青心酮抑制脂多糖诱导的小鼠巨噬细胞凋亡的机制探讨  

Mechanism of inhibition of 3, 4-dihydroxyacetophenone on LPS-induced apoptosis of RAW264.7 macrophage in mice

作　　者：李钢[1] 吴萍[2] 张代娟[2] 叶笃筠[2] 李锋[3] 

机构地区：[1]华中科技大学同济医学院附属梨园医院外科,湖北武汉430070 [2]华中科技大学同济医学院病理生理学系,湖北武汉430030 [3]华中科技大学同济医学院附属同济医院,湖北武汉430030

出　　处：《中草药》2005年第12期1835-1838,共4页Chinese Traditional and Herbal Drugs

基　　金：国家自然科学基金资助项目(30100226)

摘　　要：目的阐明青心酮对脂多糖(LPS)诱导的巨噬细胞凋亡抑制作用的可能机制。方法采用LPS刺激小鼠RAW264.7巨噬细胞株为炎症模型,采用RT-PCR检测血红素氧合酶-1(HO-1)mRNA,血红蛋白结合法测定一氧化碳(CO)的相对水平,流式细胞仪结合细胞形态学检测观察细胞凋亡。结果1×10-5mol/L青心酮作用24h,在增加细胞HO-1mRNA及CO水平的同时,可使LPS诱导的巨噬细胞凋亡率显著下降(P<0.01);加入牛血红蛋白清除CO后,青心酮对LPS所致细胞凋亡的抑制率由(63.2±3.8)%降低为(45.1±5.3)%,差异显著(P<0.01)。结论青心酮可抑制LPS所致的小鼠RAW264.7巨噬细胞的凋亡,此作用部分由HO-1/CO系统所介导。Objective To investigate the potential mechanism of inhibition of 3, 4-dihydroxyacetophenone （DHAP） on the LPS-induced apoptosis of RAW264. 7 macrophage. Methods RAW264.7 macrophage line in mice was induced by LPS to set up the inflammatory model. Heine oxygenase-1 （HO- 1） mRNA was measured by RT-PCR. The relative concentration of carbon monoxide （CO） was detected in hemoglobin binding test. Apoptosis was studied by flow cytometric assay with cytomorphology. Results Treated with 1 × 10^-5 mol/L DHAP for 24 h, LPS-induced macrophage apoptosis was decreased （P〈 0.01）, while the level of HO-1 mRNA and CO in cells was increasing. When CO was eliminated with bovine hemoglobin, the inhibitory rate of DHAP on LPS-induced apoptosis was decreased from （63.2± 3.8）% to （45.1±5.3）% to show the significant effect （P〈0.01）. Conclusion DHAP could inhibit LPS- induced apoptosis of RAW264.7 macrophage in mice. This effect is partly mediated by HO-1/CO system.

关 键 词：青心酮 细胞凋亡 巨噬细胞 血红素氧合酶-1 

分 类 号：R285.5[医药卫生—中药学]