Abstract
Anthocyanins belong to a large and widespread group of water-soluble phytochemicals and exhibit potent antioxidative and anti-inflammatory properties; however, the molecular mechanisms of these biochemical actions mediated by anthocyanins remain unclear. In this study, our data show that pretreatment of THP-1 macrophages with Cyanidin-3- O-β-glucoside (C3G) for 12 h can enhance the expression and transcriptional activities of the nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) and liver X receptor α (LXRα). Furthermore, pretreatment of these cells with C3G for 12 h causes dose-dependent inhibition of lipopolysaccharide (LPS)-induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at both the mRNA and protein levels together with a decrease in nitric oxide (NO) and prostaglandin E 2 (PGE 2) production. Consequently, addition of geranylgeranyl pyrophosphate ammonium salt (GGPP), an LXRα antagonist, significantly downregulates the inhibitory effect of C3G on LPS-induced iNOS and COX-2 expression in THP-1 macrophages, whereas the PPARγ antagonist GW9662 has no effect. Further investigation revealed that LXRα might interfere with LPS-induced iNOS and COX-2 expression by suppressing the functional activation of nuclear factor-κB (NF-κB), not – as was previously proposed – by reducing NF-κB nuclear translocation. Taken together, these results indicate that LXRα activation has an essential role in the anti-inflammatory property of C3G. Moreover, they provide new insight into the molecular basis for the anti-inflammatory property of anthocyanins.
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