Platelet-rich plasma treatment alleviates osteoarthritis-related pain, inflammation, and apoptosis by upregulating the expression levels of microRNA-375 and microRNA-337.

OBJECTIVE

The present study was designed to determine the molecular mechanism by which platelet-rich plasma (PRP) acts on Osteoarthritis (OA) -related pain, inflammation, and apoptosis and .

MATERIALS AND METHODS

An OA model was established in rats using anterior cruciate ligament transection, and an OA model was created by treating chondrocytes with IL-1β. Then, the induced rats and chondrocytes were treated with PRP. Real-time PCR were used to examine the expression of micorRNAs (miRs) and mRNAs of inflammatory cytokines. WB were performed to detect the expression of apoptotic factors and Wnt/β-catenin signals. Structural damage of the cartilage and pain in OA rats were analyzed and represented by Mankin Score, OARSIS score, Tender threshold, and Thermal pain threshold. CCK-8 assay and flow cytometry were used to determine cell viability and apoptosis.

RESULTS

The expression levels of miR-337 and miR-375 were downregulated in the and vitro OA models; however, PRP treatment elevated their levels. miR-337 and miR-375 inhibition reversed the effects of PRP of reducing tenderness and thermal pain thresholds in OA rats. Moreover, PRP decreased the mRNA expression levels of MMP-13, Bax, and inflammatory factors, such as IL-1β, IL-18, and TNF-α, as well as increased the expression levels of collagen II and antiapoptotic Bcl-2. The decrease in inflammation and apoptosis was reversed by miR-337 and miR-375 inhibition, respectively.

DISCUSSION AND CONCLUSIONS

In conclusion, miR-337 and miR-375 are involved in PRP-delayed OA progression by affecting inflammation and apoptosis.