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丁 浩, 符永健, 郑丽蓉, 等.利多卡因对兔蛛网膜下腔出血后早期脑损伤的保护机制研究.四川大学学报(医学版),2017,48(2):230-233
利多卡因对兔蛛网膜下腔出血后早期脑损伤的保护机制研究
Neuroprotection Mechanism of Lidocaine in Rabbits with Early Brain Injury Resulted from Subarachnoid Hemorrhage
  
中文关键词:  【关键词】 利多卡因 蛛网膜下腔出血 早期脑损伤 线粒体通路
英文关键词:【Key words】 Lidocaine Subarachnoid hemorrhage Early brain injury Mitochondrial pathway
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中文摘要:
      【摘要】 目的 探讨利多卡因对兔蛛网膜下腔出血(SAH)后早期脑损伤的保护机制。方法 18只新西兰大白兔随机分为3组:假手术(Sham)组、蛛网膜下腔出血(SAH)组、利多卡因(LD)组。各组动物均在麻醉下行手术操作,SAH组和LD组动物取自体动脉血1 mL/kg(按体质量计)注入枕大池,Sham组注入等量生理盐水;30 min后LD组兔经静脉注入20 mg/mL利多卡因0.6 mL,SAH组、Sham组注入等量生理盐水。72 h后进行摄食量和神经功能损害分级,采用实时荧光定量PCR(RT-PCR)及Western blot技术检测兔脑海马组织中半胱氨酸天冬氨酸蛋白酶3(Caspase-3)、细胞色素C(Cyt-c )mRNA及蛋白的表达。结果 与Sham组比较,SAH、LD组兔摄食量减少,出现不同程度的神经功能损害,脑海马组织中Caspase-3、Cyt-c mRNA及蛋白表达增加(P <0.05);与SAH组比较,LD组兔摄食量及神经功能损害差异无统计学意义(P >0.05),脑海马组织中Caspase-3、Cyt-c mRNA及蛋白表达减少(P <0.05)。结论 利多卡因对兔SAH后早期脑损伤的保护机制可能与下调脑组织Caspase-3、Cyt-c mRNA及蛋白表达,抑制线粒体通路有关。
英文摘要:
      【Abstract】 Objective To determine the neuroprotection mechanism of lidocaine on early brain injury resulted from subarachnoid hemorrhage. Methods Eighteen New Zealand white rabbits were randomly divided into three groups: Sham group, subarachnoid hemorrhage (SAH) group and lidocaine treatment (LD) group. Operations were performed on all animals under anesthesia. Autologous nonheparinized arterial blood (1 mL/kg,body mass) was injected into cisterna magna of rabbits in the SAH and LD groups, while saline (1 mL/kg,body mass) was given to rabbits in the sham group. Thirty minutes later, intravenous injection of 0.6 mL 20 mg/mL lidocaine was given to those in the LD group, and intravenous injection of 0.6 mL saline was given to those in the Sham and SAH groups. Food intake and neurological impairments of the rabbits were assessed 72 h after the induction of SAH. The protein and mRNA experssions of Caspase-3 and cytochrome-c (Cyt-c) in hippocampus tissues were detected using real-time PCR (RT-PCR) and Western blot. Results Rabbits in the SAH and LD groups had lower food intake and higher mRNA and protein expressions of Caspase-3 and Cyt-c than those in the sham groups, which was accompanied with varying degrees of neurological impairments. No significant differences in food intake and neurological impairments were found between the SAH and LD groups (P >0.05). However, rabbits in the LD group had lower levels of mRNA and protein expressions of Caspase-3 and Cyt-c than those in the SAH group (P <0.05). Conclusion The neuroprotection mechanism of lidocaine on early brain injury in rabbits with subarachnoid hemorrhage may be associated with inhibition of mitochondrial pathway and downregulated mRNA and protein expressions of Caspase-3 and Cyt-c in brain tissues.
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