羟基酪醇对过度训练大鼠心肌线粒体动力学蛋白及自噬水平的影响  

Effects of hydroxytyrosol on myocardial mitochondrial dynamic protein and autophagy in the overtraining rats

作　　者：孙云彦[1] 殷红[2] 

机构地区：[1]南阳理工学院体育教学部,河南南阳473003 [2]河南大学体育学院,河南开封4750001

出　　处：《山东体育学院学报》2014年第3期51-56,66,共7页Journal of Shandong Sport University

基　　金：国家青年科学基金资助项目(81100174)

摘　　要：目的:研究检测ET后心肌线粒体功能,观察羟基酪醇HT对线粒体功的保护效应,并通过关注动力学及自噬蛋白变化,探讨HT保护机制。方法:80只SD大鼠随机分成4组,即:正常对照组(CON),正常加羟基酪醇组(CON+HT),过度训练组(ET)及训练加羟基酪醇组(ET+HT)。灌胃给药,剂量为25 mg/kg/d,每周训练时间为周一至周六,共8周,氧耗法测定线粒体呼吸功能。Westerblot法检测线粒体生物合成(PGC-1α),复合物(I,II,III,IV,V),动力学(融合:Mfn1/2,OPA1;裂解:Drp1)及自噬相关蛋白(Atg5,Beclin-1及Lc3-B)。结果:ET可显著性降低线粒体呼吸控制率(RCR)及磷氧比值(P/O),下调PGC-1α及复合物I,IV,V表达,增加线粒体裂解(Drp1),降低融合(Mfn2,Opa1)。相对地,HT可有效提高线粒体P/O及复合物I,V表达水平;促进生物合成(Pgc-1α),提高融合(Mfn2,Opa1),降低裂解(Drp1)和自噬(Atg5,Lc3-B)。结论:ET造成的心肌线粒体功能异常与动力学蛋白及自噬水平变化相关。HT对上述病理性变化的抑制作用可能是其发挥保护作用的重要机制。Abstract：Objective：This study evaluated the changes of mitochondrial respiratory functions, observe the mitochondrial dynamics and autophagy related proteins alterations, explored HT - induced favorable protections for myocardium in excessive training animals. Methods ： 80 Sprague dawley rats were subjected and divided into four groups ： sedentary group （ CON ）, sedentary ＋ HT group （ CON ＋ HT） ,excessive exercise training group （ET） and ET ＋ HT group. Administration regimen： 25mg/ kg/d. Training from Monday to Friday every week for eight weeks. Oxygen consumption was used for evaluating the mitochondrial respiratory functions. Westerblot was used to determine the mitochondrial biogenesis （ Pgc - 1α）, complexes protein expressions, mitochondrial dynamics （ fusion ： Mfnl/2 ,Opal ; fission ： Drpl ） and autophagy associated proteins（ atgS, beclin - land lc3 - B）. Re- sults ：ET showed significant decrease on mitochondrial respiratory control rate （RCR）and value ofP/O,downregulated PGC - 1α and complex I, IV and V levels. ET also revealed to induce mitochondrial dynamics pathological remodelling （ increased fission [ Drpl ] and decreased fusion [ Mr2 and Opal ] ） and elevated autophagy level （ Atg5, Beclin - 1 ）. HT treatment efficiently increased P/ O, complex I and V levels, which were indicated to the increased protein levels of Pgc - 1α, Mfn2 and Opal, but decreased Drpl, Atg5 and Lc3 -B. Conclusion ：These results demonstrated that ET - induced myocardial mitochondrial dysfunctions may be mediated via the downregulation of mitochondrial biogenesis, dynamic proteins and upregulation of autophagy. HT may normalize the mitochondrial dynamic remodeling and decrease autophagy, thereby improve the mitochondrial functional performances.

关 键 词：过度训练 心肌 生物合成 裂解 融合 自噬 

分 类 号：G804.7[文化科学—运动人体科学]