【摘要】 【目的】研究右美托咪定对巨噬细胞吞噬功能的影响并探讨其可能的机制。【方法】RAW264.7细胞分成对照组(control)、右美托咪定组(DEX)、BRL44408+右美托咪定组(BRL44408+DEX)。Western blotting检测α2A肾上腺素受体、p-Akt、Akt的表达,Phagocytosis Assay Kit(IgG PE)检测巨噬细胞的吞噬能力。【结果】RAW264.7细胞上有α2A肾上腺素受体的表达;右美托咪定能够增强巨噬细胞的吞噬能力(P <0.001),BRL44408逆转巨噬细胞吞噬能力的增强(P <0.001);右美托咪定使RAW264.7细胞的Akt通路激活,BRL44408的使用抑制Akt通路的激活(P <0.01)。【结论】右美托咪定可能通过α2A肾上腺素受体激活Akt通路,进而增强巨噬细胞的吞噬功能。更多还原

【Abstract】 【Objective】To investigate the effect of dexmedetomidine on the phagocytosis of macrophages.【Methods】RAW264.7 cells were divided into control group,DEX group,and BRL44408+DEX group. Expression of α2 Aadrenergic receptor,p-Akt and Akt were detected by Western Blotting;Phagocytosis Assay Kit(IgG PE)was used to measure the phagocytosis of macrophages.【Results】 α2 Aadrenergic receptor was detected in RAW264.7 cells;Dexmedetomidine could enhance the phagocytosis of macrophages(P < 0.001),and BRL44408 reversed the enhancement of phagocytic ability of macrophages(P < 0.001);Dexmedetomidine upregulated the expression of Akt in RAW264.7 cells,while the use of BRL44408 inhibited the activation of the Akt pathway(P < 0.01).【Conclusion】Dexmedetomidine could enhance phagocytosis of RAW264.7 by activating the Akt pathway through the α2 Aadrenergic receptor.更多还原