Cyanidin-3-O-β-glucoside inhibits lipopolysaccharide-induced inflammatory response in mouse mastitis

• 作 者: FUYunhe;WEIZhengkai;ZHOUErshun;ZHANGNaisheng;YANGZhengtao;
• 机 构: Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University,Changch
• 出 处: 中国畜牧兽医学会家畜内科学会2014年学术研讨会
• 发表日期: 2014年期

　　Cyanidin-3-O-β-glucoside (CAS No.7084-24-4), a typical anthocyanin pigment that exists in the human diet,has been reported to have anti-inflammatory properties.However, the effect of C3G on LPS-induced mastitis and the molecular mechanisms has not been investigated.In this study,we detected the protective effects of C3G on LPS-induced mouse mastitis model and investigated the molecular mechanisms in LPS-stimulated mouse mammary epithelial cells.Our results showed that C3G could attenuate mammary histopathologic changes,and myeloperoxidase (MPO) activity;inhibit TNF-α, IL-1βand IL-6 production;caused by LPS.Meanwhile, C3 G dose-dependently inhibited TNF-α and IL-6 in LPS-stimulated mouse mammary epithelial cells.C3G suppressed LPS-induced NF-κB and IRF3 activation.Furthermore, C3G disrupted the formation of lipid rafts by depleting cholesterol.Moreover, C3G activated LXR-ABCG1-dependent cholesterol efflux.Knockdown of LXRα abrogated the anti-inflammatory effects of C3G.In conclusion, C3G has a protective effect on LPS-induced mastitis.The promising anti-inflammatory mechanisms of C3G is associated with up-regulation of the LXRα-ABCG1 pathway which result in disrupting lipid rafts by depleting cholesterol, thereby suppressing TLR4 mediated NF-κB and IRF3 signaling pathways induced by LPS.