Dihydroartemisinin ameliorated the inflammatory response and regulated miRNA-mRNA expression profile of chronic nonbacterial prostatitis.

Abstract

Chronic nonbacterial prostatitis (CNP) is a chronic inflammatory disease. Patients often have trouble urinating, experience painful and frequent urination, and pelvic floor pain, which seriously affects their quality of life. Dihydroartemisinin (DHA) is the most important artemisinin derivative with good anti-inflammatory effects. However, the mechanism of DHA for CNP has not been fully elucidated. To examine the protective effect of DHA on CNP in mice model and to explore the potential mechanisms from the perspective of microRNAs (miRNAs). The CNP mouse model was induced using a prostate protein extract solution and complete Freund's adjuvant. The pain threshold was determined using von Frey filaments. Hematoxylin and eosin (H&E) staining, TUNEL staining, western blot, real-time polymerase chain reaction (PCR), and small RNA sequencing were used to evaluate the effect of DHA on CNP. Dihydroartemisinin significantly alleviated prostate tissue damage in CNP mice, reduced the pain threshold, improved the prostate index, and reduced cell apoptosis. It also reduced the expressions of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and macrophage chemoattractant protein-1 (MCP-1). Furthermore, after screening 48 differentially expressed genes, we found 4 miRNAs significantly downregulated and 2 miRNAs upregulated in the model group, which were later significantly reversed by DHA treatment. These results indicate that DHA treatment of CNP involves several signaling pathways. Dihydroartemisinin can improve the pathological state and inflammatory response in a CNP mouse model, which may be related to the regulation of miRNAs.