论文部分内容阅读
目的:探讨甜菜碱对异丙肾上腺素(ISO)诱导的大鼠急性缺血性心肌损伤的保护作用及其对MAPK通路的影响。方法:SD雄性大鼠皮下注射ISO(85 mg·kg-1·d-1,qd,连续2 d)建立急性心肌缺血模型,研究甜菜碱(100,200,400 mg·kg-1·d-1)灌胃给药40 d对缺血性心肌病理结构、抗氧化酶活力、脂质过氧化物含量及MAPK通路相关蛋白表达的影响。结果:甜菜碱(100,200,400 mg·kg-1·d-1)对急性心肌缺血心肌病理结构的损伤具有保护作用,可升高ISO致急性心肌缺血大鼠心肌组织中T-AOC、SOD、GSH-PX的活力,并相应降低脂质过氧化物MDA的含量。甜菜碱(400 mg·kg-1·d-1)显著降低pERK1/2蛋白的表达,并增加p-JNK和p-p38 MAPK蛋白的表达(P<0.01)。单用甜菜碱(400 mg·kg-1·d-1)除可降低ERK1/2的表达外,对心肌组织结构、抗氧化物酶活性及脂质过氧化物含量及其他MAPK通路蛋白表达均无影响。结论:大剂量甜菜碱对异丙肾上腺素致大鼠急性心肌缺血性损伤的保护作用可能与MAPK通路有关。
Objective: To investigate the protective effect of betaine on isoproterenol (ISO) -induced acute ischemic myocardial injury in rats and its effect on MAPK pathway. Methods: Acute myocardial ischemia model was induced in SD male rats by subcutaneous injection of ISO (85 mg · kg-1 · d-1, qd for 2 days). The effects of betaine (100,200,400 mg · kg-1 · d-1) Effects of gastric administration for 40 d on pathological structure, antioxidase activity, lipid peroxidation and expression of MAPK pathway related proteins in ischemic. Results: Betaine (100, 200, 400 mg · kg-1 · d-1) had a protective effect on the pathological structure of acute myocardial ischemia and increased the levels of T-AOC and SOD in myocardium of ISO- GSH-PX activity, and a corresponding reduction of lipid peroxide MDA content. Betaine 400 mg · kg-1 · d-1 significantly decreased the expression of pERK1 / 2 and increased the expressions of p-JNK and p-p38 MAPK (P <0.01). In addition to decreasing the expression of ERK1 / 2, betaine alone (400 mg · kg-1 · d-1) could significantly inhibit cardiac myocyte structure, antioxidant enzyme activity, lipid peroxidation and other MAPK pathway proteins no effect. CONCLUSION: The protective effect of high-dose betaine on isoproterenol-induced acute myocardial ischemic injury may be related to MAPK pathway.