Li Huaping, Li Zhenjie, Peng Liqian, Jiang Na, Liu Qing, Zhang Erting, Liang Bihua, Li Runxiang, Zhu Huilan
a Guangzhou Institute of Dermatology , Guangzhou , China.
b Guangzhou First People's Hospital, Guangzhou Medical University , Guangzhou , China.
Free Radic Res. 2017 Feb;51(2):200-210. doi: 10.1080/10715762.2017.1294755.
Ultraviolet B (UVB) irradiation plays a key role in skin damage, which induces oxidative and inflammatory damages, thereby causing photoaging or photocarcinogenesis. Lycium barbarum polysaccharide (LBP), the most biologically active fraction of wolfberry, possesses significant antioxidative and anti-inflammatory effects on multiple tissues. In the present study, the photoprotective effects and potential underlying molecular mechanisms of LBP against UVB-induced photo-damage were investigated in immortalized human keratinocytes (HaCaT cells). The data indicated that pretreatment with LBP significantly attenuated UVB-induced decrease in cell viability, increase in ROS production and DNA damage. LBP also significantly suppressed UVB-induced p38 MAPK activation, and subsequently reversed caspase-3 activation and MMP-9 expression. Notably, LBP was found to induce Nrf2 nuclear translocation and increase the expression of Nrf2-dependent ARE target genes. Furthermore, the protective effects of LBP were abolished by siRNA-mediated Nrf2 silencing. These results showed that the antioxidant LBP could partially protect against UVB irradiation-induced photo-damage through activation of Nrf2/ARE pathway, thereby scavenging ROS and reducing DNA damage, and subsequently suppressing UVB-induced p38 MAP pathway. Thus, LBP can be potentially used for skincare against oxidative damage from environmental insults.
紫外线B(UVB)照射在皮肤损伤中起关键作用,它会引发氧化损伤和炎症损伤,从而导致光老化或光致癌作用。枸杞多糖(LBP)是枸杞中生物活性最强的成分,对多种组织具有显著的抗氧化和抗炎作用。在本研究中,我们在永生化人角质形成细胞(HaCaT细胞)中研究了LBP对UVB诱导的光损伤的光保护作用及其潜在的分子机制。数据表明,LBP预处理可显著减轻UVB诱导的细胞活力下降、活性氧(ROS)生成增加和DNA损伤。LBP还显著抑制UVB诱导的p38丝裂原活化蛋白激酶(MAPK)激活,随后逆转半胱天冬酶-3激活和基质金属蛋白酶-9(MMP-9)表达。值得注意的是,发现LBP可诱导核因子E2相关因子2(Nrf2)核转位并增加Nrf2依赖的抗氧化反应元件(ARE)靶基因的表达。此外,siRNA介导的Nrf2沉默消除了LBP的保护作用。这些结果表明,抗氧化剂LBP可通过激活Nrf2/ARE途径部分保护细胞免受UVB照射诱导的光损伤,从而清除ROS并减少DNA损伤,随后抑制UVB诱导的p38 MAP途径。因此,LBP有可能用于护肤品中,以抵御环境损伤引起的氧化损伤。