Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL.
Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL.
Photochem Photobiol. 2019 Mar;95(2):605-611. doi: 10.1111/php.13021. Epub 2018 Oct 14.
UVA irradiation is known to cause photoaging via production of reactive oxygen species (ROS) and activation of inflammatory processes. Previously, we have demonstrated that baicalin, a plant-derived flavonoid possessing both antioxidant and anti-inflammatory activity, protects mouse keratinocytes against damage from UVB irradiation. However, the role of baicalin in vivo has not been well studied, particularly in the setting of UVA irradiation. To explore the protective effects and mechanisms of baicalin treatment in mice after UVA irradiation, mice were exposed to acute and chronic doses of UVA irradiation with or without baicalin or vehicle. Skin samples were collected for histological staining, RNA isolation, flow cytometry and protein extraction. Our results demonstrate the protective effect of baicalin against UVA-induced oxidative damage and inflammation in mouse skin. These effects are likely mediated via the TLR4 pathway, which may serve as a target for photochemoprevention against skin inflammation.
UVA 辐射会通过产生活性氧（ROS）和激活炎症过程导致光老化。以前，我们已经证明，黄芩苷是一种具有抗氧化和抗炎活性的植物衍生类黄酮，可保护小鼠角质细胞免受 UVB 辐射的损伤。然而，黄芩苷在体内的作用尚未得到很好的研究，特别是在 UVA 辐射的情况下。为了探索黄芩苷在 UVA 照射后对小鼠的保护作用及其机制，我们用或不用黄芩苷或载体对小鼠进行了急性和慢性 UVA 照射。收集皮肤样本进行组织学染色、RNA 分离、流式细胞术和蛋白质提取。我们的结果表明，黄芩苷对 UVA 诱导的小鼠皮肤氧化损伤和炎症具有保护作用。这些作用可能是通过 TLR4 途径介导的，TLR4 途径可能是针对皮肤炎症的光化学预防的靶点。
