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中国精品科技期刊2020
胡戈, 曹建民, 周海涛, 郭娴, 汪毅, 牛衍龙, 任奕, 李倩. 虾青素介导Nrf2信号通路减轻大强度运动诱导大鼠心肌细胞的凋亡[J]. 食品工业科技, 2019, 40(8): 266-271. DOI: 10.13386/j.issn1002-0306.2019.08.045
引用本文: 胡戈, 曹建民, 周海涛, 郭娴, 汪毅, 牛衍龙, 任奕, 李倩. 虾青素介导Nrf2信号通路减轻大强度运动诱导大鼠心肌细胞的凋亡[J]. 食品工业科技, 2019, 40(8): 266-271. DOI: 10.13386/j.issn1002-0306.2019.08.045
HU Ge, CAO Jian-min, ZHOU Hai-tao, GUO Xian, WANG Yi, NIU Yan-long, REN Yi, LI Qian. Astaxanthin Reduces Myocardial Cell Apoptosis Induced by High Intensity Training Via Activating Nrf2 in Rats[J]. Science and Technology of Food Industry, 2019, 40(8): 266-271. DOI: 10.13386/j.issn1002-0306.2019.08.045
Citation: HU Ge, CAO Jian-min, ZHOU Hai-tao, GUO Xian, WANG Yi, NIU Yan-long, REN Yi, LI Qian. Astaxanthin Reduces Myocardial Cell Apoptosis Induced by High Intensity Training Via Activating Nrf2 in Rats[J]. Science and Technology of Food Industry, 2019, 40(8): 266-271. DOI: 10.13386/j.issn1002-0306.2019.08.045

虾青素介导Nrf2信号通路减轻大强度运动诱导大鼠心肌细胞的凋亡

Astaxanthin Reduces Myocardial Cell Apoptosis Induced by High Intensity Training Via Activating Nrf2 in Rats

  • 摘要: 目的:观察补充虾青素能否介导核因子E2相关因子2(nuclear factor-E2-related factor 2,Nrf2)通路,减少6周大强度训练致大鼠心肌组织氧化应激,降低细胞凋亡水平。方法:7周龄SD雄性大鼠,适应性饲养及训练后随机分为对照组(C组,10只)、大强度训练组(HT组,15只)、虾青素+大强度训练组(HTA组,15只),大强度训练持续6周。训练期间,HTA组每天灌胃1次虾青素,灌胃剂量为20 mg/kg/d,C组和HT组分别灌胃同体积的大豆油。实验结束24 h后取血清测试血清肌钙蛋白I(Cardiac Troponin I,cTNI),取心肌测定凋亡指数、B细胞淋巴瘤/白血病基因2(B cell lymphoma/leukemia 2,Bcl2)、Bcl2相关x蛋白(Bcl2 associated x protein,Bax)、Nrf2、血红素加氧酶-1(heme oxygenase-1,HO-1)表达,同时测定心肌总抗氧化能力(Total antioxidative capacity,T-AOC)、超氧化物歧化酶(superoxide dismutase,SOD)活性和丙二醛(Malonaldehyde,MDA)浓度。结果:经6周大强度训练,与C组比较,HT组大鼠血清cTNI、心肌凋亡水平、Bax表达、MDA浓度极显著增强(p<0.01),Bcl2/Bax、HO-1表达量、SOD、T-AOC活性极显著下降(p<0.01)。而通过6周的虾青素干预,与HT组比较,HTA组血清cTNI、心肌MDA浓度、心肌组织细胞的凋亡水平、Bax表达显著下降(p<0.05),Nrf2和HO-1表达量、Bcl2/Bax、SOD和T-AOC活性显著升高(p<0.05)。除Bcl2和HO-1外,其余指标与C组相比仍有显著性差异(p<0.05)。结论:补充虾青素可以介导Nrf2通路,上调Nrf2、HO-1的蛋白表达,提高SOD和T-AOC抗氧化酶的活性,进而有效降低6周大强度运动训练引发的大鼠心脏组织氧化应激水平和心肌细胞凋亡水平,保护心脏组织结构和功能正常。

     

    Abstract: Objective:By supplementing the astaxanthin,the effects if astaxanthin could mediate Nrf2 and reduce myocardium oxidative injury in rats after high intensity training of 6 weeks were investigated in the research. Methods:7-week SD male rats were divided into 3 groups randomly:control group(C group,n=10),high intensity training group(HT group,n=15),astaxanthin and high intensity training group(HTA group,n=15). The rats in HTA group were intragastrically daily administered astaxanthin 20 mg/kg and were intragastrically administered equal amount of soybean oil in HT group during the training day.The serum cardiac troponin I(cTNI),myocardial apoptosis index,the expression of myocardial B cell lymphoma/leukemia 2(Bcl2),Bcl2 associated x protein(Bax),nuclear factor-E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),myocardial malonaldehyde(MDA),superoxide dismutase(SOD)and total antioxidative capacity(T-AOC)activity were detected at 24 h after the last training.Results:After 6-week of high intensity training,compared with C group,the serum cTNI,myocardial apoptosis index,the Bax expression and myocardial MDA were significantly higher in HT group(p<0.01). The Bcl2/Bax,the expression of HO-1,SOD and T-AOC activity were significantly lower(p<0.01). After the intervention of 6-week astaxanthin intragastrical administration,in HTA group,the serum cTNI,myocardial MDA,the myocardial apoptosis index,the Bax expression were significantly lower than HT group(p<0.05). Finally,Bcl2/Bax,SOD,T-AOC activity,the Nrf2 expression and HO-1 were significantly improved(p<0.05). Compared with C group,all these indexes increased significantly besides Bcl2 and HO-1(p<0.05). Conclusion:These results demonstrate that supplement of astaxanthin can mediate Nrf2 signaling pathway,and elevate the expression of Nrf2 and HO-1.It can also effectively increase the activity of SOD and T-AOC,after that the astaxanthin is helpful to alleviate the myocardial oxidative level and myocardial apoptosis which are caused by 6-week high intensity training. Finally,the structure and function of heart tissue are back to normal.

     

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