表明其具有抗血管生成活性。此外,QC治疗可抑制BPH大鼠中HIF-1α的表达,以及血管内皮生长因子和碱性成纤维细胞生长因子的表达。因此,本研究首次假设QC通过抑制HIF-1α信号通路来抑制BPH大鼠前列腺组织中的血管生成,这可能是QC治疗BPH的机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/032a90d6208f/ETM-08-01-0118-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/99bf6db50532/ETM-08-01-0118-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/595fb08293a6/ETM-08-01-0118-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/ff9095a0492c/ETM-08-01-0118-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/b68c437bfca9/ETM-08-01-0118-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/032a90d6208f/ETM-08-01-0118-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/99bf6db50532/ETM-08-01-0118-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/595fb08293a6/ETM-08-01-0118-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/ff9095a0492c/ETM-08-01-0118-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/b68c437bfca9/ETM-08-01-0118-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69af/4061199/032a90d6208f/ETM-08-01-0118-g04.jpg

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