山西医科大学学报
山西醫科大學學報
산서의과대학학보
Journal of Shanxi Medical University
2015年
10期
968-972
,共5页
刘敏龙%张小玲%王国恩%骆艳妮%强雷%张军
劉敏龍%張小玲%王國恩%駱豔妮%彊雷%張軍
류민룡%장소령%왕국은%락염니%강뢰%장군
脓毒症%程序性细胞死亡配体-1%脾脏%肾脏%心脏%内毒素
膿毒癥%程序性細胞死亡配體-1%脾髒%腎髒%心髒%內毒素
농독증%정서성세포사망배체-1%비장%신장%심장%내독소
sepsis%programmed death-1 ligand%spleen%kidney%heart%endotoxin
目的 观察脓毒症小鼠脾脏、心脏和肾脏组织程序性细胞死亡配体-1(programmed cell death ligand-1,PD-L1)表达变化. 方法 40只C57BL/6小鼠随机分为脓毒症模型组及假手术组,每组20只. 采用盲肠结扎穿孔法造模,造模成功后两组小鼠分别在24 h(n=10),48 h(n=10)时间点处死. 取脾脏、心脏和肾脏组织用免疫组化法检测各组织PD-L1表达;用流式细胞仪检测各组外周血单核细胞PD-L1表达;收集腹水用酶联免疫吸附法检测腹水内毒素水平. 结果 模型组24 h和48 h脾脏、肾脏PD-L1表达明显增高,与假手术组比较差异有统计学意义(P<0. 05);各组心肌细胞未见PD-L1表达. 模型组脾脏PD-L1阳性细胞出现在红髓和脾小体,肾脏阳性细胞是肾小管上皮细胞. 模型组24 h和48 h单核细胞PD-L1的表达均较假手术组升高(P<0. 01).模型组腹水内毒素水平均较假手术组高(P<0. 01). 结论 脓毒症小鼠脾脏和肾脏PD-L1表达升高,PD-L1可能参与脓毒症发生发展.
目的 觀察膿毒癥小鼠脾髒、心髒和腎髒組織程序性細胞死亡配體-1(programmed cell death ligand-1,PD-L1)錶達變化. 方法 40隻C57BL/6小鼠隨機分為膿毒癥模型組及假手術組,每組20隻. 採用盲腸結扎穿孔法造模,造模成功後兩組小鼠分彆在24 h(n=10),48 h(n=10)時間點處死. 取脾髒、心髒和腎髒組織用免疫組化法檢測各組織PD-L1錶達;用流式細胞儀檢測各組外週血單覈細胞PD-L1錶達;收集腹水用酶聯免疫吸附法檢測腹水內毒素水平. 結果 模型組24 h和48 h脾髒、腎髒PD-L1錶達明顯增高,與假手術組比較差異有統計學意義(P<0. 05);各組心肌細胞未見PD-L1錶達. 模型組脾髒PD-L1暘性細胞齣現在紅髓和脾小體,腎髒暘性細胞是腎小管上皮細胞. 模型組24 h和48 h單覈細胞PD-L1的錶達均較假手術組升高(P<0. 01).模型組腹水內毒素水平均較假手術組高(P<0. 01). 結論 膿毒癥小鼠脾髒和腎髒PD-L1錶達升高,PD-L1可能參與膿毒癥髮生髮展.
목적 관찰농독증소서비장、심장화신장조직정서성세포사망배체-1(programmed cell death ligand-1,PD-L1)표체변화. 방법 40지C57BL/6소서수궤분위농독증모형조급가수술조,매조20지. 채용맹장결찰천공법조모,조모성공후량조소서분별재24 h(n=10),48 h(n=10)시간점처사. 취비장、심장화신장조직용면역조화법검측각조직PD-L1표체;용류식세포의검측각조외주혈단핵세포PD-L1표체;수집복수용매련면역흡부법검측복수내독소수평. 결과 모형조24 h화48 h비장、신장PD-L1표체명현증고,여가수술조비교차이유통계학의의(P<0. 05);각조심기세포미견PD-L1표체. 모형조비장PD-L1양성세포출현재홍수화비소체,신장양성세포시신소관상피세포. 모형조24 h화48 h단핵세포PD-L1적표체균교가수술조승고(P<0. 01).모형조복수내독소수평균교가수술조고(P<0. 01). 결론 농독증소서비장화신장PD-L1표체승고,PD-L1가능삼여농독증발생발전.
Objective To explore the changes of PD-L1 expression in the spleen, kidney and heart of septic mice. Methods Forty C57 mice were randomly divided into:sepsis model group and sham group( n=20 in each group) . Sepsis model was induced by cecal ligation and puncture. The mice were sacrificed at 24 h(n=10) and 48 h(n=10) in two groups, respectively. Spleen, kidney and heart at 24 h and 48 h were obtained to detect the PD-L1 expression by immunohistochemistry. Peripheral blood samples at 24 h and 48 h were taken to detect the PD-L1 expression in monocytes by flow cytometry. Ascites at 24 h and 48 h were collected to detect the en-dotoxin level by enzyme-linked immunosorbent assay. Results Compared with sham group, PD-L1 expression in the spleen and kid-ney was increased at 24 h and 48 h in sepsis model group(P<0. 05). PD-L1 expression was not observed in the heart in sepsis model group and sham group. Positive cells of PD-L1 expression were found in the red pulp, splenic corpuscle and renal tubules in sepsis model group. Compared with sham group, PD-L1 expression in the monocytes was increased in sepsis model group(P<0. 01), and the endotoxin level in ascites was also increased(P<0. 01). Conclusion PD-L1 expression is increased in spleen and kidney of sep-sis mice. Increased PD-L1 expression may be involved in the development of sepsis.