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IL-6/STAT3 通路参与调控慢性非细菌性前列腺炎细胞的自噬,且可能受 NLRP3 炎性小体的影响。

IL-6/STAT3 pathway is involved in the regulation of autophagy in chronic non-bacterial prostatitis cells, and may be affected by the NLRP3 inflammasome.

机构信息

Department Of Urology, The First Affiliated Hospital of Anhui Medical University, Institute of Urology, Anhui Medical University and Anhui Province Key Laboratory of Genitourinary Diseases, Anhui Medical University, Hefei, Anhui, P.R. China.

出版信息

Ultrastruct Pathol. 2021 Jul-Sep;45(4-5):297-306. doi: 10.1080/01913123.2021.1966149. Epub 2021 Aug 23.

Abstract

Studies have shown that the cytokine IL-6 plays an important role in the occurrence and development of chronic non-bacterial prostatitis (CNP), but the specific mechanism by which this cytokine regulates CNP is still unclear. At the same time, relevant research have also shown that autophagy is involved in regulating the occurrence and development of inflammation. The possible mechanisms are IL-6/STAT3 signaling pathway and NLRP3 inflammasome. On the basis of establishing the CNP model in rats, we found that IL-6 can regulate autophagy of CNP cells and is associated with the STAT3 pathway and NLRP3 inflammasome. Our results indicate that IL-6 is involved in the regulation of autophagy signaling pathways in CNP. IL-6/STAT3 signaling pathway can suppress cell autophagy pathway in CNP; And the NLRP3 inflammasome may regulate CNP cell autophagy by regulating the IL-6/STAT3 pathway. These findings may provide a new theoretical basis for the pathogenesis of CNP, as well as new ideas and new targets for the treatment and prevention of CNP.

摘要

研究表明细胞因子 IL-6 在慢性非细菌性前列腺炎(CNP)的发生发展中起重要作用,但该细胞因子调节 CNP 的具体机制尚不清楚。同时,相关研究还表明自噬参与调节炎症的发生和发展。其可能的机制是 IL-6/STAT3 信号通路和 NLRP3 炎性小体。在建立大鼠 CNP 模型的基础上,我们发现 IL-6 可调节 CNP 细胞的自噬,与 STAT3 通路和 NLRP3 炎性小体有关。我们的结果表明,IL-6 参与 CNP 自噬信号通路的调节。IL-6/STAT3 信号通路可抑制 CNP 细胞的自噬途径;NLRP3 炎性小体可能通过调节 IL-6/STAT3 通路来调节 CNP 细胞自噬。这些发现可能为 CNP 的发病机制提供新的理论依据,以及 CNP 的治疗和预防的新思路和新靶点。

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