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首页> 外文期刊>Life sciences >Cyanidin-3-O-beta-glucoside inhibits iNOS and COX-2 expression by inducing liver X receptor alpha activation in THP-1 macrophages.
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Cyanidin-3-O-beta-glucoside inhibits iNOS and COX-2 expression by inducing liver X receptor alpha activation in THP-1 macrophages.

机译：Cyanidin-3-O-β-葡萄糖苷通过在THP-1巨噬细胞中诱导肝X受体α活化来抑制iNOS和COX-2表达。

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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-beta-glucoside (C3G) for 12 h can enhance the expression and transcriptional activities of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) and liver X receptor alpha (LXRalpha). 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 LXRalpha antagonist, significantly downregulates the inhibitory effect of C3G on LPS-induced iNOS and COX-2 expression in THP-1 macrophages, whereas the PPARgamma antagonist GW9662 has no effect. Further investigation revealed that LXRalpha might interfere with LPS-induced iNOS and COX-2 expression by suppressing the functional activation of nuclear factor-kappaB (NF-kappaB), not - as was previously proposed - by reducing NF-kappaB nuclear translocation. Taken together, these results indicate that LXRalpha 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.
机译：花青素属于一大类水溶性植物化学物质，具有强大的抗氧化和抗炎特性。然而，花色苷介导的这些生化作用的分子机制仍不清楚。在这项研究中，我们的数据表明，用Cyanidin-3-O-β-葡萄糖苷（C3G）预处理THP-1巨噬细胞可以增强核受体过氧化物酶体增殖物激活受体γ（PPARgamma）的表达和转录活性。和肝脏X受体alpha（LXRalpha）。此外，用C3G预处理这些细胞12小时会导致脂多糖（LPS）诱导的一氧化氮合酶（iNOS）和环氧合酶2（COX-2）的剂量依赖性抑制，其mRNA和蛋白质水平都会降低。一氧化氮（NO）和前列腺素E（2）（PGE（2））生产。因此，加入LXRalpha拮抗剂香叶基香叶基焦磷酸铵盐（GGPP）会显着下调C3G对THP-1巨噬细胞中LPS诱导的iNOS和COX-2表达的抑制作用，而PPARγ拮抗剂GW9662没有作用。进一步的研究表明，LXRalpha可能通过抑制核因子-kappaB（NF-kappaB）的功能激活来干扰LPS诱导的iNOS和COX-2表达，而不是像以前建议的那样，通过减少NF-kappaB核易位来进行干预。综上，这些结果表明LXRalpha激活在C3G的抗炎特性中起着至关重要的作用。而且，它们为花色苷抗炎特性的分子基础提供了新的见识。

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