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卡利科辛通过抑制p38MAPK/NF-κB通路来保护大鼠免受慢性前列腺炎的影响

Heng Wang¹, Lei He², Zhaofei Liu¹

¹Department of Urology, Lianyungang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Lianyungang 222000, China.

Open medicine (Warsaw, Poland)

|September 4, 2023

概括

西西桑 (Qinshi Simiao San) 的关键成分卡利科辛 (Calycosin) 通过减少炎症和氧化应激减轻老鼠的慢性前列腺炎 (CP). 它通过抑制p38基因激活蛋白激酶 (p38MAPK) /NF-kappaB (NF-κB) 信号通路来实现这一目标.

科学领域:

药理学药理学是指药理学的学科.
泌尿器科泌尿器科泌尿器科泌尿器科
分子生物学分子生物学

背景情况:

慢性前列腺炎 (CP) 是一种常见的疾病,其分子机制尚不清楚.
西西苗山 (Qinshi Simiao San) 衍生出的卡利科辛 (Calycosin) 在缓解CP的过程中显示出潜在的潜力.
卡利科辛在CP中的确切作用机制需要阐明.

研究的目的:

在慢性前列腺炎的老鼠模型中研究卡利科辛的治疗效果和分子机制.
评估卡利科辛对前列腺组织病理,炎症,氧化应激和关键信号通路的影响.

主要方法:

为前列腺形态进行血素-素染色.
针对炎症性细胞因子 (IL-1β,IL-6,TNF-α) 和免疫因子 (SIgA,IgG) 的ELISA.
氧化应激标志物 (MDA,SOD,CAT) 的检测套件和活性氧物种 (ROS) 的免疫光检测套件.
西部涂抹分析p38MAPK/NF-κB信号通路.

主要成果:

卡利科辛显著改善了CP大鼠的前列腺组织形态.
卡利科辛降低了IL-1β,IL-6,TNF-α,IgG和SIgA的水平.
卡利科辛抑制了氧化应激,并抑制了p38MAPK/NF-κB通路的激活.

结论:

卡利科辛在老鼠模型中显示出对慢性前列腺炎的保护作用.
卡利科辛的抗炎和抗氧化特性通过抑制p38MAPK/NF-κB信号通路而得到介导.

关键词:

卡利科辛是一种酸盐.慢性前列腺炎慢性前列腺炎在p38MAPK/NF-κB路径中.

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