δ阿片受体激动剂对LPS诱导的巨噬细胞凋亡及坏死的影响

目的研究δ阿片受体激动剂DADLE对LPS诱导的巨噬细胞凋亡和坏死的影响。方法用LPS（100μg/L）刺激大鼠腹腔巨噬细胞，在LPS后立即或4h后加入DADLE（104M）。流式细胞仪和共聚焦成像检测巨噬细胞凋亡及坏死，ELISA法检测巨噬细胞细胞核NF—KB的活化水平，Westemblot法检测p38MAPK活化水平。ELISA法检测细胞培养上清TNF-α、IL-1β和HMGB1水平。结果DADLE明显抑制了LPS诱导的巨噬细胞凋亡及坏死，降低了细胞培养上清中TNF—α、IL-1β和HMGBl的水平，而且对巨噬细胞NF—kB及p38MAPK的活化均有抑制作用。结论DADLE通过抑制NF—kB及p38MAPK的活化。减少了LPS诱导的巨噬细胞凋亡、坏死及细胞因子的释放。

Effect of delta-opioid receptor agonist on LPS induced apoptosis and necrosis of macrophages

Objective To study the effect of deha-opioid receptor agonist （DADLE） on LPS induced apoptosis and necrosis of maerophages. Methods Peritoneal macrophages isolated from rats were challenged with LPS. DADLE at 104 M was administrated concurrently or 4h after LPS. Apoptosis and necrosis of macrophages were determined by flow cytometry analysis and confocal imaging. NF-KB activity in macrophages was determined by ELISA. Levels of activated p38 MAPK were measured by western blot. Levels of TNF-α,IL-1β and HMGB1 in culture supernatant were determined by ELISA. Results TNF-α,IL-1β and HMGB1 in supernatant were also suppressed by DADLE. LPS-induced apoptosis and necrosis of maerophages were significantly suppressed by DADLE, DADLE also inhibited the p38 MAPK and NF-KB pathways. Conclusion DADLE attenuates LPS induced apoptosis and necrosis of macrophages and cytokine release by suppressing the p38 MAPK and NF-KB pathways.