急性耐力运动使心肌氧化应激-自噬通量-凋亡信号向稳态平衡的变化趋势调整

发布时间：2018-04-22 06:06

  本文选题：急性耐力运动 + 心肌组织　； 参考：《首都体育学院学报》2017年06期

【摘要】：探讨交通相关微粒(diesel exhaust particles,DEP)悬液急性滴注对心肌氧化应激、细胞自噬和凋亡信号的影响及急性耐力运动的调节功能与干预作用。方法:8周健康雄性C57BL/6小鼠,随机分为对照组(Con)、急性耐力运动组(AE)、急性染毒组(DEP)和急性耐力运动+染毒组(AE+DEP),每组均6只。DEP组和AE+DEP组进行一次急性DEP染毒滴注(1 mg/kg)。随后,AE组和AE+DEP组进行一次75%VO_(2max)的急性耐力跑台运动(12 m/min,90 min)。运动后恢复12 h后断颈椎处死,摘取心脏。酶标仪测心肌氧化应激水平(MDA、SOD、CAT和H_2O_2等),Western blotting测心肌自噬相关蛋白(Atg5、LC3、P62、Beclin1和UVRAG等)和凋亡相关蛋白(Caspase 3和PARP等)表达水平。结果:1)DEP可使心肌MDA和H_2O_2含量显著升高,CAT活性明显下降,而急性耐力运动可显著抑制DEP介导的心肌MDA和H_2O_2含量升高,并抑制CAT活性下降;2)DEP可显著上调心肌自噬蛋白Atg5、LC3-Ⅱ表达和LC3-Ⅱ/LC3-Ⅰ比率,降低P62蛋白表达,但Beclin1通路自噬关键蛋白Beclin1和UVRAG表达却无显著变化,而急性耐力运动可显著抑制DEP介导的心肌Atg5和LC3-II蛋白表达升高、LC3-Ⅱ/LC3-Ⅰ比率上调,并抑制P62蛋白表达下降,但对Beclin1和UVRAG蛋白表达未造成显著影响;3)DEP可显著上调心肌凋亡相关蛋白Caspase 3和PARP的表达,而急性耐力运动可抑制心肌Caspase3蛋白过量表达,并显著降低PAR P蛋白表达。结论:DEP可使心肌产生明显的氧化应激反应,致使心肌自噬通量水平过量增加,进而诱导心肌细胞凋亡。急性耐力运动可下调心肌氧化应激水平,抑制DEP介导的心肌自噬过度激活和细胞凋亡。提示:急性耐力运动使心肌氧化应激-自噬通量-凋亡信号具有向稳态平衡方向发展的变化趋势。
[Abstract]:To investigate the effects of acute infusion of diesel exhaust particlesl (DEP) suspension on myocardial oxidative stress, autophagy and apoptotic signal, and the regulatory function and intervention effect of acute endurance exercise. Methods healthy male C57BL/6 mice were randomly divided into control group, acute endurance exercise group, acute endurance exercise group and acute endurance exercise group. Then the AE group and AE DEP group were given an acute endurance treadmill exercise of 12 m / min / min ~ 90 min ~ (-1) and 75 m 路min ~ (2) 路min ~ (-1) 路min ~ (-1) 路min ~ (-1) respectively. After 12 hours of exercise, the cervical vertebrae was amputated and the heart was removed. The level of oxidative stress in myocardium was measured by enzyme scale. The expressions of ATG5LC3 P62 Beclin1 and UVRAG) and apoptosis-related proteins (Caspase 3 and PARP, etc.) were measured by Western blotting. Results the content of MDA and H_2O_2 in myocardium was significantly increased and the activity of catalase was significantly decreased, while acute endurance exercise could significantly inhibit the increase of MDA and H_2O_2 in myocardium mediated by DEP. In addition, inhibiting the decrease of CAT activity could significantly up-regulate the expression of myocardial autophagy protein Atg5tLC3- 鈪，

本文编号：1785914