Wang Lusheng, Yang Kaiye, Jing Rongrong, Zhao Wengang, Guo Keke, Hu Zhenlin, Liu Guangrong, Xu Nuo, Zhao Jungang, Lin Li, Gao Shuang
School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Infinitus (China) Company Ltd., Guangzhou, China.
Front Pharmacol. 2023 Jan 17;14:1089537. doi: 10.3389/fphar.2023.1089537. eCollection 2023.
Exposure to ultraviolet B (UVB) radiation can damage the epidermis barrier function and eventually result in skin dryness. At present, little work is being devoted to skin dryness. Searching for active ingredients that can protect the skin against UVB-induced dryness will have scientific significance. polysaccharide (SIP) has been shown to have significant antioxidant and anti-photodamage effects on the skin following UVB irradiation. To evaluate the effect of SIP on UVB-induced skin dryness ex vivo, SIP-containing hydrogel was applied in a mouse model following exposure to UVB and the levels of histopathological changes, DNA damage, inflammation, keratinocyte differentiation, lipid content were then evaluated. The underlying mechanisms of SIP to protect the cells against UVB induced-dryness were determined in HaCaT cells. SIP was found to lower UVB-induced oxidative stress and DNA damage while increasing keratinocyte differentiation and lipid production. Western blot analysis of UVB-irradiated skin tissue revealed a significant increase in peroxisome proliferator-activated receptor-α (PPAR-α) levels, indicating that the underlying mechanism may be related to PPAR-α signaling pathway activation. By activating the PPAR-α pathway, SIP could alleviate UVB-induced oxidative stress and inhibit the inflammatory response, regulate proliferation and differentiation of keratinocytes, and mitigate lipid synthesis disorder. These findings could provide candidate active ingredients with relatively clear mechanistic actions for the development of skin sunscreen moisturizers.
暴露于中波紫外线(UVB)辐射会损害表皮屏障功能,最终导致皮肤干燥。目前,针对皮肤干燥的研究较少。寻找能够保护皮肤免受UVB诱导干燥的活性成分具有科学意义。已证明多糖(SIP)在UVB照射后对皮肤具有显著的抗氧化和抗光损伤作用。为了在体外评估SIP对UVB诱导的皮肤干燥的影响,在UVB照射后的小鼠模型中应用含SIP的水凝胶,然后评估组织病理学变化、DNA损伤、炎症、角质形成细胞分化、脂质含量水平。在HaCaT细胞中确定了SIP保护细胞免受UVB诱导干燥的潜在机制。发现SIP可降低UVB诱导的氧化应激和DNA损伤,同时增加角质形成细胞分化和脂质生成。对UVB照射的皮肤组织进行蛋白质印迹分析显示,过氧化物酶体增殖物激活受体-α(PPAR-α)水平显著升高,表明潜在机制可能与PPAR-α信号通路激活有关。通过激活PPAR-α途径,SIP可以减轻UVB诱导的氧化应激并抑制炎症反应,调节角质形成细胞的增殖和分化,并减轻脂质合成紊乱。这些发现可为开发皮肤防晒保湿剂提供具有相对明确作用机制的候选活性成分