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Updated: Mar 22, 2026
Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
Protective effects of curcumin against liver fibrosis through modulating DNA methylation
Peng Wu1, Rui Huang2, Ya-Li Xiong2
1The First Clinical Medical School, Nanjing University of Traditional Chinese Medicine, Nanjing 210023, China; Department of Medical Nursing, Jiangsu Jiankang Vocational College, Nanjing 210029, China.
Abstract:
Recent research has demonstrated that advanced liver fibrosis in patients could be reversed, but no approved agents are available for the treatment and prevention of liver fibrosis in humans. Curcumin (CUR) is the principal curcuminoid of turmeric. Inhibitory effects of CUR and its underlying mechanisms in liver fibrogenesis have been explored. In the present study, we hypothesized that epigenetic mechanisms contribute to the protective effects of CUR against liver fibrosis. We used CCl4-induced liver injury in BALB/c mice and the rat hepatic stellate cell line HSC-T6 as experimental models. Genomic DNA methylation was analyzed by MeDIP-chip and verified by real-time PCR on MeDIP-enriched DNA. The mRNA and protein expressions of DNMT1, α-SMA, and Col1α1 were determined by real-time PCR and Western blotting, respectively. The methylation statuses of FGFR3, FZD10, Gpx4, and Hoxd3 were further confirmed by quantitative methylation-specific PCR (qMSP). Our results showed that CUR treatment reversed liver injury in vivo and in vitro, possibly through down regulation of DNMT1, α-SMA, and Col1α1 and by demethylation of the key genes. In conclusion, aberrant methylation is closely associated with liver fibrosis and CUR treatment may reverse liver fibrosis by epigenetic mechanisms.
Insights
Curcumin (CUR) may reverse liver fibrosis by altering epigenetic mechanisms. This study found CUR treatment reduced liver injury and key fibrotic markers through DNA demethylation in mouse models and cell lines.
Area of Science:
- Hepatology
- Epigenetics
- Pharmacology
Background:
- Advanced liver fibrosis is a significant health concern with no approved treatments.
- Curcumin (CUR), derived from turmeric, shows potential in inhibiting liver fibrogenesis.
- The role of epigenetic modifications in CUR's protective effects against liver fibrosis requires further investigation.
Purpose of the Study:
- To investigate the hypothesis that epigenetic mechanisms mediate the protective effects of Curcumin (CUR) against liver fibrosis.
- To explore the impact of CUR on DNA methylation patterns and gene expression in liver fibrosis models.
Main Methods:
- CCl4-induced liver injury in BALB/c mice and HSC-T6 rat hepatic stellate cells were used as experimental models.
- Genomic DNA methylation was analyzed using MeDIP-chip, quantitative methylation-specific PCR (qMSP), and real-time PCR.
- mRNA and protein expression of key fibrotic markers (DNMT1, α-SMA, Col1α1) were assessed via real-time PCR and Western blotting.
Main Results:
- CUR treatment effectively reversed CCl4-induced liver injury in vivo and in vitro.
- CUR administration led to the downregulation of DNMT1, α-SMA, and Col1α1, key markers of liver fibrosis.
- Demethylation of specific genes (FGFR3, FZD10, Gpx4, Hoxd3) was observed following CUR treatment, suggesting an epigenetic mechanism.
Conclusions:
- Aberrant DNA methylation is strongly associated with the development of liver fibrosis.
- Curcumin (CUR) demonstrates potential for reversing liver fibrosis through epigenetic modulation, specifically via DNA demethylation.
- These findings highlight CUR as a promising therapeutic agent for liver fibrosis, acting through epigenetic pathways.
