Platelet-rich plasma improves lipopolysaccharide-induced inflammatory response by upgrading autophagy

Objectives Platelet-rich plasma (PRP) plays an important role at all stages of wound healing, including the inflammatory stage. Macrophage autophagy has been found to influence the inflammatory response process. However, it is unclear whether PRP can affect inflammatory responses via macrophage autophagy. In the present study, we explored the effect of PRP on inflammatory responses and researched the underlying mechanism. Methods RAW 264.7 macrophages were treated with PRP and/or lipopolysaccharide (LPS). The effects of PRP on the expression of inflammatory factors were determined by ELISA and qRT-PCR. Macrophage autophagosomes were also assessed by TEM and immunofluorescence. Autophagy and NLRP3-related proteins were investigated using Western blot analysis. Results PRP reduced the levels of inflammatory factors and increased autophagy in RAW 264.7 cells. Pretreatment with 3-MA, which is an autophagy inhibitor, abolished the impact of PRP on the inflammatory response. Moreover, PRP induced macrophage autophagy by activating the NLRP3 inflammasome. Conclusions These results show that PRP can attenuate LPS-induced inflammatory responses by enhancing autophagy via NLRP3. These study also provides a new perspective on the molecular mechanism of PRP therapy in wound healing.