Human skin functions go beyond serving only as a mechanical barrier. As a complex organ, the skin is capable to cope with external stressors cutaneous by neuroendocrine systems to control homeostasis. However, constant skin exposure to ultraviolet (UV) radiation causes progressive damage to cellular skin constituents, mainly due excessive reactive oxygen species (ROS) production. The present study shows new approaches of metformin (MET) as an antioxidant agent. Currently, MET is the first line treatment of type 2 diabetes and has attracted attention, based on its broad mechanism of action. Therefore, we evaluated MET antioxidant potential in cell-free systems and in UVB irradiated human keratinocyte HaCaT cells. In cell-free system assays MET did not show intrinsic scavenging activity on DPPH radicals or superoxide (O₂⁻) xanthine/luminol/xanthine oxidase-generated. Cell-based results demonstrated that MET was able to reduce UVB-induced intracellular ROS and NADPH oxidase-dependent superoxide (O₂⁻) production. MET posttreatment of HaCaT cells reduced ERK 1/2 phosphorylation, NADPH oxidase activity, and cell death by apoptosis. These findings suggest that the protection mechanism of MET may be through the inhibition of ROS formation enzyme. These results showed that MET might be a promising antioxidant agent against UV radiation induced skin damage.

人类皮肤的功能不仅仅是作为机械屏障。作为一个复杂的器官，皮肤能够通过神经内分泌系统应对皮肤的外部压力以控制体内平衡。然而，皮肤持续暴露于紫外线 (UV) 辐射会导致细胞皮肤成分逐渐受损，这主要是由于活性氧 (ROS) 产生过多。本研究展示了二甲双胍 (MET) 作为抗氧化剂的新方法。目前，MET 是 2 型糖尿病的一线治疗药物，因其广泛的作用机制而备受关注。因此，我们评估了无细胞系统和 UVB 照射的人角质形成细胞 HaCaT 细胞中的 MET 抗氧化潜力。在无细胞系统测定中，MET 对 DPPH自由基或超氧化物（O₂ ^- ) 黄嘌呤/鲁米诺/黄嘌呤氧化酶产生。基于细胞的结果表明，MET 能够减少 UVB 诱导的细胞内 ROS 和 NADPH 氧化酶依赖性超氧化物 (O ₂ ^- ) 的产生。HaCaT 细胞的 MET 后处理降低了 ERK 1/2 磷酸化、NADPH 氧化酶活性和细胞凋亡导致的细胞死亡。这些发现表明MET的保护机制可能是通过抑制ROS形成酶。这些结果表明 MET 可能是一种很有前途的抗氧化剂，可以对抗紫外线辐射引起的皮肤损伤。