Platelet‐rich plasma protects human keratinocytes from UVB‐induced apoptosis by attenuating inflammatory responses and endoplasmic reticulum stress.

Background: Although the role of platelet‐rich plasma (PRP) in ultraviolet light B (UVB)‐induced photoaging has been confirmed in many studies, the specific mechanism is still not clear. Therefore, we attempted to investigate the effect and mechanism of PRP on UVB‐induced human keratinocyte (HaCaT cells) apoptosis. Methods: HaCaT cells were collected to construct UVB‐induced photoaging models. Then, the cells were divided into Sham group, 5% PRP group, UVB group, and UVB + 5% PRP group. Next, MTT assay was used to detect the level of cell proliferation; flow cytometry to check the level of apoptosis; ELISA to determine the TNF‐α, IL‐18, IL‐6, and IL‐1β levels in the supernatant; and Western blot to test Bax, Bcl‐2, cytochrome c (Cyt.c), GRP78, CHOP, and ATF4 protein expression levels. Results: Briefly, 5% PRP intervention could relieve the inhibition of UVB on HaCaT cell proliferation, inhibit the promotion of UVB to cell apoptosis, up‐regulate UVB‐induced Bcl‐2 protein expression, and decrease Bax and Cyt.c protein level. In addition, 5% PRP significantly down‐regulated the inflammatory factor levels of TNF‐α, IL‐18, IL‐6, and IL‐1βin UVB‐induced cells and reduced the inflammatory response. Moreover, 5% PRP also greatly reduced the protein expression levels of GRP78, CHOP, and ATF4 in UVB‐induced cells and alleviated endoplasmic reticulum (ER) stress. Conclusion: PRP may protect HaCaT cells from UVB‐induced apoptosis by alleviating inflammatory response and ER stress. [ABSTRACT FROM AUTHOR]