期刊文献+

Cdk5活性抑制肽对2型糖尿病小鼠模型血糖和体重的影响

Cdk5 activity inhibitory peptide for T2DM Experimental study on the impact of blood glucose and body weight in mice
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摘要 目的观察Cdk5抑制短肽(TFP5)对2型糖尿病小鼠模型体重和血糖的干预作用。方法早期干预:分为正常小鼠生理盐水组(1 m L·只-1,组1),正常小鼠注射TFP5组(200 mmol,1 m L·只-1,组2),db/db小鼠注射生理盐水组(1 m L·只-1,组3),db/db小鼠注射TFP5(200 mmol,1 m L·只-1,组4)。从第5周开始每日注射1次,以后均为隔日注射1次,注射至第8周,共注射3周,第8周时处死小鼠。晚期干预:分db/db小鼠注射生理盐水组(组5)和db/db小鼠注射TFP5(400 mmol,组6),从第15周开始每日注射1次,第16周改为隔日1次,第17周停止注射1周,18周处死。注射方式均为腹腔注射,由第5周时体重每周测2次,处死之前测体重,取血送血糖监测。结果 2组正常小鼠的血糖和体重差异均无统计学意义(P<0.05);db/db小鼠注射生理盐水组血糖明显高于注射TFP5组(P<0.05),6周后db/db小鼠注射生理盐水组体重明显高于注射TFP5组(P<0.05);2组在第18周时,体重及血糖均差异无统计学意义(P>0.05)。结论应用TFP5能够降低T2DM模型小鼠的血糖及体重,但其治疗效果可能受到治疗时机、疗程的长度等的影响。 Objective To study and observe TFP5 on weight and blood glucose in T2 DM animal models. Methods Experiment1( early intervention) : group 1 was not treated control group of normal mice,and group 2 of mice injected TFP5 the normal group,the third group of db / db mice injected with saline( 1 ml),and group 4 of db / db mice injected TFP5( 200 mmol,1ml). From the beginning of the first five weeks to eight weeks for injection,injected once a day the first week,after both injected once every other day of injection three weeks,the mice were sacrificed 8 weeks. Experiment 2( late intervention),a group of db / db mice were injected with saline group( Group 5),another group of db / db mice injected TFP5( 400 mmol,group 6). Injection time is to start from the first 15 weeks,daily injections once every other day the second week of injection two weeks,stop the injection a week,18 weeks to death. Mice were injected intraperitoneally way,weight measured twice weekly until death measure weight,blood biochemical tests sent. Results The blood glucose was significantly higher in group 3 than that in group 4( P 〈 0. 05); 6 weeks after group 3 was significantly higher than the weight of the group 4,and the gap between the two weight increase with time( P 〈 0. 05); Between group 5 and 6,body weight and blood glucose were not significantly different at all in the 18 week( P 〉 0. 05). Conclusion Application TFP5 confirmed T2 DM can improve islet function in mice with reduced blood glucose and weight; its therapeutic effect may be the timing of treatment,length of treatment of other effects.
出处 《宁夏医学杂志》 CAS 2015年第3期200-202,共3页 Ningxia Medical Journal
基金 国家自然科学基金资助项目(NSFC81160093 NSFC81460161) 宁夏自然科学基金资助项目(NZ14160) 宁夏科技攻关资助项目(KGX1910-16) 宁夏科技攻关国际合作项目(2011ZYH169) 宁夏科技支撑资助项目(2013ZY503)
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参考文献8

  • 1Wei FY,Nagashima K,Ohshima T,et al. Cdk5 一 dependent regula-(10):1104-1108.
  • 2Ya Li Zheng, Ya Fang Hu, Aiping Zhang,et al. Overexpression ofp35 in Min6 pancreatic beta cells induces a stressed neuron - likeapoptosis[ J]. J Neurol Sci,2010,15( 1/2) : 101 - 107.
  • 3郑亚莉,陆晓华,曹丽,王慧,李博,鄂静,保莉,罗红艳,兰晓梅.蛋白激酶5过度激活诱发β细胞凋亡和调节胰岛素分泌的机制研究[J].中国全科医学,2013,16(24):2823-2827. 被引量:1
  • 4Varsha Shukla, YaLi Zheng,Santosh K, et al. A truncated peptidefrom p35 a Cdk5 activator prevents Alzheimer1 s disease phenotype-sin model mice[ J] . The FASEB Journal Article,2013 ,10(4) :12.
  • 5Bk B,Zheng YL,Shukla V,et al. TFP5,apeptide derived from p35,a Cdk5 neuronal activator,rescues cortical neurons from glucose tox-icity [J] . J Alzheimers Dis,2014,39(4) :899 -909.
  • 6Bonora E. Protection of pancreatic beta - cells: is it feasible[ J].Nutr Metab Cardiovasc Dis,2008,18( 1) :74 -83.
  • 7Ya Li Zheng,Ya Fang Hu,Aiping Zhang,et al. Pant overexpressionof p35 in Min6 pancreatic beta cells induces a stressed neuron -like apoptosis[J].J Neurol Sci,2010,15( 1/2) :101 -107.
  • 8Matveyenko AV,Butler PC. Relationship between beta - cell nwss anddiabetes onset[ J]. Diabetes Obes Metab,2008,11(10) :23 -31.

二级参考文献14

  • 1Matveyenko AV, Butler PC. Relationship between beta - cell mass and diabetes onset [J]. Diabetes Obes Metab, 2008, 10 (Suppl 4) : 23 -31.
  • 2Kaneto H, Kawamori D, Matsuoka TA, et al. Oxidative stress and pancreatic beta-cell dysfunction [J]. Am J Ther, 2005, 12 (6) : 529 - 533.
  • 3Jonas JC, Bensellam M, Duprez J, et al. Glucose regulation of islet stress responses and beta - cell failure in type 2 diabetes [ J ]. Diabetes Obes Metab, 2009, 11 (Suppl4) : 65 -81.
  • 4Andrali SS, Sampley ML, Vanderford NL, et al. Glucose regulation of insulin gene expression in pancreatic beta - cells [ J ]. Biochem J, 2008, 415 (1): 1-10.
  • 5Wei FY, Nagashima K, Ohshima T, et al. Cdk5 - dependent regula- tion of glucose- stimulated insulin secretion [J]. Nat Med, 2005, 11 (10): 1104 -1108.
  • 6Hisanaga S, Saito T. The regulation of cyclin - dependent kinase 5 ac- tivity through the metabolism of p35 or p39 Cdk5 activator [J]. Neu- rosignals, 2003, 12 (4/5): 221-229.
  • 7Li L, Holscher C. Common pathological processes in Alzheimer diseaseand type 2 diabetes : a review [ J ]. Brain Res Rev, 2007, 56 (2) : 384 - 402.
  • 8Ubeda M, Rukstalis JM, Habener JF. Inhibition of cyclin - depend- ent kinase 5 activity protects pancreatic beta ceils from glucotoxicity [J]. J Biol Chem, 2006, 281 (39) : 28858 -28864.
  • 9Dhavan R, Tsai LI-I. A decade of CDK5 J]. Nat Rev Mol Cell Bi- ol, 2001, 2 (10): 749-759.
  • 10Patrick GN, Zukerberg L, Nikolic M, et al. Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration [ J 1. Nature, 1999, 402 (6762): 615-622.

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