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首页> 外文期刊>Biological trace element research >Cardioprotective Effect of Aloe vera Biomacromolecules Conjugated with Selenium Trace Element on Myocardial Ischemia-Reperfusion Injury in Rats
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Cardioprotective Effect of Aloe vera Biomacromolecules Conjugated with Selenium Trace Element on Myocardial Ischemia-Reperfusion Injury in Rats

机译:芦荟生物致铬与硒微量元素缀合的心脏保护作用对大鼠心肌缺血再灌注损伤的影响

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The present study was undertaken to evaluate the cardioprotection potential and underlying molecular mechanism afforded by a selenium (Se) polysaccharide (Se-AVP) from Aloe vera in the ischemia-reperfusion (I/R) model of rats in vivo. Myocardial I/R injury was induced by occluding the left anterior descending coronary artery (LAD) for 30 min followed by 2-h continuous reperfusion. Pretreatment with Se-AVP (100, 200, and 400 mg/kg) attenuated myocardial damage, as evidenced by reduction of the infarct sizes, increase in serum and myocardial endogenous antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT)), and decrease in the malondialdehyde (MDA) level in the rats suffering I/R injury. This cardioprotective activity afforded by Se-AVP is further supported by the decreased levels of cardiac marker enzymes creatine kinase (CK) and lactate dehydrogenase (LDH), as well as the rise of myocardial Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities in I/R rats. Additionally, cardiomyocytic apoptosis was measured by terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining and the result showed that the percent of TUNEL-positive cells in myocardium of Se-AVP-treated groups was lower than I/R rats. In conclusion, we clearly demonstrated that Se-AVP had a protective effect against myocardial I/R injury in rats by augmenting endogenous antioxidants and protecting rat hearts from oxidative stress-induced myocardial apoptosis.
机译:本研究旨在评估由芦荟(SE)多糖(SE-AVP)在体内大鼠缺血再灌注(I / R)模型中的亚硒酸钠(SE-AVP)提供的心脏保护潜力和潜在的分子机制。通过封闭左前期下降冠状动脉(LAD)诱导心肌I / R损伤30分钟,然后连续再灌注2-H连续再灌注。通过减少梗塞尺寸的减少,血清和心肌内源性抗氧化剂(超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH)增加,可通过减少心肌损伤的预处理(100,200和400 mg / kg)减弱的心肌损伤过氧化氢酶(猫)),并降低患有I / R损伤的大鼠的丙二醛(MDA)水平。通过SE-AVP提供的这种心脏保护活性进一步支持通过减少的心脏标记酶肌酸​​激酶(CK)和乳酸脱氢酶(LDH)以及心肌Na + -K + -ATP酶和CA2 + -MG2 + -ATP酶活性的升高在I / R大鼠。另外,通过末端 - 脱氧核苷酸转移酶介导的切口末端标记(TUNEL)染色测量心肌细胞凋亡,结果表明,SE-AVP处理基团心肌中的TUNEL阳性细胞的百分比低于I / R大鼠。总之,我们清楚地证明,通过增强内源性抗氧化剂和保护大鼠心脏免受氧化应激诱导的心肌细胞凋亡,SE-AVP对大鼠心肌I / R损伤具有保护作用。

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