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作 者:张锟[1] 陈立波[1] 郑海[1] 程平[1] 汪理[1]
机构地区:[1]华中科技大学同济医学院附属协和医院急诊外科,武汉430022
出 处:《中华实验外科杂志》2014年第5期979-981,共3页Chinese Journal of Experimental Surgery
摘 要:目的通过阻断内源性糖皮质激素受体观察其在创伤应激时是否参与了髓源抑制细胞的扩增。方法将BALB/c小鼠分为两组,一组建立腹部创伤模型,另一组于建模前30min给予糖皮质激素受体阻滞剂RU486腹腔注射,观察7d两组小鼠的生存情况。以流式细胞术和免疫组织化学检测脾脏、外周血和骨髓中CD11b^+/Gr-1^+髓源抑制细胞的比例。结果RU486能够降低创伤后髓源抑制细胞的大量扩增,以创伤模型建立后6h最为明显,模型组和RU486干预组髓源抑制细胞比例在脾脏中分别为(6.222±0.339)%和(3.303±0.385)%、在外周血分别为(29.108±9.814)%和(13.160±2.554)%、骨髓中分另0为(24.802±5.577)%和(12.920±2.114)%。同时,生存实验发现RU486干预后的创伤小鼠死亡率超过1/3,而模型组则未见死亡。结论内源性的糖皮质激素参与了创伤后髓源抑制细胞的扩增,也是内源性糖皮质激素发挥促炎症转归作用的机制之一。Objective To investigate if endogenous glucocorticoids play a role in the expansion of myeloid-derived suppressor cells (MDSCs) following trauma by blocking the glucocorticoid receptor. Methods After anesthesia, BALB/c mice treated or untreated with RU486 (mifepristone) were subjected to laparotomy to mimic traumatic condition. The percentage of CD11b ^+/Gr-1^+ MDSCs in the spleen, periph- eral blood and bone marrow was determined by flow cytometry or immunohistochemistry. Results RU486 not only blunted MDSCs expansion induced by trauma in the spleen [trauma: (6.222 ± 0.339)%, RU486: (3. 303 ± 0. 385)% ], peripheral blood [ trauma: (29. 108 ± 9. 814)%, RU486: ( 13. 160 ± 2. 554) % ] and bone marrow [ trauma: (24. 802 ± 5. 577 ) %, RU486 : ( 12. 920 ± 2. 114 ) % ] especially at 6 h after traumatic stress, but also resulted in decreased survival rate of 20% traumatic mice within 7 days. Conclusion Endogenous glucocorticoid may promote MDSCs expansion in a murine trauma model. This process may lead to the outcome of inflammation.
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