Improvement of chronic non-bacterial prostatitis by Jiedu Huoxue decoction through inhibiting TGF-β/SMAD signaling pathway.

Improvement of chronic non-bacterial prostatitis by Jiedu Huoxue decoction through inhibiting TGF-β/SMAD signaling pathway.
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DOI:
10.1016/j.biopha.2022.113193
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发表时间:
2022-06
期刊:
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
影响因子:
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通讯作者:
Jun Yi;Junqing Pan;Sina Zhang;Wenli Mao;Jiangang Wang;Wanchun Wang;Zhangren Yan
Jun Yi;Junqing Pan;Sina Zhang;Wenli Mao;Jiangang Wang;Wanchun Wang;Zhangren Yan
中科院分区:
其他
文献类型:
--
作者:
Jun Yi;Junqing Pan;Sina Zhang;Wenli Mao;Jiangang Wang;Wanchun Wang;Zhangren Yan

文献摘要

相似文献

慢性非细菌性前列腺炎(CNBP)占临床前列腺炎病例的90%以上,目前尚无特异性有效的治疗方法。解毒活血汤(JDHXD)在CNBP中的调节作用尚不清楚。方法采用1%角叉菜胶(50 μL)注射角叉菜胶建立CNBP动物模型。研究前列腺指数、上皮厚度、管腔面积和疼痛反应时间。分别用TUNEL染色和流式细胞术检测细胞凋亡水平。采用ELISA法测定血清炎症因子。结果JDHXD治疗可显著改善CNBP大鼠前列腺组织损伤。前列腺指数、疼痛反应时间等反映前列腺功能的指标均得到改善。JDHXD在体内具有抑制细胞凋亡、活性氧(ROS)和炎症反应的作用。JDHXD显著抑制TGF-β/SMAD信号通路,激活TGF-β/SMAD信号通路可逆转JDHXD对CNBP损伤的改善作用。证实了JDHXD具有抗炎、抗氧化和抗凋亡的作用。结论jdhxd可能通过靶向TGF-β/SMAD信号通路,抑制炎症反应、ROS和细胞凋亡,改善CNBP损伤。本研究可能为通过抑制TGF-β/SMAD信号通路预防和治疗CNBP提供新的思路。
BackgroundChronic non-bacterial prostatitis (CNBP) accounts for more than 90 % of clinical prostatitis cases, and there is no specific and effective treatment for CNBP. The regulatory role of Jiedu Huoxue decoction (JDHXD)in CNBP remains unclear. We investigated if JDHXD could improve CNBPMethodsThe animal model of CNBP was established by carrageenan injection with 1 % carrageenan (50 μL). The prostate index, epithelial thickness, lumen area, and pain response time were investigated. The apoptosis levels were measured with TUNEL staining and flow cytometry, respectively. Inflammatory factors in the serum were measured with ELISA method.ResultsTreatment with JDHXD significantly improve prostate tissues injury in CNBP rats. Some parameters, such as prostate index, and pain response time, reflecting the prostate function were improved by JDHXD. Inhibition of apoptosis, reactive oxygen species (ROS), and inflammatory response were achieved by JDHXD in vivo. JDHXD markedly suppressed the TGF-β/SMAD signaling pathway, and activation of TGF-β/SMAD signaling pathway could reverse the improvement of CNBP injury by JDHXD. The anti-inflammatory, anti-oxidative and anti-apoptotic effects of JDHXD were proved.ConclusionJDHXD might improve CNBP injury through suppressing inflammation response, ROS, and apoptosis by targeting TGF-β/SMAD signaling pathway. This research might provide a new thought for the prevention and treatment of CNBP through inhibiting TGF-β/SMAD signaling pathway.