chrysin and Fatty-Liver

Chrysin (5,7-di-OH-flavone), a widely distributed natural flavonoid, has been well documented for involving in various biological activities, especially in regulation of peroxisome proliferator activated receptor γ (PPARγ) activity as a modest modulator. However, the exact molecular mechanism is still unrevealed. In the current study, for the first time, we discovered that, chrysin not only significantly attenuated inflammation in high-fat feeding mice, but also alleviated high fat diet-induced hepatic, muscular steatosis in obese mice without altering the body weight. Chrysin decreases the infiltration of macrophages into adipose tissue in obese mice. In addition, chrysin was also found to induce an anti-inflammatory M2 phenotype and decreases M1 phenotype, both in peritoneal macrophages of obese mice and cultured macrophages in vitro, and thereby, chrysin changed the M1/M2 status. Our data further showed that chrysin regulated the phenotype of macrophages through enhancing the transcriptional activation of PPARγ and the expression of its target genes. Taken together, we conclude that chrysin may serve as an effective modulator of PPARγ during the pathogenesis of inflammation, thereby our findings shed light on the potential therapeutic feature of chrysin in recovering inflammatory diseases via regulating M1/M2 status.

Topics: Adipose Tissue; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Division; Cell Line, Transformed; Cell Survival; Cells, Cultured; Dose-Response Relationship, Drug; Fatty Liver; Flavonoids; Humans; Liver; Macrophages, Peritoneal; Male; Mice; Mice, Inbred C57BL; Muscle, Skeletal; Myositis; Non-alcoholic Fatty Liver Disease; Obesity; PPAR gamma; Random Allocation; Specific Pathogen-Free Organisms; Transcription, Genetic

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease and its incidence is rising worldwide. We compared the antioxidant capacity of seventeen flavonoids with their inhibitory effects on oleic acid-induced triglyceride (TG) over-accumulation in HepG2 cells. The results showed significant correlations (P < 0.01) between the inhibition of intracellular TG levels and the suppression effects on reactive oxygen species. Nevertheless, the radical-reducing activities of flavonoids assessed by chemical assays (cyclic voltammetry and Folin-Ciocalteu reagent assay) were poorly correlated with their intracellular TG inhibitory effects. The relationships between structural properties of flavonoids and their inhibitory effects on TG over-accumulation were discussed.

Topics: Antioxidants; Cell Line; Fatty Liver; Flavonoids; Humans; In Vitro Techniques; Oleic Acid; Reactive Oxygen Species; Triglycerides