摘要
目的:研究长期大负荷训练致运动免疫抑制后大鼠胸腺蛋白质组表达的变化及其生理意义。方法:建立大鼠8周长期大负荷训练的运动免疫抑制模型,取训练组与对照组大鼠胸腺,提取胸腺组织总蛋白,通过二维凝胶电泳分离蛋白质,经考马斯亮蓝染色及图像分析,选取有表达差异的蛋白质点进行质谱分析。结果:长期大负荷训练后大鼠胸腺明显萎缩,其胸腺组织总蛋白经二维电泳可分离得到(639±39)个蛋白点,平均匹配率82.9%,22种蛋白质表达差异在1.5倍以上,9种表达差异在2倍以上。通过质谱鉴定出其中7种变化显著的蛋白质。这些蛋白是泛素羧基端水解酶L5(ubiquitin carboxyl-terminal hydrolase 5,UCHL5)、主要急性期蛋白-α1(major acute phase-α1,MAP-α1)、激肽原2前体(T-kininogen 2 precursor,T-KNNG2p)、角蛋白复合体2(keratin complex 2,KRTC2)、谷胱甘肽合成酶(glutathione synthetase,GSS)、前促触珠蛋白(preprohaptoglobin,PPHG)、丙酮酸脱氢酶E1-β(pyruvate dehydrogenase E1 component subunit-β,PDHE1-β)。结论:长期大负荷的耐力训练可使大鼠胸腺发生明显萎缩,蛋白质组表达发生显著改变;UCHL5对胸腺蛋白谱表达变化具有重要意义,它影响并调控了急性期蛋白MAP-α1、T-KNNG2p、KRTC2的表达,并可能与胸腺中大量的细胞凋亡有关;长期大负荷的训练可造成机体的炎症反应,表现在急性期蛋白表达的升高;胸腺中存在以表达KRTC2为特征的组织重建修复。
Objective：To study the changes in thymus proteomics expressions induced by long term heavy load training and to explore their physiological significances.Methods：Exercise-induced immunosuppression rat’s model with thymus atrophy was established by SD rats after 8 weeks’ long term heavy load swimming training.Whole tissue protein was extracted from thymus of rats in both train ing group and control group and was seperated by 2-dimensional electrophoresis（2-DE）.After stained with Coomassie brilliant blue,the differentially expressed protein spots were identified by flight mass spectrometry（MALDI-TOF） and then subjected to mass fingerprint analysis.Results：Long term heavy load training can induce thymus atrophy and 2-DE of rat ’s thymus whole protein can separate（639±39） protein spots with an average spot matching rate 82.9%.Twenty-two protein spots were expressed differentially by 1.5 folds or more and 9 protein spots by 2 folds or more.Seven most differential expressed protein spots were identified by MALDI-TOF.These protein spots were ubiquitin carboxyl-terminal hydrolase 5（UCHL5）,major acute phase-α1（MAP-α1）,T-kininogen 2 precursor（T-KNNG2p）,keratin complex 2（KRTC2）,glutathione synthetase（GSS）,preprohaptoglobin（PPHG） and pyruvate dehydrogenase E1 component subunit-β（PDHE1-β）.Conclusions：Long term heavy load training can induce thymus atrophy and rat ’s thymus proteomics changes.UCHL5,which affects and regulates MAP-ɑ1,T-KNNG2p and PPHG’s synthesis and may associate with cell apoptosis,is of great significance to this change.Long term heavy load training can induce body’s inflammation and make protein expression at the acute phase increase.The restoration of the tissue characterized by KRTC2’s expressions exists in the thymus.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2013年第4期381-388,共8页
Journal of Chongqing Medical University
