期刊文献+

限制性应激对1型糖尿病模型大鼠的影响

Restraint stress effects in type 1 diabetes rats
下载PDF
导出
摘要 背景:限制性应激为构建心理应激的一种方法。目的:建立合适的糖尿病及限制性应激模型,分析限制性应激与1型糖尿病的关系。方法:选取48只雄性SD大鼠,在腹腔内注射链脲佐菌素构建1型糖尿病大鼠模型。建模成功后将其随机分为2组,实验组施加限制性应激,对照组不施加。于施加限制性应激后的1,2,3和4周分别处死实验组和对照组的大鼠各6只,检测相关应激标识物:促肾上腺皮质激素、皮质酮以及胰高血糖素在血清中的浓度。并定期进行空腹血糖测试。结果与结论:实验组大鼠在施加限制性应激1周后血糖及胰高血糖素增高显著高于对照组(P<0.05或P<0.001);血清中促肾上腺皮质激素,皮质酮等应急标识物水平显著高于对照组(P<0.05或P<0.01)。说明限制性应激可以升高糖尿病大鼠的血糖水平。 BACKGROUND: A way to build psychological stress is restraint stress. OBJECTIVE: To study the relationship of restraint stress and type 1 diabetes METHODS: Forty-eight male Sprague-Dawley rats underwent intraperitoneal injection of streptozotocin to rat models of type 1 diabetes mellitus. After the successful modeling, rats were randomly divided into two groups: stress group (the rats were exerted with restraint stress) and control group (no intervention). Six rats from either group were executed at 1, 2, 3 and 4 weeks after exerting stress, and the related stress markers were detected, including the levels of adrenal cortical hormone, corticosterone and glucagon in the serum. Fasting blood glucose was measured regularly in rats. RESULTS AND CONCLUSION: In the stress group, the levels of glucose and glucagon, after a week of the stress, were higher than those in the control group (P 〈 0.05 or P 〈 0.001). Simultaneously, the levels of adrenal cortical hormone and corticosterone in serum were higher in the stress group compared with the control group (P 〈 0.05 or P 〈 0.001 ). These indicate that restraint stress can raise the blood sugar level of diabetic rats.
出处 《中国组织工程研究》 CAS CSCD 2013年第11期1946-1950,共5页 Chinese Journal of Tissue Engineering Research
基金 重庆市教委科学技术研究项目基金资助课题(KJ090316)~~
关键词 组织构建 组织构建实验造模 限制性应激 1型糖尿病 SD大鼠 促肾上腺皮质激素 皮质酮 他基金 tissue construction experimental modeling in tissue construction restraint stress type 1 diabetesmellitus Sprague-Dawley rats adrenal cortical hormone corticosterone other grants-supported paper
  • 相关文献

参考文献16

  • 1Al an FN,Wil is T. Diabetes three hundred years ago[J].{H}DIABETES,1953,(01):74-77.
  • 2Buynitsky T,Mostofsky DI. Restraint stress in biobehavioral research:Recent developments[J].{H}Neuroscience and Biobehavioral Reviews,2009,(07):1089-1098.
  • 3Peng H,Hagopian W. Environmental factors in the development of type 1 diabetes[J].{H}Reviews in Endocrine and Metabolic Disorders,2006,(03):149-162.
  • 4Konturek PC,Brzozowski T,Burnat G. Gastric ulcer healing and stress-lesion preventive properties of pioglitazone are attenuated in diabetic rats[J].{H}Journal of Physiology and Pharmacology,2010,(04):429-436.
  • 5Lehmann AE,Ennis K,Georgieff MK. Evidence for a hyporesponsive limbic-hypothalamic-pituitary-adrenal axis fol owing early-life repetitive hypoglycemia in adult male rats[J].{H}American Journal of Physiology Regulatory Integrative and Comparative Physiology,2011,(02):R484-R490.
  • 6Sakai A. Animal models for bone and joint disease. Animal models of immobilization and unloading[J].Clin Calcium,2011,(02):181-188.
  • 7Jaggi AS,Bhatia N,Kumar N. A review on animal models for screening potential anti-stress agents[J].{H}Neurological Sciences,2011,(06):993-1005.
  • 8魏泓.医学实验动物学[M]{H}成都:四川科学技术出版社,1998163-169.
  • 9沈亚非,徐焱成.链脲佐菌素诱导实验性糖尿病大鼠模型建立的研究[J].实用诊断与治疗杂志,2005,19(2):79-80. 被引量:91
  • 10Herlinda Aguilar-Zavala,Ma. Eugenia Garay-Sevil a,Juan Manuel Malacara. Stress, inflammatory markers and factors associated in patients with type 2 diabetes mel itus[J].{H}STRESS AND HEALTH,2008,(03):49-54.

二级参考文献8

  • 1Ueda H, Ikegami H, Yamato E, et al. The NSY Mouse: a new animal model of spontaneous NIDDM with moderate obesity[J].Diabetologia , 1995,38 : 503
  • 2Rackietan N, Rackietan M L, Nadkarni M R. Studies on diabetogenic action of streptozocin (NSC-37917) [J ]. Cancer Chemother Rep, 1993,29:91
  • 3Pettepher C C, Ledoux S P, Bohr V A, et al. Repair of Alkalilabile sites within the mitochondrial DNA of RINr 38 cells after exposure to the nitrosourea streptozotocin[J]. J Bio Chem,1991,266:3113
  • 4Lupi R, Dotta F, Marscella L, et al. Prolonged exposure to free fatty acids has cytosatatic and pro-apototic effects on human pancreastic islets: evidence that beta-cell death is caspase mediated, partially dependent on ceramide pathway and Bcl-2redulated[J]. Diabetes, 2002,51 : 1437
  • 5Mauricio D, Mandrup-Palsen T. Apoptosis and the pathogenesis of IDDM: a question of life and death[J]. Diabetes, 1998,47:1537
  • 6Liuk, Parterson A J, Chin E, et al. Glucose stimulates protein modification by o-linked GlcNAC pancreastic beta cell: Linkage of o-linked GlcNAC to bete cell death [J]. PNAS, 2000,97(6):2820
  • 7Amos A F, Mc Carty D J, Zim Met P [J]. The rising global burden of diabetes and its complications :estimates and projections to the year 2010[J]. Diabet Med, 1997,14(Suppl 5) :SI
  • 8赵志刚.糖尿病防治若干研究进展[J].实用诊断与治疗杂志,2004,18(3):157-160. 被引量:76

共引文献90

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部