期刊文献+

VitE对动脉粥样硬化模型兔肝脏肌球蛋白轻链激酶活性及表达的影响 被引量:3

Effect of Vit E on myosin light chain kinase activity and expression in the liver of atherosclerosis model rabbit
下载PDF
导出
摘要 目的 探讨维生素E(VitE)对动脉粥样硬化模型兔肝脏MLCK活性及表达的影响。方法 复制兔动脉粥样硬化模型 ,用γ 3 2 P参入法检测肝脏MLCK活性 ,免疫荧光法检测肝组织MLCK的表达。结果 动脉粥样硬化兔模型建立成功 ,在喂胆固醇 4wk及 12wk的动物组 ,肝脏MLCK活性[分别为 (1884 8 7± 74 34 3)、(18818 3± 346 9 9)cpm·mg-1protein]与正常对照比较 [(6 6 77 5± 10 9 6 0 )cpm·mg-1pro tein]升高 (P <0 0 5 ) ;但在喂胆固醇同时添加VitE后 ,肝脏MLCK活性 [(10 898 8± 2 0 4 1 2 )cpm·mg-1protein]与正常对照组比较升高不明显 (P >0 0 5 )。荧光显微镜下观察显示 ,兔肝在喂食胆固醇膳食 4wk后MLCK的表达有所增强 ,12wk后显著增强 ,12wk组的膳食中同时加VitE后 ,MLCK表达有所下降。结论 在动脉粥样硬化过程中 ,肝脏病变可能与MLCK活性增强有关 ,VitE可能是降低肝脏MLCK活性的因素 。 AIM To study the effect of Vit E on the MLCK activity and expression in the liver of atherosclerosis model rabbits. METHODS The MLCK activity of rabbit liver was measured by the method of γ- 32P incorporated and its expression was detected by immunofluorescent. RESULTS The model of atherosclerosis was estabilished. After rabbits were fed with cholesterol for four weeks and twelve weeks, the activity of MLCK increased markedly, and there was significantly statistical difference compared with the normal control (P<0.05). As for the rabbits fed with cholesterol and vitamin E for twelve weeks, the activity of MLCK did not change markedly, there was no statistical difference compared with the normal control (P>0.05). MLCK expression increased after the rabbits was fed with cholesterol for four weeks, and this increase became more obvious had been the rabbits was fed with cholesterol for twelve weeks. The expression decreased when vitamin E had been added into the cholesterol fed. CONCLUSION The pathology of liver may be associated with the increase of the activity of MLCK. Vit E may reduce MLCK activity and protect hepatocyte from injury.
出处 《中国药理学通报》 CAS CSCD 北大核心 2003年第11期1299-1302,共4页 Chinese Pharmacological Bulletin
基金 国家自然科学基金 (No 3 9870 3 2 4) 国家教委优秀年轻教师研究基金资助项目
关键词 肌球蛋白轻链激酶 VITE 动脉粥样硬化 肝脏 myosin light chain kinase Vit E atherosclerosis liver
  • 相关文献

参考文献4

二级参考文献5

共引文献36

同被引文献17

  • 1江志奎,朱华庆,胡勇,王健,周青,桂淑玉,汪渊.Vit E对动脉粥样硬化模型兔动脉肌球蛋白轻链激酶表达的影响[J].中国药理学通报,2004,20(6):652-656. 被引量:4
  • 2马强,吴永贵,吴国仲,齐向明,林辉.LY333531下调大鼠糖尿病模型肾组织结缔组织生长因子表达[J].安徽医科大学学报,2005,40(1):34-37. 被引量:5
  • 3Persechini A,Stull J T.Phosphorylation kinetics of skeletal musucle myosin and the effect of phosphorylation on actomyosin adenosine triphosphatase activity[J].Biochemistry,1984,23(18):4144-50.
  • 4Li,L Eto M,Lee M R.et al.Possible involvement of the novel CIP-17 Protein in protein kinase C signal transduction of rabbit arterial smooth musle[J].J Physiol(Lond),1998,508(3):871-81.
  • 5Archer S L.Huang J M C,Hampl V,et al.Nitric oxide and cGMP cause vasorelaxation by activation of a charybolotoxin-sensitive K channel by cGMP-dependent protein kinase[J].Proc Nail Acad Sci USA,1994,91(16):7583-7.
  • 6Torrecillas G,Diez-Marques M L,Carcia-Escribanoc et al.Mechanisms of cGMP-dependent mesangial-cell relaxation:a role for myosirt light-chain phosphatase activation[J].Biochem J,2000,346(1):217-22.
  • 7Herring B P,Englnd PJ.The turnover of phosphate bound to myosin light chain-2 in perfused rat heart[J].Biochem J,1986,240(1):205-14.
  • 8Ho-Jae H C,Choi H J,Park S H.High gluose inhibits uptake in renal proximal tubule cells by oxidative stress and protein kinase C[J].Kidney Int,2000,57(3):918-26.
  • 9Haoyou Chu and H,Glenn B.Hight concentration of glucose inhibits glomerular endothelial cNOS through a PKC mechanism[J].Am J physiol Renal Physiol,2004,287(3):F384-F92.
  • 10Anderson S.Rennke H G,Garcia D L.et al.Short and long term effects of antibypertensive therapy in the diabetic rat[J].Kidey,1989,36(4):526-36.

引证文献3

二级引证文献7

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