ArticleCell biochemistry and biophysics2026
Luteolin Modulates DNA Methylation and Histone Acetylation To Restore Nrf2 and Alleviate Hyperglycemia-Induced Oxidative Stress in Vitro.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Recent experimental and epidemiological studies highlight the advantages of dietary polyphenols in preventing a wide range of diseases and disorders, including diabetes. One key mechanism involves the epigenetic regulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a redox cellular defense transcription factor, whose modulation aids in mitigating the oxidative damage associated with diabetes. This study investigates the epigenetic reactivation of Nrf2 by Luteolin (LUT) in Hyperglycemic microenvironment (HGM)- induced MIN6 cells. The activation potential of LUT was determined through qRT-PCR, Western blot, and epigenetic modulation. Following 24 h exposure to HGM, both mRNA and protein expression levels of Nrf2 and its downstream targets were significantly reduced. However, pretreatment with LUT restored their expression levels. Epigenetic markers, such as Histone deacetylases (HDAC 1 and 3) and DNA methyltransferases (DNMT1, 3 A, and 3B), were upregulated, while HDAC2 was downregulated under HGM conditions. These expressions were reversed by LUT pretreatment in MIN6 cells. Additionally, LUT was predicted to bind to the conserved catalytic domain of DNMTs directly, leading to changes in the expression pattern. The methylation percentage of the Nrf2 promoter region showed an increase under HGM conditions, which was significantly reversed by LUT in a dose-dependent manner. Collectively, our results demonstrate that LUT promotes Nrf2 activation through epigenetic regulation, highlighting its therapeutic potential in diabetes management.
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