UVA comprises more than 90% of the solar UV radiation reaching the Earth. Artificial lightening lamps have also been reported to emit significant amounts of UVA. Exposure to UVA has been associated with dermatological disorders including skin cancer. At the molecular level, UVA damages different cellular biomolecules and triggers inflammatory responses. The current study was devoted to investigate the potential protective effect of L-carnitine against UVA-induced skin tissue injury using rats as a mammalian model. Rats were distributed into normal control group (NC), L-carnitine control group (LC), UVA-Exposed group (UVA), and UVA-Exposed and L-carnitine-treated group (UVA-LC). L-carnitine significantly attenuated UVA-induced elevation of the DNA damage markers 8-oxo-2′-deoxyguanosine (8-oxo-dG) and cyclobutane pyrimidine dimers (CPDs) as well as decreased DNA fragmentation and the activity of the apoptotic marker caspase-3. In addition, L-carnitine substantially reduced the levels of lipid peroxidation marker (MDA) and protein oxidation marker (PCC) and significantly elevated the levels of the total antioxidant capacity (TAC) and the antioxidant reduced glutathione (GSH) in the skin tissues. Interestingly, L-carnitine upregulated the level of the DNA repair protein proliferating cell nuclear antigen (PCNA). Besides it mitigated the UVA-induced activation of the oxidative stress-sensitive signaling protein p38 and its downstream target c-Fos. Moreover, L-carnitine significantly downregulated the levels of the early response proinflammatory cytokines TNF-α, IL-6, and IL-1β. Collectively, our results highlight, for the first time, the potential attenuating effects of L-carnitine on UVA-induced skin tissue injury in rats that is potentially mediated through suppression of UVA-induced oxidative stress and inflammatory responses.

UVA占到达地球的太阳UV辐射的90％以上。人工照明灯也据报道会发出大量的UVA。接触UVA与包括皮肤癌在内的皮肤疾病有关。在分子水平上，UVA会破坏不同的细胞生物分子并引发炎症反应。当前的研究致力于使用大鼠作为哺乳动物模型研究左旋肉碱对UVA诱导的皮肤组织损伤的潜在保护作用。将大鼠分为正常对照组（NC），左旋肉碱对照组（LC），暴露于UVA的组（UVA），以及暴露于UVA和L-肉碱的组（UVA-LC）。左旋肉碱可显着减弱UVA诱导的DNA损伤标记物8-oxo-2'-脱氧鸟苷（8-oxo-dG）和环丁烷嘧啶二聚体（CPDs）的升高，并减少DNA片段化和凋亡标记胱天蛋白酶的活性-3。此外，左旋肉碱可显着降低皮肤组织中脂质过氧化标志物（MDA）和蛋白质氧化标志物（PCC）的水平，并显着提高总抗氧化剂能力（TAC）和抗氧化剂还原型谷胱甘肽（GSH）的水平。有趣的是，左旋肉碱上调了DNA修复蛋白增殖细胞核抗原（PCNA）的水平。此外，它减轻了UVA诱导的氧化应激敏感信号蛋白p38及其下游目标c-Fos的活化。而且，左旋肉碱显着下调了早期反应性促炎细胞因子TNF-α，IL-6和IL-1β的水平。总的来说，我们的研究结果首次突显了左旋肉碱对UVA诱导的大鼠皮肤组织损伤的潜在减弱作用，这可能是通过抑制UVA诱导的氧化应激和炎症反应而介导的。