Dihydroquercetin composite nanofibrous membrane prevents UVA radiation-mediated inflammation, apoptosis and oxidative stress by modulating MAPKs/Nrf2 signaling in human epidermal keratinocytes - 23/09/22

Doi : 10.1016/j.biopha.2022.113727

Jinping Zhang ^a,^{^{1
These authors have contributed equally to this work}}, Yongchun Zheng ^b,^{^{1
These authors have contributed equally to this work}}, Bo Hong ^a, Lina Ma ^b, Yingchun Zhao ^a, Shuai Zhang ^a, Shuwen Sun ^a, Qiteng Ding ^a, Yue Wang ^a, Wencong Liu ^a,^⁎ , Chuanbo Ding ^b,^⁎
^a College of traditional Chinese Medicine, Jilin Agricultural University, Changchun 130118, China
^b College of traditional Chinese Medicine, Jilin Agriculture Science and Technology College, Jilin 132101, China

^⁎Correspondence to: Department of Pharmacy Jilin Agricultural University, Changchun 130000, China.Department of Pharmacy Jilin Agricultural UniversityChangchun130000China^⁎⁎Correspondence to: Jilin Agricultural Science and Technology College, Jilin 132000, China.Jilin Agricultural Science and Technology CollegeJilin132000China

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Abstract

Exposure to ultraviolet (UV) radiation is a key cause of skin inflammation and photodamage in the environment. Dihydroquercetin composite nanofiber membrane (CPD) is a nano-scale membrane cloth prepared by electrospinning technology. The results in this study showed that CPD could enhance the activities of endogenous antioxidant enzymes such as SOD and GSH-Px induced by UVA radiation, and reduce the overexpression of ROS. MAPKs/Nrf2 signaling is associated with inflammation, apoptosis and oxidative stress. Compared with control HaCaT cells, we found that CPD pretreatment prevents MAPK (p-ERK, p-JNK, and p-P38)/Nrf2-induced inflammation, apoptosis, and oxidative stress signaling during UVA exposure pathway overexpression. Immunofluorescence experiments also showed that CPD could reduce the fluorescence intensity of Caspase-3 and TNF-α. These results suggest that CPD may be a successful healing agent that provides reinforcement against UVA-induced oxidative and irritating skin compensation.

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