Ma Ming-Ming, Li Yan, Liu Xiang-Yong, Zhu Wei-Wei, Ren Xiang, Kong Gui-Qing, Huang Xiao, Wang Li-Peng, Luo Li-Qing, Wang Xiao-Zhi
Department of Respirator Medicine and Intensive Care Unit, Affiliated Hospital of Binzhou Medical University, Binzhou, 256603, Shandong Province, China.
Inflammation. 2015 Aug;38(4):1669-82. doi: 10.1007/s10753-015-0144-y.
Cyanidin-3-O-glucoside (C3G), an anthocyanin belonging to the flavonoid family and commonly present in food and vegetables in human diet, has exhibited anti-inflammatory and anti-oxidant effects. This study aimed to investigate the protective ability of C3G against inflammatory and oxidative injuries, as well as to clarify the possible mechanism in lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) in vitro and acute respiratory distress syndrome mouse model in vivo. HUVECs or male Kunming mice were pretreated with C3G 1 h before LPS stimulation. C3G significantly inhibited the production of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin (IL) -6, and IL-1β) in cell supernatants and bronchoalveolar lavage fluid (BALF) as determined by enzyme-linked immunosorbent assay. Histopathologic examination with hematoxylin and eosinstaining showed that C3G pretreatment substantially suppressed inflammatory cell infiltration, alveolar wall thickening, and interstitial edemain lung tissues. C3G markedly prevented LPS-induced elevation of malondialdehyde and myeloperoxidase levels in lung tissue homogenates, wet to dry ratio of lung tissues, total cells, and inflammatory cells (neutrophils and macrophages) in BALF. Moreover, C3G reduced superoxide dismutase activity in the lung tissue homogenates. Western blot assay also showed that C3G pretreatment significantly suppressed LPS-induced activation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways by blocking the phosphorylation of inhibitor κB-α, NF-κB/P65, extracellular signal-regulated kinase, p38, and c-Jun NH2-terminal kinase in the lung tissues. In summary, C3G may ameliorate LPS-induced injury, which results from inflammation and oxidation, by inhibiting NF-κB and MAPK pathways and playing important anti-inflammatory and anti-oxidative roles.
矢车菊素 - 3 - O - 葡萄糖苷（C3G）是一种属于黄酮类家族的花青素，普遍存在于人类饮食中的食物和蔬菜中，已表现出抗炎和抗氧化作用。本研究旨在探讨C3G对炎症和氧化损伤的保护能力，并阐明其在体外脂多糖（LPS）刺激的人脐静脉内皮细胞（HUVECs）和体内急性呼吸窘迫综合征小鼠模型中的可能机制。在LPS刺激前1小时用C3G预处理HUVECs或雄性昆明小鼠。通过酶联免疫吸附测定法测定，C3G显著抑制细胞上清液和支气管肺泡灌洗液（BALF）中促炎细胞因子（肿瘤坏死因子 - α、白细胞介素（IL） - 6和IL - 1β）的产生。苏木精和伊红染色的组织病理学检查表明，C3G预处理可显著抑制肺组织中的炎症细胞浸润、肺泡壁增厚和间质水肿。C3G显著阻止LPS诱导的肺组织匀浆中丙二醛和髓过氧化物酶水平升高、肺组织湿干比、BALF中的总细胞和炎症细胞（中性粒细胞和巨噬细胞）增加。此外，C3G降低了肺组织匀浆中的超氧化物歧化酶活性。蛋白质免疫印迹分析还表明，C3G预处理通过阻断肺组织中抑制蛋白κB - α、NF - κB/P6５、细胞外信号调节激酶、p38和c - Jun氨基末端激酶的磷酸化，显著抑制LPS诱导的核因子 - κB（NF - κB）和丝裂原活化蛋白激酶（MAPK）信号通路的激活。总之，C3G可能通过抑制NF - κB和MAPK途径并发挥重要的抗炎和抗氧化作用，改善LPS诱导的由炎症和氧化引起的损伤。
