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传统中药黄芩苷对急性力竭运动后大鼠心肌损伤保护作用 被引量:3

Protective Effect of Baicalin on Myocardial Injury in Rats after Acute Exhaustive Exercise
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摘要 黄芩苷(Baicalin)是从双子叶唇形科植物黄芩(Scutellaria baicalensis Georgi)的干燥根中提取分离出来的一种黄酮类化合物,具有显著的抑菌、利尿、抗炎、抗变态及解痉等生物活性。为了试图探究黄芩苷对急性力竭运动后大鼠心肌损伤的影响及可能机制。研究结果显示,与对照组比较,力竭运动组大鼠左心室短轴缩短率(LVFS)和射血分数(LVEF)显著降低(P<0.05),左心室收缩期直径(LVIDs)和舒张期直径(LVIDd)显著升高(P<0.05);与力竭运动组比较,中、高剂量黄芩苷组大鼠LVFS和LVEF显著升高(P<0.05),LVIDs和LVIDd显著降低(P<0.05),而低剂量黄芩苷组各指标无显著变化(P>0.05)。对照组大鼠心肌组织细胞排列紧密且规则,结构清晰,染色较为均匀;力竭运动组大鼠心肌组织细胞排列紊乱,细胞质中出现空泡,染色不均匀;中、高剂量黄芩苷组心肌组织细胞排列紊乱和染色不均现象较力竭运动组大鼠得到明显改善。与对照组比较,力竭运动组大鼠心肌组织MDA含量显著升高(P<0.05),SOD和GSH-Px水平显著降低(P<0.05),胞浆Nrf2、胞核Nrf2和HO-1蛋白表达水平均显著升高(P<0.05);与力竭运动组比较,中、高剂量黄芩苷组大鼠心肌组织MDA含量显著降低(P<0.05),SOD和GSH-Px水平显著升高(P<0.05),胞核Nrf2和HO-1蛋白表达水平均显著升高(P<0.05),胞浆Nrf2蛋白表达水平显著降低(P<0.05),而低剂量黄芩苷组各指标无显著变化(P>0.05)。黄芩苷可保护力竭运动后大鼠心肌损伤,其作用机制可能与激活Nrf2/HO-1信号通路降低氧化应激反应有关。 To investigate the effect of baicalin on myocardial injury in rats after acute exhaustion and its possible mechanism.Sixty rats were randomly divided into control group,exhausted exercise group,low-dose baicalin group,middle-dose baicalin group and high-dose baicalin group,12 rats in each group.Rats in the low,medium and high dose baicalin group were administrated with 20,40,80 mg/kg baicalin solution daily,while the control group and the exhausted exercise group were administrated with an equal volume of normal saline.After continuous intragastric administration for 14 days,the rats in the exhausted exercise group and the low,medium and high dose baicalin group were subjected to exhausted exercise,while the control group rats were not exercised.Echocardiography was used to detect cardiac function indicators in rats,and HE staining were used to observe changes in rat myocardial tissue structure.Enzyme-linked immunosorbent assay was used to detect the level of MDA,SOD and GSH-Px in rat myocardial tissue.Western Blot method was used to detect the expression level of Nrf2 and HO-1 protein in myocardial tissue.Compared with the control group,LVFS and LVEF of the exhausted exercise group were significantly reduced(P<0.05),while LVIDs and LVIDd were significantly increased(P<0.05);compared with the exhausted exercise group,LVFS and LVEF in the medium and high dose baicalin group were significantly increased(P<0.05),LVIDs and LVIDd were significantly reduced(P<0.05),but there was no significant change in each index in the low-dose baicalin group(P>0.05).Myocardial tissue cells in the control group were arranged tightly and regularly with clear structure and uniform staining.Myocardial tissue cells in the exhausted exercise group were disordered with vacuoles in the cytoplasm and uneven staining.Disorders of cell arrangement and uneven staining were significantly improved compared with those in the exhausted exercise group.Compared with the control group,MDA content of myocardial tissue in the exhausted exercise group was significantly increased(P<0.05),the levels of SOD and GSH-Px were significantly reduced(P<0.05),and the expression levels of cytoplasmic Nrf2,nuclear Nrf2 and HO-1 protein were significantly increased(P<0.05);compared with the exhausted exercise group,MDA content in the myocardial tissue of the rats in the medium and high dose baicalin group were significantly reduced(P<0.05),the levels of SOD and GSH-Px were significantly increased(P<0.05),the expression levels of nuclear Nrf2 and HO-1 protein protein were increased significantly(P<0.05),while the expression levels of cytoplasmic Nrf2 protein were decreased significantly(P<0.05),but there was no significant change in the indexes of the low-dose baicalin group(P>0.05).Baicalin can protect myocardial injury in rats after exhaustive exercise,and its mechanism may be related to activation of Nrf2/HO-1 signaling pathway to reduce oxidative stress response.
作者 靳莉丹 Jin Lidan(Zhengzhou Institute of Industrial Application Technology,Zhengzhou,451100)
出处 《分子植物育种》 CAS 北大核心 2022年第6期2070-2075,共6页 Molecular Plant Breeding
基金 河南省软科学研究支持项目(212400410172)资助。
关键词 黄芩苷 心肌损伤 氧化应激 Nrf2/HO-1信号通路 Baicalin Myocardial injury Oxidative stress Nrf2/HO-1 signaling pathway
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