Arbutin Inhibited Heat Stress-Induced Apoptosis and Promoted Proliferation and Migration of Heat-Injured Dermal Fibroblasts and Keratinocytes by Activating PI3K/AKT Signaling Pathway

Abstract

Objective. Studies have shown that arbutin has antioxidant and anti-inflammatory activities, which makes it suitable for treating skin wounds. We designed this study to investigate the effect of arbutin on heat-induced apoptosis, proliferation, and migration of dermal fibroblasts and keratinocytes and to explore the molecular mechanism. Methods. In vitro, HaCAT and dermal fibroblast (DFL) cells were cultured and used to establish a heat stress-injured skin cell model. We investigated the effects of arbutin on apoptosis, proliferation, and migration of HaCAT and DFL cells after heat stress injury. We then used immunoblotting to detect the expression of p-PI3K, PI3K, p-AKT, and AKT proteins for studying the underlying mechanisms and used a PI3K/AKT inhibitor (LY294002) to verify the efficacy of arbutin in HaCAT and DFL cells with heat stress injury. Results. Arbutin strongly inhibited heat stress-induced apoptosis, proliferation inhibition, and migration inhibition of HaCAT and DFL cells in vitro. Our results also showed that arbutin strongly decreased the ratio of Bax/Bcl2 protein expression and PCNA protein expression in HaCAT and DFL cells after treatment with heat stress. Furthermore, we also found that arbutin significantly increased the ratio of p-PI3K/PI3K and p-AKT/AKT protein expression, and LY294002 markedly reversed the effect of arbutin on heat stress-induced apoptosis, proliferation inhibition, and migration inhibition of HaCAT and DFL cells. Conclusion. Our finding indicated that arbutin inhibited heat stress-induced apoptosis and promoted proliferation and migration of heat-injured dermal fibroblasts and epidermal cells by activating the PI3K/AKT signaling pathway, suggesting that arbutin may provide an alternative therapeutic approach for the treatment of skin injury.

Analysis of CircRNA Expression in Peripheral Blood of Holstein Cows in Response to Heat Stress

“…In our results, overlapped DE in cows’ circRNAs under heat stress was most enriched in choline metabolism, which is related to alleviating heat-stress-induced damages by reducing oxidative stress [ 39 ]. Furthermore, PI3K/AKT [ 40 ], sphingolipid [ 36 ] and cAMP [ 37 ] have been proved to be important signaling molecules participating in adaptation to heat stress by affecting multi-level regulatory networks. From our results, the RT and RR significantly increased but the milk yield decreased with the THI in cows ( Table 2 ), which revealed that Holstein cows in Beijing were undergoing severe temperature stress in July.…”