促炎细胞因子
膀胱出口梗阻
炎症
前列腺
癌症研究
基因表达
细胞因子
增生
医学
免疫学
生物
内科学
基因
遗传学
癌症
作者
Mitsuhiro Tagaya,Michiko Oka,Makoto Ueda,Kazuchika Takagaki,Mitsushi Tanaka,Tadaaki Ohgi,Junichi Yano
出处
期刊:Cytokine
[Elsevier]
日期:2009-09-01
卷期号:47 (3): 185-193
被引量:19
标识
DOI:10.1016/j.cyto.2009.06.004
摘要
Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antioxidant, antiinflammatory phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. Because Eviprostat is a mixture of compounds from multiple natural sources, however, its mechanism of action has been difficult to investigate. Here, we describe the use of oligonucleotide microarrays to investigate changes in gene expression in the prostate of rats with surgically induced partial bladder-outlet obstruction and the effect of Eviprostat on those changes. Several dozen proinflammatory genes were activated in obstructed rats, including cytokine, arachidonic acid cascade enzyme, Toll-like receptor (TLR), and transcription factor genes, and their expression was suppressed by Eviprostat. Pathway analysis revealed that several proinflammatory pathways were activated, including cytokine and TLR signaling pathways. The differential expression of selected genes was verified by real-time reverse-transcriptase polymerase chain reaction. Our findings suggest that prostate inflammation in our rat model of partial bladder-outlet obstruction is related to the increased expression of nuclear factor κB (NF-κB) and the induction of proinflammatory cytokines, and that Eviprostat suppresses their expression at the transcriptional level. The prostate inflammation seen in BPH and the clinical benefits of Eviprostat may be similarly explained.
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