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Inhibition of Ultraviolet-B Radiation Induced Photodamage by Trigonelline Through Modulation of Mitogen Activating Protein Kinases and Nuclear Factor-κB Signaling Axis in Skin
Photochemistry and Photobiology ( IF 3.3 ) Pub Date : 2020-12-20 , DOI: 10.1111/php.13369
Lone A Nazir 1, 2 , Malik A Tanveer 1, 2 , Sheikh A Umar 1, 2 , Sharma Love 1, 2 , Gupta Divya 1, 2 , Sheikh A Tasduq 1, 2
Affiliation  

Cutaneous photodamage is incited via exposure of ultraviolet-B (UV-B) radiation to skin, characterized by the manifestation of oxidative stress, inflammation, collagen degradation and apoptosis which translates to external aging signs such as wrinkle formation and leathery skin appearance. Meanwhile, it increases cellular susceptibility to photocarcinogenesis. Several studies have accumulated evidence regarding the usage of natural agents in reversing the clinical signs of photoaging as well as preventing photo-toxicity at molecular level. In this study, we have explored the therapeutic potential of natural agent Trigonelline (TG) against UV-B radiation mediated skin photodamage. Various parameters modulated by the exposure of UV-B radiation were investigated in human skin cells and chronic photodamage mice model (Balb/c). We found that TG alleviates UV-B radiation induced photodamage in human skin cells and Balb/c skin mice. TG treatment in UV-B irradiated skin cells abates UV-B radiation mediated phototoxicity, oxidative stress, inflammation and apoptosis. At molecular level, we observed TG treatment significantly prevents the reactive oxygen species (ROS) generation and lipid peroxidation, restores collagen synthesis and matrix metalloproteinase (MMPs) levels. The in vitro findings were replicated in the in vivo model. We found that the TG acts potentially via modulation of ROS-MAPKs-NF-κB axis. Collectively, we propose that TG acts antagonistically against UV-B mediated skin damage and has strong potential to be developed as a therapeutic and cosmetical agent against photodamage disorders.

中文翻译:

葫芦巴碱通过调节皮肤中的丝裂原活化蛋白激酶和核因子-κB信号轴抑制紫外线-B辐射诱导的光损伤

皮肤光损伤是通过暴露在皮肤上的紫外线-B (UV-B) 辐射引起的,其特征在于氧化应激、炎症、胶原蛋白降解和细胞凋亡的表现,这会转化为外部衰老迹象,例如皱纹形成和皮肤革质外观。同时,它增加了细胞对光致癌的易感性。几项研究已经积累了关于使用天然药物逆转光老化的临床症状以及在分子水平上防止光毒性的证据。在这项研究中,我们探索了天然药剂葫芦巴碱的治疗潜力(TG) 抗 UV-B 辐射介导的皮肤光损伤。在人体皮肤细胞和慢性光损伤小鼠模型 (Balb/c) 中研究了由 UV-B 辐射暴露调制的各种参数。我们发现 TG 减轻了人类皮肤细胞和 Balb/c 皮肤小鼠中 UV-B 辐射引起的光损伤。对 UV-B 照射的皮肤细胞进行 TG 治疗可减轻 UV-B 辐射介导的光毒性、氧化应激、炎症和细胞凋亡。在分子水平上,我们观察到 TG 治疗显着防止活性氧 (ROS) 生成和脂质过氧化,恢复胶原合成和基质金属蛋白酶 (MMP) 水平。体外研究结果在体内重复模型。我们发现 TG 可能通过调节 ROS-MAPKs-NF-κB 轴发挥作用。总的来说,我们提出 TG 对 UV-B 介导的皮肤损伤具有拮抗作用,并且具有被开发为针对光损伤疾病的治疗和美容剂的强大潜力。
更新日期:2020-12-20
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