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

Abstract

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. 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. 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. PRP may protect HaCaT cells from UVB-induced apoptosis by alleviating inflammatory response and ER stress.