Wang Heng, He Lei, Liu Zhaofei, Xu Xiangjun, Zhang Haitao, Mao Pengfei, Li Ming
Department of Urology, Lianyungang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Lianyungang 222000, China.
Department of Acupuncture, Lianyungang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Lianyungang 222000, China.
Open Med (Wars). 2023 Aug 28;18(1):20230770. doi: 10.1515/med-2023-0770. eCollection 2023.
Currently, the effect and molecular mechanism of calycosin, the main active ingredient of Qinshi Simiao San, which can alleviate chronic prostatitis (CP), on CP remain unclear. This study aimed to elucidate the potential mechanism of action of calycosin in CP in a rat CP model. The prostate tissue morphology was evaluated based on hematoxylin-eosin staining. Enzyme-linked immunosorbent assay was conducted to evaluate inflammatory cytokine and immune factor levels (secretory immunoglobulin A [SIgA]; immunoglobulin G [IgG]) in prostate tissues and serum. Additionally, representative biomarkers of oxidative stress, including malondialdehyde, superoxide dismutase, and catalase were detected using detection kits, and reactive oxygen species release was evaluated using immunofluorescence staining. Furthermore, the p38 mitogen-activated protein kinase (p38MAPK)/NF-kappaB (NF-κB) signaling pathway was analyzed by western blotting. The results showed that calycosin substantially ameliorated the pathological damage to prostate tissues of the CP rats. Moreover, calycosin significantly downregulated interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha, IgG, and SIgA levels. Furthermore, we found that calycosin considerably suppressed oxidative stress and inhibited the activation of the p38MAPK/NF-κB signaling pathway in rats with CP. In summary, our findings revealed that calycosin protects against CP in rats by inhibiting the p38MAPK/NF-κB pathway.
目前，秦氏四妙散的主要活性成分毛蕊异黄酮可缓解慢性前列腺炎（CP），但其对CP的作用及分子机制仍不清楚。本研究旨在通过大鼠CP模型阐明毛蕊异黄酮在CP中的潜在作用机制。基于苏木精-伊红染色评估前列腺组织形态。采用酶联免疫吸附测定法评估前列腺组织和血清中的炎性细胞因子和免疫因子水平（分泌型免疫球蛋白A [SIgA]；免疫球蛋白G [IgG]）。此外，使用检测试剂盒检测氧化应激的代表性生物标志物，包括丙二醛、超氧化物歧化酶和过氧化氢酶，并采用免疫荧光染色评估活性氧释放。此外，通过蛋白质印迹法分析p38丝裂原活化蛋白激酶（p38MAPK）/核因子-κB（NF-κB）信号通路。结果表明，毛蕊异黄酮显著改善了CP大鼠前列腺组织的病理损伤。此外，毛蕊异黄酮显著下调白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α、IgG和SIgA水平。此外，我们发现毛蕊异黄酮在CP大鼠中显著抑制氧化应激并抑制p38MAPK/NF-κB信号通路的激活。总之，我们的研究结果表明，毛蕊异黄酮通过抑制p38MAPK/NF-κB途径保护大鼠免受CP侵害。
