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Cyanidin-3-rutinoside(C3R) Attenuates Free Fatty Acid-Induced Hepatic Lipid Accumulation in HepG2 Cells

ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is characteristic by pathological lipid accumulation in hepatocytes. This study investigates how Cyanidin-3-rutinoside(C3R), a natural anthocyanin with antioxidant and metabolic regulatory properties, counteracts this process. In a free fatty acid (FFA)-induced HepG2 steatosis model, C3R significantly reduced intracellular triglycerides, total cholesterol, and LDL-C levels, suppressed lipid droplet formation, and alleviated oxidative stress by enhancing SOD/CAT activities and GSH content while lowering MDA and ROS. RNA-seq analysis revealed that C3R reversed FFA-induced transcriptomic alterations. Mechanistically, C3R inhibited SREBP2-mediated cholesterol synthesis, activated the PCSK9/LDLR pathway to promote cholesterol clearance, and upregulated PPARγ-dependent CYP7A1 expression to stimulate bile acid synthesis from cholesterol. C3R also enhanced autophagic flux, facilitating lipid droplet degradation. Molecular docking confirmed high-affinity binding of C3R to INSIG1, PCSK9, and PPARγ, with hydroxyl groups forming specific hydrogen bonds at active sites, supporting direct target engagement. These findings establish a multi-targeted mechanism for C3R in ameliorating hepatic steatosis and provide a molecular basis for anthocyanin-mediated regulation of lipid metabolism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE316562 | GEO | 2026/01/23

REPOSITORIES: GEO

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Project description:Pink-flowered strawberry is a new promising ornamental flower derived from intergeneric hybridization (Fragaria × Potentilla) with bright color, prolonged flowering period and edible fruits. However, the transcriptional events underlying anthocyanins biosynthesis pathway have not been fully characterized in its petal coloration. The pigment compounds accumulated in its fruits were the same as cultivated strawberry, but different from in its flowers. To gain insights into the regulatory networks related to anthocyanin biosynthesis and identify key genes, we performed an integrated analyses of the transcriptome and metabolomes involved in red petals at three development stages (Bud stage (L), Coloration beginning stage (Z) and Big bud stage (D)) of pink-flowered strawberry. Transcript and metabolite profiles were generated through high-throughput RNA-sequencing and high-performance liquid chromatography coupled with mass spectrometry, respectively. The results showed that the main pigments of red and dark pink petals were anthocyanins, among which cyanidins were the main compounds. There were no anthocyanins detected in white-flowered hybrids. A total of 50 285 non-redundant unigenes were obtained from the transcriptome databases, among which 59 differentially expressed genes could be identified as putative homologues of flower coloration related genes. Based on a comprehensive analysis relating pigmentation compounds to gene expression profiles, the mechanism of flower color formation was examined in pink-flowered strawberry. Furthermore, a new hypothesis explaining the lack of color phenotype of the white-flowered strawberry hybrids from the level of the transcriptome. The expression patterns of FpDFR gene and FpANS gene corresponded to the accumulation patterns of cyanidin contents in pink-flowered strawberry hybrids with different shades of pink; Whereas other anthocyanin biosynthesis genes were weakly related flower color deepened. Moreover, FpANS, FpBZ1 and FpUGT75C1 genes were the key factors that lead to the inability to accumulate anthocyanins in the white petals of PFS hybrids. Meanwhile, the competitive effect of FpFLS gene and FpDFR gene may further inhibit anthocyanin synthesis. The data presented herein are important for understanding of the molecular mechanisms underlying the petal pigmentation and will be powerful for integrating into novel genes that are potential targets for breeding new valuable pink-flowered strawberry cultivars.

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Cyanidin-3-rutinoside(C3R) Attenuates Free Fatty Acid-Induced Hepatic Lipid Accumulation in HepG2 Cells

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