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[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(<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(<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。
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[Abstract]
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. Heme 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 (P0.01), 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 (P0.01). Conclusion DHAP could inhibit LPS-induced apoptosis of RAW264.7 macrophage in mice. This effect is partly mediated by HO-1/CO system.
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[基金项目]
国家自然科学基金资助项目(30100226)