【摘要】：目的:研究青年期開(kāi)始規(guī)律運(yùn)動(dòng)對(duì)心臟Ca-α1D基因沉默老齡果蠅心臟功能、運(yùn)動(dòng)能力和生命周期的影響,探討Ca-α1D基因在心臟衰老及運(yùn)動(dòng)抗心臟衰老中的作用。方法:基因型為w1118;P{GD1737}v51491的處女蠅分別與W1118品系、Hand-GAL4品系雄蠅雜交,獲得F1代處女蠅分為安靜組、干擾組、運(yùn)動(dòng)組、運(yùn)動(dòng)干擾組,每組400只,飼養(yǎng)至2周齡開(kāi)始運(yùn)動(dòng),2小時(shí)/天,5天/周,訓(xùn)練持續(xù)時(shí)間為4周。采用qRT-PCR測(cè)定心肌Ca-α1D基因mRNA表達(dá)量,M-mode心動(dòng)圖檢測(cè)評(píng)價(jià)心臟功能,測(cè)量攀爬指數(shù)評(píng)定運(yùn)動(dòng)能力,統(tǒng)計(jì)生命周期反映壽命情況。結(jié)果:(1)干擾組心肌Ca-α1D的相對(duì)表達(dá)量較對(duì)照組約下降50%(P0.01)。(2)與對(duì)照組相比,干擾組心動(dòng)周期(HP)增加(P0.01),收縮間期(SI)上升(P0.05)。纖維性震顫(FL)、心動(dòng)徐緩發(fā)生率增加(P0.01)。舒張直徑(DD)、收縮直徑(SD)增加(P0.01),射血分?jǐn)?shù)(FS)降低(P0.05)。與對(duì)照組相比,運(yùn)動(dòng)組HP、DI上升(P0.05),心動(dòng)徐緩發(fā)生率增加(P0.01)。與對(duì)照組相比,運(yùn)動(dòng)干擾組HP、心動(dòng)徐緩發(fā)生率增加(P0.01)。DD、SD增加(P0.01),而FS變化不具有顯著性差異(P0.05)。與干擾組相比,運(yùn)動(dòng)干擾組心動(dòng)徐緩發(fā)生率減少(P0.01)。DD增加(P0.05)�；虺聊�(lián)合耐力運(yùn)動(dòng)對(duì)心動(dòng)徐緩發(fā)生率的結(jié)果有協(xié)同作用(P0.05)。其中基因是對(duì)HP、DD、SD、FS、FL結(jié)果產(chǎn)生作用的主效應(yīng),運(yùn)動(dòng)是對(duì)DI結(jié)果產(chǎn)生作用的主效應(yīng)。(3)與對(duì)照組相比,運(yùn)動(dòng)組攀爬能力增強(qiáng)(P0.01)、干擾組攀爬能力降低(P0.05);基因沉默聯(lián)合耐力運(yùn)動(dòng)對(duì)攀爬能力具有協(xié)同作用(P0.05)。(4)運(yùn)動(dòng)組平均壽命高于對(duì)照組(P0.01),運(yùn)動(dòng)干擾組高于干擾組(P0.01),干擾組平均壽命低于對(duì)照組(P0.01)。結(jié)論:規(guī)律運(yùn)動(dòng)的干預(yù)能夠維持心臟正常節(jié)律、提高運(yùn)動(dòng)能力和增進(jìn)生命周期有一定作用。心臟特異性Ca-α1D基因沉默是導(dǎo)致該果蠅心臟收縮功能減退、節(jié)律紊亂以及壽命縮減的主要原因。運(yùn)動(dòng)能夠有效改善因Ca-α1D基因敲減引起的心動(dòng)過(guò)緩、提高運(yùn)動(dòng)能力,但是對(duì)心臟收縮能力的改善作用不顯著,其原因是否與老齡果蠅自身的機(jī)能水平衰退有關(guān),值得進(jìn)一步研究。
[Abstract]:Objective: To study the effect of Ca- alpha 1D gene on cardiac function, exercise ability and life cycle of aged Drosophila melanogaster, and to explore the role of Ca- alpha 1D gene in cardiac senescence and anti cardiac senescence. Methods: gene type is w1118; P{GD1737}v51491 virginity flies respectively with W1118 strain and Hand-GAL4 strain male flies, respectively. The F1 virginity flies were divided into the quiet group, the interference group, the exercise group and the exercise interference group, 400 rats in each group, and were fed to 2 weeks of age to start the movement, 2 hours / day, 5 days / week, and the training duration was 4 weeks. The mRNA expression of Ca- alpha 1D gene was measured by qRT-PCR, and the cardiac function was evaluated by M-mode cardiogram, and the climbing index was used to assess the ability of exercise and to measure climbing index to assess exercise ability and to measure the ability of climbing index. Life cycle reflected life expectancy. Results: (1) the relative expression of Ca- alpha 1D in the myocardium of the interference group decreased by 50% (P0.01). (2) compared to the control group, the cardiac cycle (HP) increased (P0.01), the Systolic Interval (SI) increased (P0.05), fibrous tremor (FL), the rate of bradycardia increased (P0.01). The diastolic diameter (DD), the contraction diameter (SD) increased. Plus (P0.01), ejection fraction (FS) decreased (P0.05). Compared with the control group, the exercise group was HP, DI (P0.05), and the incidence of bradycardia increased (P0.01). Compared with the control group, the incidence of HP in the exercise group was increased (P0.01).DD, SD increased (P0.01), but there was no significant difference between the exercise group and the disturbance group. The incidence of P0.01.DD increased (P0.05). Gene silencing combined with endurance exercise had synergistic effects on the incidence of bradycardia (P0.05). Gene was the main effect on HP, DD, SD, FS, and FL, and movement was the main effect on the results of DI. (3) compared with the control group, the climbing ability of the exercise group was enhanced (P0.01), dry The climbing ability of the group was reduced (P0.05); gene silencing combined with endurance exercise had synergistic effect on climbing ability (P0.05). (4) the average life span of the exercise group was higher than that of the control group (P0.01), the exercise interference group was higher than the interference group (P0.01), and the average life span of the interference group was lower than that of the control group (P0.01). Conclusion: the intervention of regular exercise can maintain the normal rhythm of the heart, and improve the normal rhythm of the heart. The heart specific Ca- alpha 1D gene silencing is the main cause of the Drosophila's systolic dysfunction, rhythmic disorder, and life expectancy. Exercise can effectively improve the bradycardia caused by Ca- alpha 1D knockout and improve the movement ability, but the improvement of cardiac contractility is improved. It is not obvious whether the reason is related to the decline of the functional level of the Drosophila melanogaster.
【作者單位】： 湖南師范大學(xué)體育學(xué)院;
【基金】：湖南省自然科學(xué)基金項(xiàng)目(2015JJ2102)
【分類(lèi)號(hào)】：G804.2

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