紫外线诱导的脂质过氧化机制与相关皮肤病的研究进展

Mechanism of ultraviolet- induced lipid peroxidation and related skin diseases

紫外线可干扰细胞的信号传导过程，诱导细胞产生过量的活性氧。脂质是生物膜的主要成分，也是活性氧的主要攻击靶点。活性氧与多不饱和脂肪酸为主的脂质发生脂质过氧化反应，在中高水平脂质过氧化作用下，细胞发生凋亡和坏死细胞的程序性死亡，最终导致细胞损伤，促进多种病理状态的发展和加速老化过程。脂质过氧化作用产生丙二醛、4羟基壬烯醛和丙烯醛等高亲电子活性的醛，这些醛类可对磷脂、蛋白质和DNA造成不可逆的修饰和损伤。脂质过氧化作用与许多皮肤病相关，对脂质过氧化作用的进～步研究可能会为皮肤病的预防与治疗提供新方法。

Uhraviolet light can interfere with cell signal transduction and induce cells to generate excessive reactive oxygen species （ROS）. Lipids are the major component of biological membranes and the main target of ROS for attack. ROS can react with the polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation. The middle to high level of lipid peroxidation can induce cell apoptosis and programmed necrotic cell death, finally leading to cell damage, promoting the development of a variety of pathological states and accelerating the aging process. Lipid peroxidation can lead to the formation of various highly reactive electrophilic aldehydes, such as malondialdehyde, 4-hydroxy-2-nonenal （4-HNE） and acrolein, which can cause irreversible modification and damage to phospholipids, proteins and DNA. Lipid peroxidation is associated with many skin diseases. Further studies on lipid peroxidation may provide new methods for the prevention and treatment of skin diseases.