目的 通过体外培养巨噬细胞,探讨外源性一氧化碳对游离脂肪酸(FFA)引起炎症反应的抑制作用。方法 取状态良好的RAW264.7巨噬细胞,分为空白对照组、FFA组和一氧化碳释放分子2组(CORM2组),用含100μmol/LFFA及100μmol/LCORM2的高糖DMEM培养基分别作用于RAW264.7巨噬细胞24h。采用Western blot法检测pNFκB的表达水平,酶联免疫吸附试验法测定肿瘤坏死因子(TNF)α与白介素(IL)6水平。结果 FFA组pNFκB、TNFα及IL6水平均明显高于空白对照组,且CORM2组pNFκB、TNFα及IL6水平均明显低于FFA组,差异均有统计学意义(P〈0.05)。结论 外源性一氧化碳对FFA所致的慢性低炎症状态具有抑制作用。
Objective To investigate the inhibition effect of carbon monoxide on free fatty acid (FFA) stimulating in-flammatory response through cultivating macrophage in vitro. Methods RAW264. 7 macrophages in good condition were picked up and were divided into blank control group, FFA group and carbon monoxide molecule releasing group ( CORM - 2 group). High sugar DMEM medium containing 100 μmol/L FFA and 100 μmol/L carbon monoxide releasing molecule (CORM -2 ) were used for RAW264. 7 macrophage for 24 h. The p - NF - kappa B expression was detected by using Western - blot method. The TNF - alpha and IL - 6 levels were detected by Enzyme - linked immunosorbent assay. Results Compared with the blank con- trol group, the p - NF - kappa B protein expression level in FFA group increased significantly, the p - NF - kappa B protein ex- pression level in CORM - 2 group decreased significantly. TNF - alpha expression level in FFA group increased significantly, TNF- alpha expression level in CORM -2 intervention group decrease significantly; IL- 6 expression level in FFA group in- creased significantly and IL - 6 expression level in CORM - 2 group decrease significantly, and all the differences were statistical- ly significant ( P 〈 0.05 ). Conclusion The external carbon monoxide has an inhibitory effect on low chronic inflammation state caused by FFA.