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

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.

KEYWORDS:

• Chronic non-bacterial prostatitis (CNP)
• autophagy
• interleukin-6 (IL-6)
• STAT3 pathway
• NLRP3 inflammasome

Acknowledgments

This research was supported by grants from the National Natural Science Foundation of China Government (No. 8150040310).

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Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

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Funding

This work was supported by the Natural Science Foundation of China [No. 81500576].