p38丝裂原活化蛋白激酶通路在电针减轻兔内毒素休克诱发急性肺损伤中的作用
p38사렬원활화단백격매통로재전침감경토내독소휴극유발급성폐손상중적작용
Role of p38 mitogen-activated protein kinase pathway in electro-acupuncture-induced reduction of endotoxic shock-induced acute lung injury in rabbits
  • 万方数据
    中华麻醉学杂志 중화마취학잡지
    CHINESE JOURNAL OF ANESTHESIOLOGY
    2013年 8期 989-992 ,共4页

    张桂诚%余剑波%宫丽荣%张圆%董树安%王曼%曹新顺%唐林

    장계성%여검파%궁려영%장원%동수안%왕만%조신순%당림

    电针%p38丝裂原活化蛋白激酶类%呼吸窘迫综合征,成人%休克,脓毒性 電針%p38絲裂原活化蛋白激酶類%呼吸窘迫綜閤徵,成人%休剋,膿毒性
    전침%p38사렬원활화단백격매류%호흡군박종합정,성인%휴극,농독성
    Electro acupuncture%p38Mitogen-activated protein kinases%Lung%Shock,septic
    目的 评价p38MAPK通路在电针减轻兔内毒素休克诱发急性肺损伤中的作用.方法 健康清洁级雄性新西兰大白兔70只,体重1.5 ～ 2.0kg,2月龄,采用随机数字表法,将其分为7组(n=10):正常对照组(C组)、无水乙醇组(A组)、p38MAPK特异性阻断剂SB203580组(SB组)、内毒素休克诱发急性肺损伤组(ALI组)、电针+ALI组(EA组)、假电针+ALI组(SEA组)、电针+ALI +SB组(EAS组).EA、EAS组于模型制备前1～4d及模型制备过程中电针双侧足三里和肺俞穴,参数设置:疏密波,频率2/100 Hz,波宽0.2 ～ 0.6 ms,刺激强度2～3 mA,以兔出现轻微肌颤为宜,1次/d,30min/次.SEA组以同样方法电针刺激足三里穴和肺俞穴旁开0.5 cm处.ALI组、EA组、SEA、EAS组采用静脉缓注射脂多糖5 mg/kg的方法制备内毒素性休克诱发急性肺损伤模型,C组、A组和SB组给予等容量生理盐水.模型制备成功后SB组、EAS组静脉输注SB203580 5 μmol/kg,输注速率0.05ml/min,C组给予等容量生理盐水,其余组给予等容量无水乙醇.静脉注射LPS或生理盐水后6h时,采集动脉血样,检测血清TNF-α和IL-10浓度；处死后取肺组织,观察病理学结果,并进行病理学评分,测定肺组织p38MAPK的磷酸化水平.结果 与C组比较,ALI组、SEA组、EA组和EAS组肺组织病理学评分、血清TNF-α、IL-10浓度升高,ALI组、SEA组、EA组肺组织p38MAPK磷酸化水平升高(P＜0.05),A组和SB组上述指标差异无统计学意义(P＞0.05)；与ALI组比较,EA组肺组织病理学评分和血清TNF-α浓度降低,血清IL-10浓度和肺组织p38MAPK磷酸化水平升高,EAS组肺组织病理学评分、血清TNF-α浓度和肺组织p38MAPK磷酸化水平降低(P＜0.05),SEA组上述指标差异无统计学意义(P＞0.05)；与EA组比较,EAS组肺组织病理学评分、血清TNF-α浓度升高,肺组织p38MAPK磷酸化水平降低(P＜0.05).结论 p38MAPK通路介导了电针减轻兔内毒素休克诱发急性肺损伤的作用.
    목적 평개p38MAPK통로재전침감경토내독소휴극유발급성폐손상중적작용.방법 건강청길급웅성신서란대백토70지,체중1.5 ～ 2.0kg,2월령,채용수궤수자표법,장기분위7조(n=10):정상대조조(C조)、무수을순조(A조)、p38MAPK특이성조단제SB203580조(SB조)、내독소휴극유발급성폐손상조(ALI조)、전침+ALI조(EA조)、가전침+ALI조(SEA조)、전침+ALI +SB조(EAS조).EA、EAS조우모형제비전1～4d급모형제비과정중전침쌍측족삼리화폐유혈,삼수설치:소밀파,빈솔2/100 Hz,파관0.2 ～ 0.6 ms,자격강도2～3 mA,이토출현경미기전위의,1차/d,30min/차.SEA조이동양방법전침자격족삼리혈화폐유혈방개0.5 cm처.ALI조、EA조、SEA、EAS조채용정맥완주사지다당5 mg/kg적방법제비내독소성휴극유발급성폐손상모형,C조、A조화SB조급여등용량생리염수.모형제비성공후SB조、EAS조정맥수주SB203580 5 μmol/kg,수주속솔0.05ml/min,C조급여등용량생리염수,기여조급여등용량무수을순.정맥주사LPS혹생리염수후6h시,채집동맥혈양,검측혈청TNF-α화IL-10농도；처사후취폐조직,관찰병이학결과,병진행병이학평분,측정폐조직p38MAPK적린산화수평.결과 여C조비교,ALI조、SEA조、EA조화EAS조폐조직병이학평분、혈청TNF-α、IL-10농도승고,ALI조、SEA조、EA조폐조직p38MAPK린산화수평승고(P＜0.05),A조화SB조상술지표차이무통계학의의(P＞0.05)；여ALI조비교,EA조폐조직병이학평분화혈청TNF-α농도강저,혈청IL-10농도화폐조직p38MAPK린산화수평승고,EAS조폐조직병이학평분、혈청TNF-α농도화폐조직p38MAPK린산화수평강저(P＜0.05),SEA조상술지표차이무통계학의의(P＞0.05)；여EA조비교,EAS조폐조직병이학평분、혈청TNF-α농도승고,폐조직p38MAPK린산화수평강저(P＜0.05).결론 p38MAPK통로개도료전침감경토내독소휴극유발급성폐손상적작용.
    Objective To evaluate the role of p38 mitogen-activated protein kinase (p38MAPK) pathway in electro-acupuncture (EA)-induced reduction of endotoxic shock-induced acute lung injury (ALI) in rabbits.Methods Seventy healthy male New Zealand white rabbits,aged 2 months,weighing 1.5-2.0kg,were randomly divided into 7 groups (n=10 each):normal control group (group C),anhydrous alcohol group (group A),specific p38MAPK blocker SB203580 group (group SB),endotoxic shock-induced ALI group (group ALI),EA + endotoxic shock-induced ALI group (group EA),sham EA + endotoxic shock-induced ALI group (group SEA),and EA + endotoxic shock-induced ALI + SB203580 group (group EAS).The animals were anesthetized with iv 20％ urethane 5ml/kg and tracheostomized and kept spontaneous breathing.Right common carotid artery was cannulated for mean arterial pressure monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg (in 2 ml of normal saline) was injected intravenously in groups ALI,EA,SEA,EAS,while the equal volume of normal saline was injected in the other groups.Endotoxic shock was confirmed by decrease in mean arterial pressure to 75％ of the baseline value within 2h after LPS injection.SB203580 5 μmol/kg (in 0.5ml of anhydrous alcohol) was then infused intravenously at 0.05ml/min in groups SB and EAS,while the equal volume of normal saline was infused in group C and the equal volume of anhydrous alcohol was given in the other groups.Bilateral 30 min EA (wave length 0.2-0.6 ms,frequency 2/100 Hz,intensity ≤ 2-3 mA) stimulation of Zusanli and Feishu was performed once a day for 4 days before establishment of endotoxic shock model and during the process of establishment of endotoxic shock model in EA and EAS groups.EA was performed at the points 0.5 cm lateral to the acupoints of Zusanli and Feishu according to the method previously described in group SEA.Arterial blood samples were taken at 6h after LPS or normal saline administration for detection of concentrations of serum tumor necrosis factor-α (TNF-α) and interleukin-10 (L-10).The rabbits were then sacrificed by exsanguination.The lungs were removed for microscopic examination and for measurement of phosphorylation of p38MAPK in lung tissues.The pathological changes of the lung were scored.Results Compared with group C,the pathological scores and serum TNF-α and L-10 concentrations were significantly increased in ALI,SEA,EA and EAS groups and phosphorylation of p38MAPK was increased in ALI,SEA and EA groups (P ＜ 0.05),and no significant changes were found in the parameters mentioned above in A and SB groups (P ＞ 0.05).Compared with group ALI,the pathological scores and serum TNF-α concentrations were significantly decreased and serum L-10 concentrations and phosphorylation of p38MAPK were increased in EA group,the pathological scores,serum TNF-α concentrations and phosphorylation of p38MAPK were decreased in EAS group (P ＜ 0.05),and no significant changes in the parameters mentioned above were found in SEA group (P ＞ 0.05).The pathological scores and serum TNF-α concentrations were significantly higher and phosphorylation of p38MAPK was lower in EAS group than in EA group (P ＜ 0.05).Conclusion p38MAPK pathway mediates EA-induced reduction of endotoxic shock-induced ALI in rabbits.文章序号>=10.3760/cma.j.issn.0254-1416.2013.08.022
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