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清眩润目饮通过抑制影响铁死亡的HMOX1/HIF-1通路来缓解干眼症。

Qingxuan Runmu Yin alleviates dry eye disease via inhibition of the HMOX1/HIF-1 pathway affecting ferroptosis.

作者信息

Wang Jiadi, Liu Yue, Zong Beiting, Zhao Shanshan, Li Yue, Zhang Zhirui, Yao Jing

机构信息

The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, China.

Heilongjiang University of Traditional Chinese Medicine, Harbin, China.

出版信息

Front Pharmacol. 2024 Sep 11;15:1391946. doi: 10.3389/fphar.2024.1391946. eCollection 2024.

DOI:10.3389/fphar.2024.1391946
PMID:39329129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11425584/
Abstract

The prevalence of dry eye disease (DED), a multifactorial ocular surface disease characterized by tear film instability, is increasing yearly. Qingxuan Run Mu Yin (QXRMY) is a traditional Chinese medicine (TCM) consisting of It has excellent therapeutic effects on dry eye syndrome and a good anti-inflammatory effect on immune-related inflammation. However, the molecular mechanism of Qing Xuan Run Mu Yin in treating dry eye syndrome is largely unknown. The present study used an online database to identify potential target genes of QXRMY for treating DED. The possible mechanisms of these target genes for the treatment of DED were obtained through Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) databases, Hub genes screened by Cytoscape and intersected with ferroptosis-related genes, and the essential genes were finally obtained based on the results of the analyses. DED cell model and rat model were constructed in this study to validate the critical genes and pathways, and it was confirmed that QXEMY alleviated DED by repressing ferroptosis through inhibiting the HMOX1/HIF-1 pathway. In conclusion, this study integrated network pharmacological analyses and experimental validation to provide an effective method to investigate the molecular mechanism of QXRMY in treating DED.

摘要

干眼疾病（DED）是一种以泪膜不稳定为特征的多因素眼表疾病，其患病率逐年上升。清宣润目饮（QXRMY）是一种中药方剂，它对干眼综合征具有出色的治疗效果，对免疫相关炎症具有良好的抗炎作用。然而，清宣润目饮治疗干眼综合征的分子机制在很大程度上尚不清楚。本研究利用在线数据库鉴定清宣润目饮治疗DED的潜在靶基因。通过基因本体论（GO）和京都基因与基因组百科全书（KEGG）数据库获得这些靶基因治疗DED的可能机制，通过Cytoscape筛选枢纽基因并与铁死亡相关基因进行交集分析，最终根据分析结果获得关键基因。本研究构建了DED细胞模型和大鼠模型以验证关键基因和通路，并证实清宣润目饮通过抑制HMOX1/HIF-1通路抑制铁死亡来减轻DED。总之，本研究整合了网络药理学分析和实验验证，为研究清宣润目饮治疗DED的分子机制提供了一种有效方法。

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