临床儿科杂志
臨床兒科雜誌
림상인과잡지
2010年
1期
30-33
,共4页
肺损伤%吡咯烷二硫代氨基甲酸盐%孤儿核受体%核因子-κB%IL-17
肺損傷%吡咯烷二硫代氨基甲痠鹽%孤兒覈受體%覈因子-κB%IL-17
폐손상%필각완이류대안기갑산염%고인핵수체%핵인자-κB%IL-17
lung injury%pyrrolidine dithiocarbamates%RORC%NF-кB%IL-17
目的 观察脓毒症肺损伤大鼠孤儿核受体RORC基因表达及血清IL-17水平,探讨Th17细胞在肺损伤中的作用及可能的调控机制.方法 24只SD雄性大鼠随机分为对照组、模型组,吡咯烷二硫代氨基甲酸盐(pyrrolidine dithiocarbamates,PDTC)预防组.静脉注射脂多糖(LPS,6 mg/kg)复制急性肺损伤(ALI)的动物模型,在注射后12h处死.PDTC预防组在注射LPS前30 min予以PDTC(120 mg/kg)腹腔注射.测定肺湿/干重比(W/D),石蜡包埋切片经苏木素-伊红(HE)染色行肺组织病理评分,免疫组织化学法检测肺泡巨噬细胞(alveolar macrophages,AM)核因子-KBP65(nuclear factor-κBP65,NF-κBP65)表达,EUSA法检测血清IL-17水平,实时荧光定量PCR法检测AM孤儿核受体RORC基因表达.结果与对照组相比,模型组肺干/湿比、肺组织病理评分、AM的NF-κBP65表达、血清IL-17水平、AM孤儿核受体RORC基因表达增加(P<0.05);与模型组相比,PDTC预防组上述改变得以逆转.结论 Th17细胞可能参与了肺损伤的病理过程.NF-κB活化可影响RORC基因表达,诱导,Th17分化,使血清IL-17水平升高.
目的 觀察膿毒癥肺損傷大鼠孤兒覈受體RORC基因錶達及血清IL-17水平,探討Th17細胞在肺損傷中的作用及可能的調控機製.方法 24隻SD雄性大鼠隨機分為對照組、模型組,吡咯烷二硫代氨基甲痠鹽(pyrrolidine dithiocarbamates,PDTC)預防組.靜脈註射脂多糖(LPS,6 mg/kg)複製急性肺損傷(ALI)的動物模型,在註射後12h處死.PDTC預防組在註射LPS前30 min予以PDTC(120 mg/kg)腹腔註射.測定肺濕/榦重比(W/D),石蠟包埋切片經囌木素-伊紅(HE)染色行肺組織病理評分,免疫組織化學法檢測肺泡巨噬細胞(alveolar macrophages,AM)覈因子-KBP65(nuclear factor-κBP65,NF-κBP65)錶達,EUSA法檢測血清IL-17水平,實時熒光定量PCR法檢測AM孤兒覈受體RORC基因錶達.結果與對照組相比,模型組肺榦/濕比、肺組織病理評分、AM的NF-κBP65錶達、血清IL-17水平、AM孤兒覈受體RORC基因錶達增加(P<0.05);與模型組相比,PDTC預防組上述改變得以逆轉.結論 Th17細胞可能參與瞭肺損傷的病理過程.NF-κB活化可影響RORC基因錶達,誘導,Th17分化,使血清IL-17水平升高.
목적 관찰농독증폐손상대서고인핵수체RORC기인표체급혈청IL-17수평,탐토Th17세포재폐손상중적작용급가능적조공궤제.방법 24지SD웅성대서수궤분위대조조、모형조,필각완이류대안기갑산염(pyrrolidine dithiocarbamates,PDTC)예방조.정맥주사지다당(LPS,6 mg/kg)복제급성폐손상(ALI)적동물모형,재주사후12h처사.PDTC예방조재주사LPS전30 min여이PDTC(120 mg/kg)복강주사.측정폐습/간중비(W/D),석사포매절편경소목소-이홍(HE)염색행폐조직병리평분,면역조직화학법검측폐포거서세포(alveolar macrophages,AM)핵인자-KBP65(nuclear factor-κBP65,NF-κBP65)표체,EUSA법검측혈청IL-17수평,실시형광정량PCR법검측AM고인핵수체RORC기인표체.결과여대조조상비,모형조폐간/습비、폐조직병리평분、AM적NF-κBP65표체、혈청IL-17수평、AM고인핵수체RORC기인표체증가(P<0.05);여모형조상비,PDTC예방조상술개변득이역전.결론 Th17세포가능삼여료폐손상적병리과정.NF-κB활화가영향RORC기인표체,유도,Th17분화,사혈청IL-17수평승고.
Objective To detect the expression of orphan nuclear receptor RORC gene and the level of serum interleukin-17 in acute lung injury (ALI) rats, and to explore the effects and possible regulation mechanisms of helper T lymphocyte 17 (Th17) in the ALI.Methods Twenty four SD male rats were randomly assigned to three groups, control group, model group, and pyrrolidine dithiocarbamates (PDTC) prevention group.The rats in model group and PDTC prevention group were intravenously injected LPS (6 mg/kg) for inducing ALI.The PDTC prevention group had been intraperitoneally injected PDTC (120 mg/kg) thirty minutes before LPS injection.All rats were killed twelve hours after LPS injecttion.The lung wet/dry weight ratio was measured.Lung pathologic tissue scored after hematoxylin-eosin (HE) stain.The expression of alveolar macrophages (AM) nuclear factor-KBP65 (NF-κBP65) was detected by immunohistochemistry.The level of serum IL-17 was detected by ELISA method.The expression of AM orphan nuclear receptor RORC gene was determined by SYBR Green Ⅰ real-time polymerase chain reaction.Results Compared with control group.the lung wet/dry weight ratio.lung pathologic tissue score, the expression of AM NF-κBP65.the level of serum IL-17 and the expression of AM orphan nuclear receptor RORC gene were significantly increased (P < 0.05).However, compared with model group, these changes were prevented in PDTC prevention group.Conclusions Th17 might participate in the pathological process of ALI.Activation of NF-кB might influence RORC gene expression, induce Th17 differentiation, and elevate the level of serum IL-17.
