Ryu Jina, Kwon Mi-Jin, Nam Taek-Jeong
Department of Food and Life Science, Pukyong National University, Busan 608-737, Korea.
Mar Drugs. 2015 Jul 31;13(8):4721-32. doi: 10.3390/md13084721.
In this study, we examined the protective effects of porphyra-334 against UVA-irradiated cellular damage and elucidated the underlying mechanisms. Porphyra-334 prevented UVA-induced cell death and exhibited scavenging activities against intracellular oxidative stress induced by UVA irradiation in skin fibroblasts. We found that porphyra-334 significantly reduced the secretion and expression of IL-6 and TNF-α, reduced nuclear expression of Nuclear factor-κB (NF-κB), and sustained NF-E2-related factor 2 (Nrf2) activation. Further mechanism research revealed that porphyra-334 promoted the Nrf2 signaling pathway in UVA-irradiated skin fibroblasts. Our results show that the antioxidant effect of porphyra-334 is due to the direct scavenging of oxidative stress and its inhibitory effects on NF-κB-dependent inflammatory genes, such as IL-6 and TNF-κ. Therefore, we hypothesize that boosting the Nrf2- NF-κB-dependent response to counteract environmental stress is a promising strategy for the prevention of UVA-related damage.
在本研究中,我们检测了紫菜多糖-334对紫外线A(UVA)照射所致细胞损伤的保护作用,并阐明了其潜在机制。紫菜多糖-334可预防UVA诱导的细胞死亡,并对UVA照射诱导的皮肤成纤维细胞内氧化应激具有清除活性。我们发现,紫菜多糖-334可显著降低白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的分泌及表达,降低核因子-κB(NF-κB)的核表达,并维持核因子E2相关因子2(Nrf2)的激活。进一步的机制研究表明,紫菜多糖-334可促进UVA照射的皮肤成纤维细胞中Nrf2信号通路。我们的结果表明,紫菜多糖-334的抗氧化作用是由于其对氧化应激的直接清除及其对NF-κB依赖性炎症基因(如IL-6和TNF-κ)的抑制作用。因此,我们推测增强Nrf2-NF-κB依赖性反应以对抗环境应激是预防UVA相关损伤的一种有前景的策略。