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升糖速度对低血糖大鼠脑损伤影响机制初探 被引量:8

Influence of different glucose rising speed on hypoglycemic brain injury in rats
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摘要 目的 研究及探讨不同升糖速度对低血糖性大鼠脑损伤影响的机制.方法 采用健康SD雄性大鼠36只,体重250~ 300 g,采用简单随机抽样分组的方式将其分为6组:空白组、假手术组和4个实验组,每组6只大鼠.空白组不作任何处理,假手术组胰岛素腹腔注射的同时静脉泵注葡萄糖并维持正常血糖,4组实验组在胰岛素诱导的低血糖后按照不同的泵注速度进行升糖,根据1h后血糖的不同水平分为> 1.0 ~ 3.0 mmoL/L组、>3.0 ~6.0 mmoL/L组、>6.0 ~9.0 mmol/L组和>9.0 mmol/L组.采用Western blotting法检测不同组之间抗凋亡基因Bax及Bcl-2蛋白在大脑皮层及海马神经细胞上表达,采用流式细胞仪检测不同组之间大脑海马及皮层神经细胞内Ca^2+的浓度.各组间计量资料比较采用单因素方差分析.结果 Bax/Bcl-2比值:相对于空白组,假手术组、4个实验组大脑皮层及海马的Bax/Bcl-2比值有显著性的提高,差异有统计学意义(F=265.8、42.7,均P<0.05),其中>9.0 mmol/L组Bax/Bcl-2最大,>1.0~3.0 mmol/L组次之,与>3.0~ 6.0 mmol/L组、>6.0 ~9.0 mmol/L组之间差异有统计学意义(F=212.1、27.4,均P<0.05).钙离子浓度:相对于空白组,假手术组和4个实验组的钙离子浓度显著性的提高,差异有统计学意义(F=79.8、355.0,均P<0.05),其中>9.0 mmol/L组钙离子浓度最大,>1.0~ 3.0 mmol/L组次之,与3.0 ~6.0 mmol/L组、>6.0 ~ 9.0 mmol/L组之间差异有统计学意义(F=50.1、71.1,均P<0.05).结论 过慢、过快的升糖速度都不利于低血糖性脑损伤的恢复. Objective To explore the mechanism of the effect of different glucose rising speed on hypoglycemic brain injury in rats.Methods A total of 36 male SD rats (weight:250-300 g) were divided into 6 groups with simple random sample:the blank group,sham group and 4 experimental groups,6 rats in each group.The blank group was subjected to no disposal,the sham group was given femoral vein infusion of glucose and intraperitoneal injection of insulin to maintain normal blood glucose.The experimental groups were given femoral vein infusion of glucose with different speed after hypoglycemia induced by insulin injection.According to the glucose concentration after 1 hour of vein glucose infusion,the experimental groups were further divided into 4 groups (〉 1.0-3.0,〉3.0-6.0,〉6.0-9.0 and 〉9.0 mmol/L group).Western blotting was used to detect the protein expression levels of gene Bax and Bcl-2.Flow cytometry was used to detect the Ca2+ concentration in the neurocyte in hippocampus and cerebral cortex of the different groups.Comparison of measurement data among groups was done by using one-way analysis of variance.Results Ratio of Bax to Bcl-2:compared with those in blank group and sham group,Bax/Bcl-2 in cerebral cortex and hippocampus in 4 experimental groups increased significantly (F =265.8,42.7,both P〈0.05),〉9.0 mmol/L group had the highest Bax/Bcl-2,〉 1.0-3.0 mmol/L group had the second highest.There was significant differences in Bax/Bcl-2 among the 4 experimental groups (F =212.1,27.4,both P 〈 0.05).Ca^2+ concentration:compared with those in the blank group and sham group,the Ca^2+ concentration in cerebral cortex and hippocampus in 4 experimental groups increased significantly (F =79.8,355.0,both P 〈0.05).〉9.0 mmol/L group had the highest and 〉 1.0-3.0 mmol/L group had the second highest level of Ca^2 + concentration.There was significant differences in Ca^2 + concentration among the 4 experimental groups (F =50.1,71.1,both P 〈 0.05).Conclusion Both too fast and too slow glucose rising speed will aggravate the hypoglycemic brain injury.
出处 《中华糖尿病杂志》 CAS CSCD 2014年第5期317-320,共4页 CHINESE JOURNAL OF DIABETES MELLITUS
关键词 低血糖 升糖速度 脑损伤 Hypoglycemia Speed of blood glucose rising Brain injury
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参考文献12

  • 1Derakhshan F, Toth C. Insulin and the brain[ J]. Curr Diabetes Rev, 2073, 9:102-116.
  • 2郭立新.低血糖与葡萄糖再灌注脑损伤[J].中华糖尿病杂志,2012,4(3):136-138. 被引量:2
  • 3Suh SM, Hamby AM, Swanson RA. Hypoglycemia, brain energetic, and hypoglycemic neuro death [ J ]. Glia, 2007,55:1280-1286.
  • 4中华医学会糖尿病学分会.中国2型糖尿病防治指南(2010年版)[J].中华糖尿病杂志,2010,2增刊2:1-56.
  • 5Kamenov ZA, Traykov LD. Diabetic autonomic neuropathy [ J].Ady Exp Med Biol, 2012, 771:176-193.
  • 6褚秀丽,赵玉武,沈洁,王喜云,刘建芝,米亚静,金卫林.血糖升高水平对大鼠低血糖性脑损伤的影响[J].中华糖尿病杂志,2012,4(3):170-176. 被引量:14
  • 7Arya AK, Pokharia D, Tripathi K. Relationship between oxidative stress and apoptotic markers in lymphocytes of diabetic patients with chronic non healing wound [ J ]. Diabetes Res Clin Pract, 2011,94:377-384.
  • 8Wisessmith W, Phansuwan-Pujito P, Govitrapong P, et al. Melatonin reduces induction of Bax, easpase and cell death in methamphetamine-treated human neuroblastoma SH-SY5Y cultured ceils[ J]. J Pineal Res, 2009,46:433-440.
  • 9Lee MS, Chao J, Yen JC, et al. Sehizandrin protects primary rat cortical cell euhures from glutamate-induced apoptosis by inhibiting activation of the MAPK family and the mitochondria dependent pathway[ J]. Molecules, 2012,18:354-372.
  • 10Cartagena CM, Schmid KE, Phillips KL, et al. Changes in apoptotic mechanisms following penetrating ballistic-like brain injury[J]. Mol Neurosci, 2013,49:301-311.

二级参考文献16

  • 1Suh SM,Hamby AM,Swanson RA. Hypoglycemia,brain energetic,and hypoglycemic neuro death[J].Glia,2007.1280-1286.
  • 2Auer RN. Hypoglycemic brain damage[J].Forensic Science International,2004.105-110.
  • 3Vannucci RC,Vammucci SJ. Hypoglycemic brain injury[J].Seminars in Neonatology,2001.147-155.doi:10.1053/siny.2001.0044.
  • 4Giurqea L,Ulinski T,Touati G. Factitious hyperinsulinism leading to pancreatectomy:severe forms of Munchausen syndrome by proxy[J].Pediatrics,2005.145-148.
  • 5Davis EA,Keating B,Byrne GC. Impact of improved glycogenic control on rates of hypoglycaemia in insulin dependent diabetes mellitus[J].Archives of Disease in Childhood,1998.111-115.
  • 6Suh SW,Gum ET,Hamby AM. Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase[J].Journal of Clinical Investigation,2007.910-918.
  • 7Auer RN,Hugh J,Cosgrove E. Neuropathologic findings in three cases of profound hypoglycemia[J].Clinical Neuropathology,1989.63-68.
  • 8Auer RN,Siesjo BK. Hypoglycaemia:brain neurochemistry and neuropathology[J].Baillieres Cho Endocrinol Metab,1993.611-625.
  • 9Patrick AW,Campbell IW. Fatal hypoglycaemia in insulin-treated diabetes Mellitus:clinical features and neuropathological changes[J].Diabetic Medicine,1990.349-354.
  • 10Kalimo H,Olsson Y. Effects of severe hypoglycemia on the human brain.Neuropathological case reports[J].Acta Neurologica Scandinavica,1980.345-356.

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同被引文献47

  • 1汤文璐,王永铭,杜文民,程能能,陈斌艳.老年糖尿病人群低血糖风险和抗高血压药物应用的队列研究(英文)[J].中国临床药学杂志,2005,14(4):214-219. 被引量:3
  • 2王凯杰,程爱国.重型颅脑损伤后高血糖与颅内压及预后的关系[J].中华创伤杂志,2005,21(10):761-763. 被引量:18
  • 3何朝晖,支兴刚,孙晓川,唐文渊.大鼠创伤性脑损伤后胰岛素抵抗与伤后高血糖的相关分析[J].南方医科大学学报,2007,27(3):315-317. 被引量:12
  • 4OHTA M,HIGASHI Y,YAWATA T,et al.Attenuation of axonal injury and oxidative stress by edaravone protects against cognitive impairments after traumatic brain injury[J].Brain Research,2013,1490:184-192.
  • 5Ropper AH,Adams RD,Victor M,et a1.Adams and Victor sprincipies of neurology[M].8th ed.New York:McGrawHil,2005:959-982.
  • 6MALOUF R,BRUST J C.Hypoglycemia:causes,neurologicalmanifestations,and outcome[J].Ann Neuro,1985,17(5):421-430.
  • 7POH Z X,GOH K P.A current update on the use of alpha lipoic acid in the management of type 2 diabetes mellitus[J].Endocrine,Metabolic&Immune Disorders Drug Targets,2009,9(4):392-398.
  • 8Fujioka M,Okuchi K,Hiramatsu KL,et al.Specific changes in human brain after hypoglycemic injury[J].Stroke,1997,28(3):584-587.
  • 9Higgins PG,Dammhayn C,Hackel M,et al.Global spread of carbapenem-resistant acietobacter baumannii[J].J Antimicrob chemother,2010,65(2):233-238.
  • 10LU F,SELAK M,O'CONNOR J,et al.Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronic active lesions of multiple sclerosis[J].Journal of the Neurological Sciences,2000,177(2):95-103.

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