Anti-inflammatory effect of Calycosin glycoside on lipopolysaccharide-induced inflammatory responses in RAW 264.7 cells
Anti-inflammatory effect of Calycosin glycoside on lipopolysaccharide-induced inflammatory responses in RAW 264.7 cells
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DOI：
10.1016/j.gene.2018.06.057
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发表时间：
2018-10-30
期刊：
影响因子：
3.5
通讯作者：
Fu, Xueyan
中科院分区：
文献类型：
--
作者：
Dong, Lin;Yin, Lei;Fu, Xueyan
目的探讨毛蕊异黄酮苷（CG）潜在的抗炎作用。采用脂多糖（LPS）诱导的RAW 264.7细胞检测CG的抗炎活性，ELISA法检测其IL-6、IL-1 β、tnf - α和PGE2水平；采用Griess反应法测定培养基中的NO水平。qRT-PCR检测iNOS和COX-2 mRNA表达，western blotting检测I κ B α、65、ERK、JNK和p38的磷酸化水平。CG能显著抑制NO和PGE的产生(2)，显著抑制tnf - α、IL-1 β和IL-6的产生。CG可抑制lps诱导的RAW 264.7细胞iNOS、COX-2 mRNA表达及I κ B α、p65、ERK、JNK和p38蛋白磷酸化。这些发现表明，CG通过nf - κ B和MAPK信号通路表现出强大的抗炎活性，并作为一种潜在的治疗炎症性疾病的药物。
Objective to find the Calycosin glycoside (CG) potential anti-inflammatory effect. The anti-inflammatory activity of CG was evaluated by lipopolysaccharide (LPS)-induced RAW 264.7 cells, and the IL-6, IL-1 beta, TNF-alpha and PGE2 level were measured by ELISA; NO levels in the culture media were determined using the Griess reaction. The iNOS and COX-2 mRNA expressions were measured by qRT-PCR and the phosphorylation of I kappa B alpha, 65, ERK, JNK, and p38 was determined by western blotting. The CG could markedly inhibit the productions of NO and PGE(2) and markedly inhibit the productions of TNF-alpha, IL-1 beta and IL-6. CG could suppress mRNA expression of iNOS, COX-2 and protein phosphorylation of I kappa B alpha, p65, ERK, JNK, and p38 in LPS-induced RAW 264.7 cells. These findings indicate that CG exhibited potent anti-inflammatory activity through the NF-kappa B and MAPK signal pathway, and as a potential therapeutic agent against inflammatory diseases.