CAJ | 학술논문

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30 min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)％、骨髓中分别为(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.
목적 통과조단내원성당피질격소수체관찰기재창상응격시시부삼여료수원억제세포적확증.방법 장BALB/c소서분위량조,일조건립복부창상모형,령일조우건모전30 min급여당피질격소수체조체제RU486복강주사,관찰7d량조소서적생존정황.이류식세포술화면역조직화학검측비장、외주혈화골수중CD11b +/Gr-1+수원억제세포적비례.결과 RU486능구강저창상후수원억제세포적대량확증,이창상모형건립후6h최위명현,모형조화RU486간예조수원억제세포비례재비장중분별위(6.222±0.339)％화(3.303±0.385)％、재외주혈분별위(29.108±9.814)％화(13.160±2.554)％、골수중분별위(24.802±5.577)％화(12.920 ±2.114)％.동시,생존실험발현RU486간예후적창상소서사망솔초과1/3,이모형조칙미견사망.결론 내원성적당피질격소삼여료창상후수원억제세포적확증,야시내원성당피질격소발휘촉염증전귀작용적궤제지일.
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 CD1 l b +/Gr-1 + MDSCs in the spleen,peripheral 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.