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白细胞介素-6和髓鞘碱性蛋白在急性一氧化碳中毒迟发性脑病中的作用 被引量:6

Study on the correlation between IL-6, MBP and delayed encephalopathy after acute carbon monoxide poisoning
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摘要 目的本研究通过制备急性一氧化碳中毒迟发性脑病(DEACMP)动物模型,探讨白细胞介素-6(IL-6)和髓鞘碱性蛋白(MBP)在DEACMP中的作用。方法Wistar雄性健康成年大鼠78只,随机分为对照组(BC组=6只)和实验组(实验组=72只)。实验组通过腹腔注射一氧化碳(CO)制造DEACMP动物模型,并按中毒时间(1h、3h、5h、7h、9h、11h、19h、24h、3d、5d、7d、14d)分为12个亚组,分别命名为1h组、3h组、5h组、7h组、9h组、11h组、19h组、24h组、3d组、5d组、7d组、14d组。通过Morris水迷宫实验评估认知功能,应用苏木精-伊红染色法观察大脑海马区的病理变化,采用ELISA方法测定大鼠血清中IL-6及MBP浓度的变化。结果①中毒大鼠呈现典型急性CO中毒表现;②Morris水迷宫实验结果:与BC组相比较,3d组、5d组以及7d组大鼠的平均逃避潜伏期差异无统计学意义(P>0.05),14d组大鼠的平均逃避潜伏期明显延长(P<0.05);③苏木精-伊红染色结果:BC组、3d组、5d组以及7d组大鼠海马区脑组织切片可见细胞大小、形态正常,核膜完整,核仁清晰,胞核呈淡蓝色;14d组大鼠海马区出现大量变性和坏死的神经元,以及神经元结构的紊乱,细胞间隙扩大,胞体缩小,染色质浓缩甚至碎裂,细胞核固缩深染、结构不清;④ELISA结果:IL-6在中毒后5h开始升高,7h达高峰,11h后恢复至正常,7h组、9h组与BC组相比较差异有统计学意义(P<0.05);MBP在中毒后1h开始升高,9h恢复到正常,5d^14d再次升高,1h组、3h组、5h组、7h组、5d组、7d组及14d组与BC组相比较有统计学意义(P<0.05)。结论中毒后7~9h血清中升高的IL-6及中毒后1~7h和5~14d血清中升高的MBP可能对于DEACMP具有早期诊断价值。 Objective In this study,an animal model of delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)was established to investigate the role of interleukin-6(IL-6)and myelin basic protein(MBP)in early diagnosis of DEACMP.Methods 78 healthy male Wistar rats were randomly divided into control group(group BC)of 6 rats,experimental group of 72 rats.In the experimental group,The rats were intraperitoneally injected with CO(150 ml·kg^-1)to establish an animal model of DEACMP.The experimental group was divided into 12 subgroups according to the poisoning time(3 h,5 h,7 h,11 h,19 h,24 h,3 d,5 d,7 d,14 d),which were named 3 h group,5 h group,7 h group,9 h group,11 h group,19 h group,24 h group,3 d group,5 dgroup,7 dgroup,14 d group.Morris water maze experiment was used to observe the cognitive function of rats’memory and orientation.HE staining was used to observe the pathological changes of hippocampus in rats.ELISA method was used to determine the concentration of IL-6 and MBP in rat serum.Results①The establishment of DEACMP animal model:5-15 min after poisoning,the rats in experience group gradually appeared irritability,hyperactivity,mild behavior;after poisoning 20 min,rats began to appear less limp,antifeedant,shortness of breath,acral skin showing cherry red fur,fur standing up,slow action,incontinence,and even coma;②Positioning navigation experiment(spatial learning ability):7 d group after poisoning compared with BC group,the average escape latency difference was not statistically significant(P<0.05);14 d group after poisoning compared with the BC group,the average escape latency was longer than the control group,the difference was statistically significant(P<0.05);③HE staining results:the brain tissue sections of hippocampus of rats in the BC group showed normal morphology,cell size,nuclear membrane integrity,clear nucleolus,the nuclei showing pale blue;after 7 d,the cells in hippocampus showed a lot of degeneration and necrosis,and neuronal structure disorder.The intercellular space was enlar
作者 项文平 王宝军 薛慧 陈超 庞江霞 张军 王静波 王洁 牛翻燕 Xiang Wenping;Wang Baojun;Xue Hui;Chen Chao;Pang Jiangxia;Zhang Jun;Wang Jingbo;Wang Jie;Niu Fanyan(Department of Neurology,the Baotou Central Hospital,Nei Mongol 014040,China)
出处 《脑与神经疾病杂志》 2020年第11期697-702,共6页 Journal of Brain and Nervous Diseases
基金 国家自然科学基金项目资助(81860210) 内蒙古人才开发基金项目资助
关键词 急性一氧化碳中毒迟发性脑病 白细胞介素-6 髓鞘碱性蛋白 疾病模型 Delayed encephalopathy after acute carbon monoxide poisoning Interleukin-6 Myelin basic protein Animal model
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  • 1Atalay H, Aybek H, Koseoqlu M, et al. The effects of anli- fostine and dexamethasone on brain tissue lipid peroxidation during oxygen treatment of carbon monoxide-poisoned rats. Adv Ther, 2006, 23 : 332-341. 被引量:1
  • 2Thom SR, Bhopale VM, Fisher D, et al. Delayed neuropa- thology after carbon monoxide poisoning is Immune-mediated. Proc Nat Acad Sci USA, 2004, 101 : 13660-13665. 被引量:1
  • 3Stephenson D, Yin T, Smalstig EB, et al. Transcription fac- tor nuclear factor-kappa B is activated in neurons after focal cerebral ischemia. J Cereb Blood Flow Metab, 2000, 20: 592-603. 被引量:1
  • 4Thorn SR, Bhopale VM, Han S T, et al. Intravascular neu- trophil activation due to carbon monoxide poisoning. Am J Re- spir Crit Care Med, 2006, 174: 1239-1248. 被引量:1
  • 5Han ST, Bhopale VM, Thom SR. Xanthine oxidoreductase and neurological sequelae of carbon monoxide poisoning. Toxi- col Lett, 2007, 170: 111-115. 被引量:1
  • 6Shprecher D, Mehta L. The syndrome of delayed post-hy- poxic leukoencephalopathy. NeuroRehabilitation, 2010, 26 : 65 -72. 被引量:1
  • 7Thorn SR, Bhopale VM, Fisher D. Hyperbaric oxygen re- duces delayed immune-mediated neuropathology in experimen- tal carbon monoxide toxicity. Toxicol Appl Pharmaco 1, 2006, 213(2) : 152-159. 被引量:1
  • 8Cobb JP, Hotchkiss RS, Karl E, et al. Mechanisms of cell injury and death. Br J Anaesth, 1996, 77: 3-10. 被引量:1
  • 9Omaye ST. Metabolic modulation of carbon monoxide toxicity. Toxicology, 2002, 180: 139-150. 被引量:1
  • 10Rocksen D, Lillichook B, Larsson R, et al. Differential an- ti-inflammatory and anti-oxidative effects of dexamethasone and N- acetylcysteine in endotoxin- induced lung inflammation. Clin Exp Immunol, 2000, 122: 249-256. 被引量:1

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