微循环学杂志
微循環學雜誌
미순배학잡지
Chinese Journal of Microcirculation
2015年
4期
7-10
,共4页
脂多糖%脓毒血症%内皮细胞%凋亡%大鼠
脂多糖%膿毒血癥%內皮細胞%凋亡%大鼠
지다당%농독혈증%내피세포%조망%대서
Lipopolysaccharide (LPS)%Endotoximia%Vascular endothelial cell (VEC)%Apoptosis%Rat
目的：：观察细菌脂多糖(LPS)致脓毒血症大鼠血管内皮细胞(VEC)凋亡的器官靶向性及时相性特征。方法：70只 SD 大鼠经尾静脉一次性注射 LPS(10mg/kg)复制脓毒血症模型后平分为30min 组、1h 组、2h 组、4h组、8h 组、16h 组和24h 组。另选10只 SD 大鼠作为正常对照组。眼眶采血,ELISA 检测各组血清中血管性血友病因子(vWF)及炎性介质白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)的变化特征。断头处死对照组、1h 组、4h 组和8h 组大鼠,取肺、肝、心、脑、肾制作组织切片,采用地高辛标记凋亡细胞,免疫组化染色检测上述各组大鼠各脏器VEC 凋亡。结果：2h-24h 组 TNF-α浓度均较对照组升高,4h 组达峰值(P <0.01)；IL-1β在2h 组和4h 组显著高于对照组,2h 组为峰值(P <0.01),8h-24h 组与对照组无显著差异(P >0.05)。4h-8h 组大鼠血清 vWF 浓度较对照组升高,4h 组达峰值(P <0.05),其它时相组与对照组差异无统计学意义(P >0.05)。LPS 致脓毒血症大鼠肺、肝、心、脑、肾存在不同程度 VEC 凋亡现象,其中肺部受累较早。结论：LPS(10mg/ml)所致脓毒血症大鼠重要脏器可出现 VEC 凋亡,以肺部较早。
目的：：觀察細菌脂多糖(LPS)緻膿毒血癥大鼠血管內皮細胞(VEC)凋亡的器官靶嚮性及時相性特徵。方法：70隻 SD 大鼠經尾靜脈一次性註射 LPS(10mg/kg)複製膿毒血癥模型後平分為30min 組、1h 組、2h 組、4h組、8h 組、16h 組和24h 組。另選10隻 SD 大鼠作為正常對照組。眼眶採血,ELISA 檢測各組血清中血管性血友病因子(vWF)及炎性介質白介素-1β(IL-1β)、腫瘤壞死因子-α(TNF-α)的變化特徵。斷頭處死對照組、1h 組、4h 組和8h 組大鼠,取肺、肝、心、腦、腎製作組織切片,採用地高辛標記凋亡細胞,免疫組化染色檢測上述各組大鼠各髒器VEC 凋亡。結果：2h-24h 組 TNF-α濃度均較對照組升高,4h 組達峰值(P <0.01)；IL-1β在2h 組和4h 組顯著高于對照組,2h 組為峰值(P <0.01),8h-24h 組與對照組無顯著差異(P >0.05)。4h-8h 組大鼠血清 vWF 濃度較對照組升高,4h 組達峰值(P <0.05),其它時相組與對照組差異無統計學意義(P >0.05)。LPS 緻膿毒血癥大鼠肺、肝、心、腦、腎存在不同程度 VEC 凋亡現象,其中肺部受纍較早。結論：LPS(10mg/ml)所緻膿毒血癥大鼠重要髒器可齣現 VEC 凋亡,以肺部較早。
목적：：관찰세균지다당(LPS)치농독혈증대서혈관내피세포(VEC)조망적기관파향성급시상성특정。방법：70지 SD 대서경미정맥일차성주사 LPS(10mg/kg)복제농독혈증모형후평분위30min 조、1h 조、2h 조、4h조、8h 조、16h 조화24h 조。령선10지 SD 대서작위정상대조조。안광채혈,ELISA 검측각조혈청중혈관성혈우병인자(vWF)급염성개질백개소-1β(IL-1β)、종류배사인자-α(TNF-α)적변화특정。단두처사대조조、1h 조、4h 조화8h 조대서,취폐、간、심、뇌、신제작조직절편,채용지고신표기조망세포,면역조화염색검측상술각조대서각장기VEC 조망。결과：2h-24h 조 TNF-α농도균교대조조승고,4h 조체봉치(P <0.01)；IL-1β재2h 조화4h 조현저고우대조조,2h 조위봉치(P <0.01),8h-24h 조여대조조무현저차이(P >0.05)。4h-8h 조대서혈청 vWF 농도교대조조승고,4h 조체봉치(P <0.05),기타시상조여대조조차이무통계학의의(P >0.05)。LPS 치농독혈증대서폐、간、심、뇌、신존재불동정도 VEC 조망현상,기중폐부수루교조。결론：LPS(10mg/ml)소치농독혈증대서중요장기가출현 VEC 조망,이폐부교조。
Objective:To evaluate vascular endothelium cell (VEC)apoptosis and its characteristics in lipopo-lysaccharide (LPS)induced endotoxic model in rat.Method:LPS (10mg/kg)was administered in one bout via cau-dal vein in 70 rats and then divided randomly into LPS-administered after 30min,1h,2h,4h,8h,1 6h,and 24h group.Another 10 rats was adopted as control group.Blood was collected from orbit.The concentrations of von Willebrand factor (vWF)and interleukin 1β(IL-1β)and tumor necrosis factorα(TNF-α)were detected by ELISA. Rats were sacrificed by decaptitation.The tissue of heart,liver,brain,kidney,lung were collected and made tissue slice.VEC apoptosis of these organs was evaluated with immunohistochemisty staining labeled with digoxin dUTP after LPS was administered.Results:The concentration of TNF-αin serum increased in LPS-administered 2h-24h group compared with the control group,and peaked at 4h group (P <0.01).The concentration of IL-1βin serum al-so increased in LPS- administered 2h- 4h group,peaked at 2h group (P < 0.01 ),and there were no significant difference between 8h-24h and control group respectivly (P >0.05).The concentration of vWF in serum enhanced gradually after LPS in LPS-administered 2h-8h group,peaked at 4h group (P <0.05),decreased in 1 6h and 24h group compared with 4h group (P <0.05).The apoptosis of VEC from vital organ (lung,heart,brain,kidney and liver)occurred after LPS administered for 2-4h,and lung was the most early organ involved.Conclusion:VEC ap-optosis occurred in LPS (10mg/ml)induced endotoximia in rat,and lung is the much earlier organ involved.
