急性肺损伤中性粒细胞凋亡异常及甲基强的松龙调控的研究  被引量:3

Abnormality of PMN apoptosis and effect of methylprednisolone in acute lung injury induced by administrating oleic acid

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作  者:韩守信[1] 陈复辉[1] 周丹[1] 吴晓梅[1] 

机构地区:[1]哈尔滨医科大学附属第二医院呼吸内科,黑龙江哈尔滨150086

出  处:《中国现代医学杂志》2007年第2期169-171,共3页China Journal of Modern Medicine

基  金:黑龙江省自然科学基金项目编号:D0313

摘  要:目的探讨急性肺损伤时支气管肺泡灌洗液(BALF)中的中性粒细胞(PMN)凋亡发生规律及甲基强地松龙调控关系。方法豚鼠30只,分为3组:1组生理盐水正常对照组,2组油酸致病组,3组油酸+甲基强的松龙组。组2、组3分别由尾静脉注射油酸(0.12mL/kg)造成豚鼠急性肺损伤模型。组1则注入生理盐水。油酸+甲基强的松龙组在实验造模前2d由腹腔注射甲基强地松龙0.10mg/kg体质量,1次/d。组1、组2、组3分别于注射后2h用生理盐水进行全肺支气管肺灌洗,收集BALF。用梯度密度法离心收集PMN。用原位末端标记法检测BALF中PMN凋亡。结果油酸致病组、油酸+甲基强的松龙组和正常对照组BALF中PMN凋亡百分比分别是:(2.500±1.080)%、(4.200±1.033)%和(6.400±1.505)%。油酸致病组、油酸+甲强龙组较正常对照组BALF中PMN凋亡均显著降低(均P<0.01)。结论急性肺损伤炎性细胞PMN凋亡延迟,PMN持续激活和释放毒性内容物与肺损伤有密切关系。甲基强地松龙能调控干预急性肺损伤时PMN凋亡延迟。[Objective] To investigate the law of apoptosis of PMN and effect of methylprednisolone in acute lung injury induced by administrating oleic acid. [Methods] 30 guinea pigs were randomly distributed into control group, OA group, OA+MPL group. OA group and OA+MPL group both had intraveneos injection of oleic acid (0.12 ml/kg) to make acute lung injury. OA+MPL group had methyprednisolone (MPL) 0.10 mg/kg injection by abdominal once a day for 2 days before. Control group had injection of normal saline. All the 3 groups had taken BALF 2 hours later. PMNs were isolated by density gradient centrifugation. PMN apoptosis were detecded by Terminal deoxynueleotidy transferase-mediated dUTP biotin nick end labeling (TUNEL). [Results] PMN apoptosis of BALFs of OA group, OA+MPN group and control group were: (2.500±1.080)%, (4.200±1.033)% and (6.400±1.505)%. The level of PMN apoptosis of BALF of OA group compared with OA+MPN group and control group were decreased markedly (both P 〈0.01). [Conclusion] The apoptosis of PMN in acute lung injury were delayed. Methyprednisolone could reverse the level of apoptosis of PMN in acute lung injury.

关 键 词:急性肺损伤 中性粒细胞 凋亡 甲基强地松龙 

分 类 号:R563[医药卫生—呼吸系统]

 

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