Chen Huimei, Shi Jian, Tang Yu, Chen Xiong, Wang Ziyan, Liu Qianhong, Wu Kai, Yao Xiaolei
The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, Hunan, China; Hunan University of Chinese Medicine, Changsha, 410208, Hunan, China; Hunan Provincial Key Laboratory for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine, Changsha, 410208, Hunan, China.
Hunan University of Chinese Medicine, Changsha, 410208, Hunan, China; Yong Zhou Hospital of Traditional Chinese Medicine, Yongzhou, 425000, Hunan, China.
Eur J Pharmacol. 2025 Mar 15;991:177311. doi: 10.1016/j.ejphar.2025.177311. Epub 2025 Jan 30.
Dry eye disease (DED) is closely associated with oxidative stress (OS); its high prevalence and the limitations of current treatments highlight the need for highly effective antioxidants. Chlorogenic acid (CGA) can upregulate the activity of antioxidant enzymes, hinder the process of lipid peroxidation, and exert potent antioxidant effects. In this study, we established an OS-induced DED mouse model to investigate the protective effect and mechanism of CGA against OS-induced DED. Three aspects were examined: oxidative damage, apoptosis, and autophagy. The results demonstrated that CGA improved ocular surface signs in DED mice, decreased inflammatory responses in the meibomian gland (MG), downregulated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), inhibited apoptosis and autophagy, and regulated proteins related to the AMPK (AMP-activated protein kinase)/ULK1 (UNC-51-like Kinase 1) signaling pathway in the MG of DED mice. These findings suggest that CGA can attenuate oxidative damage and inhibit related apoptosis and autophagy in the MG of DED mice by affecting the expression of proteins related to the AMPK/ULK1 signaling pathway.
干眼症（DED）与氧化应激（OS）密切相关；其高患病率以及当前治疗方法的局限性凸显了对高效抗氧化剂的需求。绿原酸（CGA）可上调抗氧化酶的活性，阻碍脂质过氧化过程，并发挥强大的抗氧化作用。在本研究中，我们建立了OS诱导的DED小鼠模型，以研究CGA对OS诱导的DED的保护作用及其机制。研究了三个方面：氧化损伤、细胞凋亡和自噬。结果表明，CGA改善了DED小鼠的眼表体征，降低了睑板腺（MG）的炎症反应，下调了活性氧（ROS）和丙二醛（MDA）水平，抑制了细胞凋亡和自噬，并调节了DED小鼠MG中与AMPK（AMP激活蛋白激酶）/ULK1（UNC-51样激酶1）信号通路相关的蛋白质。这些发现表明，CGA可通过影响与AMPK/ULK1信号通路相关的蛋白质表达，减轻DED小鼠MG中的氧化损伤并抑制相关的细胞凋亡和自噬。
