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Article Publish Status: FREE
Abstract Title:

Genipin protects against mitochondrial damage of the retinal pigment epithelium under hyperglycemia through thepathway mediated by thesignaling axis.

Abstract Source:

Ann Transl Med. 2022 May ;10(10):587. PMID: 35722358

Abstract Author(s):

Wenshuang Xu, Qingyou Chen, Xiaofeng Zhang, Yue Zhao, Shuang Wu, Chao Yang, Yubao Liu, Lijie Liang, Di Jia, Chaojun Li, Li Fan, Yan Shi

Article Affiliation:

Wenshuang Xu

Abstract:

BACKGROUND: To investigate the protective effect and mechanism of genipin (GE) on mitochondrial damage in retinal pigment epithelial (RPE) cells induced by high glucose.

METHODS: Differential genes of GE in the treatment of diabetic retinopathy (DR) were screened by the Gene Expression Omnibus (GEO) database. Differential genes located in thepathway were obtained. TargetScan, miRDB, and DIANA databases were used to predict the targeted microRNAs (miRNAs) of differential genes. A high-fat diet combined with streptomycin (STZ) intraperitoneal injection were used to establish a diabetic mouse model. Diabetic mice were treated with GE by intragastric administration. The functional and molecular changes of the retina were detected by electroretinogram (ERG) and reverse transcription-polymerase chain reaction (RT-PCR). ARPE-19 cells were cultured under hyperglycemic conditions withandinhibitors.was knocked down/overexpressed to detect changes in cell function, activity, and mitochondrial function. The dual luciferase reporter assay confirmed the targeted binding ofwith

RESULTS: Bioinformatics analysis finally yieldedas the research target gene.was predicted to be the targeted miRNA ofby online databases. The results of animal experiments showed that the retinal function of mice recovered after GE administration (P<0.05), the expression ofandin RPE cells was significantly increased (P<0.05), and the expression ofwas significantly decreased (P<0.05). The results of cell experiments showed that the functions of cells and mitochondria recovered after the addition of GE under hyperglycemia (P<0.05). Cell and mitochondrial functions were decreased after the addition ofinhibitor (P<0.05). Overexpression ofor inhibition ofincreased cell activity and mitochondrial function (P<0.05). The results of the dual luciferase reporter assay showed thathad a targeted binding site with

CONCLUSIONS: GE protects ARPE-19 cell functional activity, inflammatory responses, and mitochondrial damage by promoting thesignaling pathway and regulating the expression of the/signaling axis.

Study Type : Human Study

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