本文選題：BNIP3 + LC3�。� 參考：《上海體育學(xué)院》2017年碩士論文

【摘要】：研究目的:運動預(yù)適應(yīng)(exercise preconditioning,EP)能夠通過運動誘導(dǎo)機體產(chǎn)生內(nèi)源性心肌保護效應(yīng),其機制涉及到很多方面。其中線粒體是EP心臟保護中重要的參與者,線粒體自噬的上調(diào),可以及時清除受損線粒體,有利于維持細胞生存。而Bcl-2 19-k Da相互作用蛋白3(Bcl-2 19-k Da interacting protein 3,BN IP3)具有調(diào)控細胞自噬的功能,能與受損線粒體結(jié)合參與線粒體自噬。因此,本研究通過檢測和觀察心肌線粒體自噬相關(guān)蛋白BN IP3在EP晚期保護效應(yīng)中的表達變化,探討EP晚期保護效應(yīng)和心肌線粒體自噬的關(guān)系。研究方法:SD大鼠隨機分為對照組(C組)、力竭運動組(EE組)、晚期運動預(yù)適應(yīng)組(LEP組)、晚期運動預(yù)適應(yīng)+力竭運動組(LEP+EE組)和wortmannin+晚期運動預(yù)適應(yīng)+力竭運動組(W+LEP+EE組)。在EP動物模型的基礎(chǔ)上,用力竭運動致大鼠急性心肌損傷,用血漿c TnI含量和HBFP染色綜合評價心肌損傷和保護的程度,用免疫熒光雙標法檢測大鼠心肌線粒體BNIP3和TOM20的共定位程度,用免疫印跡法檢測大鼠心肌組織線粒體BN IP3和LC 3的表達變化。研究結(jié)果:與C組相比,EE組血漿c TnI和MOD值顯著升高,BNIP3轉(zhuǎn)位線粒體程度、BNIP3水平和LC3II/I水平顯著升高;LEP組BNIP3轉(zhuǎn)位線粒體程度和BNIP3水平顯著升高,血漿c TnI、MOD值和LC3II/I水平無顯著性差異。與EE組相比,LEP+EE組血漿c TnI和MOD值顯著降低,BNIP3轉(zhuǎn)位線粒體程度、BNIP3水平和LC3II/I水平顯著降低。與LEP+EE組相比,W+LEP+EE組血漿c TnI和MO D值顯著升高,BN IP3轉(zhuǎn)位線粒體程度和BN IP3水平顯著升高,LC3II/I水平無顯著性差異。研究結(jié)論:EP晚期保護期可以減輕一次大強度力竭運動對心肌所造成的運動性損傷,細胞自噬部分參與EP晚期保護效應(yīng)。一次大強度力竭運動和晚期EP均會導(dǎo)致BNIP3表達升高,參與誘導(dǎo)心肌細胞線粒體自噬。在EP晚期心肌保護效應(yīng)中,BNIP3誘導(dǎo)的線粒體自噬參與了EP對運動性心肌損傷的保護作用。
[Abstract]:Objective: exercise preconditioning can induce endogenous myocardial protection through exercise, and its mechanism involves many aspects. Mitochondria is an important participant in EP heart protection. The upregulation of mitochondrial autophagy can clear damaged mitochondria in time and help to maintain cell survival. Bcl-2 19-k Da interacting protein 3n BN IP3) has the function of regulating autophagy, and can bind with damaged mitochondria to participate in mitochondrial autophagy. Therefore, the relationship between late EP protective effect and myocardial mitochondrial autophagy was studied by detecting and observing the expression of myocardial mitochondrial autophagy related protein BN IP3 in the late stage of EP. Methods Twenty SD rats were randomly divided into three groups: control group (C), exhaustive exercise group (EE group), advanced exercise preconditioning group (Lemp group), late exercise preconditioning exhaustive exercise group (Lemp EE group) and wortmannin advanced exercise preconditioning exhaustive exercise group (WLEP EE group). On the basis of EP animal model, acute myocardial injury induced by exhaustive exercise was used to evaluate the degree of myocardial injury and protection by plasma c TNI content and HBFP staining. The co-localization of BNIP3 and TOM20 in rat myocardial mitochondria was detected by immunofluorescence double labeling method, and the expression of BNIP3 and LC3 in myocardial mitochondria was detected by Western blot. Results: compared with group C, the levels of c TnI and MOD in plasma of EE group were significantly higher than those in group C, and the levels of BNIP3 and LC3II- / I were significantly higher than those of group C, but there was no significant difference between plasma c TnI mod value and LC3IIP I level in LEP group (P < 0.05). The level of BNIP3 translocation mitochondria and BNIP3 level in LEP group were significantly higher than those in group C. There was no significant difference in the level of plasma c TnI mod and LC3IIP I. Compared with EE group, plasma c TnI and MOD levels in LEP EE group were significantly lower than those in EE group. Compared with the LEP EE group, the plasma c TnI and MO D values in the WLEP EE group were significantly higher than those in the LEP EE group. There was no significant difference in the degree of mitochondrial translocation of BN IP3 and the level of BN IP3. There was no significant difference in the level of LC3II / I between the two groups. Conclusion during the late stage of protection, the myocardial injury caused by one intensive exhaustive exercise can be alleviated, and autophagy partly participates in the late protective effect of EP. Both a high intensity exhaustive exercise and late EP could increase the expression of BNIP3 and participate in the induction of mitochondrial autophagy in cardiomyocytes. Mitochondrial autophagy induced by BNIP3 is involved in the protective effect of EP on exercise induced myocardial injury.
【學(xué)位授予單位】：上海體育學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R87

【參考文獻】

相關(guān)期刊論文 前10條

1 原陽;潘珊珊;;活性氧介導(dǎo)氧化應(yīng)激在心血管應(yīng)激及運動中對心肌線粒體和自噬作用的新進展[J];體育科學(xué);2015年05期

2 李麗君;唐圣松;;BNIP3調(diào)控腫瘤細胞自噬及凋亡的研究進展[J];臨床與病理雜志;2014年06期

3 劉澤廣;潘珊珊;郝U，

本文編號：2015188