电针刺激足三里和肺俞穴对兔内毒素休克诱发急性肺损伤的影响

Effects of electro-acupuncture at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits

目的评价电针刺激足三里和肺俞穴对兔内毒素休克诱发急性肺损伤的影响。方法健康雄性新西兰大白兔60只，体重1．5～2．0kg，2月龄，采用随机数字表法，将其随机分为6组（n=10）：假手术组（S组）、血红素加氧酶-1（HO-1）抑制剂锌原卟啉-Ⅸ组（z组）、内毒素组（L组）、电针刺激穴位＋内毒素组（EL组）、电针刺激非穴位＋内毒素组（SEL组）、电针刺激穴位＋锌原卟啉-Ⅸ＋内毒素组（ELZ组）。EL组和ELZ组电针刺激双侧足三里和肺俞穴，疏密波，频率15Hz，刺激强度以兔出现轻微肌颤为宜，1次，d，15rain／次，连续5d；SEL组刺激足三里和肺俞穴旁开0．5cm处。停止电针刺激后24h，L组、EL组、SEL组和ELZ组静脉注射脂多糖5mg／kg，S组和Z组给予等容量生理盐水0．5ml。Z组和ELZ组给予脂多糖后2h腹腔注射锌原卟啉-Ⅸ10btmol／kg，其他4组给予等容量NaHCO，1ml。注射脂多糖后6h时处死兔，取肺组织，进行肺损伤评分，测定肺泡上皮细胞凋亡指数、HO-1和HO-1mRNA表达。结果与S组比较，Z组肺损伤评分、肺泡上皮细胞凋亡指数、HO-1和HO-1mRNA表达差异无统计学意义（P〉0．05），其他4组肺损伤评分和肺泡上皮细胞凋亡指数升高，HO-1和HO-1mRNA表达上调（P〈0．01）；与L组比较，EL组肺损伤评分和肺泡上皮细胞凋亡指数降低，HO-1和HO-1mRNA表达上调（P〈0．01），其他2组上述指标差异无统计学意义（P〉0．05）；与EL组比较，ELZ组肺损伤评分和肺泡上皮细胞凋亡指数升高，HO-1和HO-1mRNA表达下调（P〈0．01）。结论电针刺激足三里和肺俞穴可减轻兔内毒素休克诱发急性肺损伤，其机制与上调肺组织HO-1表达，抑制肺泡上皮细胞凋亡有关。

Objective To evaluate the effect of electro-acupuncture （EA） at Zusanli and Feishu on endo- toxin shock-induced acute lung injury in rabbits. Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups （ n = 10 each） ： group sham operation （group S）; group zinc protoporphyrin-IX （ZnPP-IX） （group Z）; group lipopolysaecharide （LPS） （group L）; group LPS ＋ EA （group EL） ; group LPS＋ sham EA （group SEL） and group LPS＋ EA＋ ZnPP-IX （group ELZ）. The animals were anesthetized with intraperitoneal 10% chloral hydrate 400 mg/kg and tracheostomized. The animals kept spontaneous breathing. Right internal carotid artery was cannulated for BP monitoring. Ear vein was cannulated for drug administration. LPS 5 mg/kg was injected iv in groups L, EL, SEL, ELZ. Endotoxin shock was confirmed by decrease in BP by 20 % of the baseline value and PaO2/FiO2 ≤ 300. ZnPP-IX （heme oxygenase （HO-1 ） inhibitor） 10 μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ. Bilateral 15 min EA stimu- lation of Zusanli and Feishu （according to atlas of animal acu-points） was performed once a day for 5 days before LPS administration in groups EL and ELZ. The animals were sacrificed by blood-letting at 6 h after LPS administra- tion. The lungs were removed for microscopic examination （0 = no injury, 4 = most severe injury）, detection of al- veolar epithelial cell apoptosis （by TUNEL） and determination of HO-1 protein and mRNA expression. Results LPS significantly increased lung injury scores, alveolar epithelial cell apoptosis index （the number of apoptotic cells/total cells） and HO-1 protein and mRNA expression. EA significantly attenuated lung injury and alveolar epi- thelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L. The protective effects of EA was counteracted by ZnPP- lX in group ELZ. Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.