英姿,黄斌,匡希斌.痰热清注射液及药效成分黄芩苷对心梗模型小鼠心肌细胞损伤的保护作用.[J].中南医学科学杂志.,2017,(6):567-571. |
痰热清注射液及药效成分黄芩苷对心梗模型小鼠心肌细胞损伤的保护作用 |
Protective effects of Tan-Re-Qing and its absorbed components baicalin on myocardial cell injury after myocardial infarction in mice |
投稿时间:2017-07-04 修订日期:2017-09-26 |
DOI:10.15972/j.cnki.43-1509/r.2017.06.008 |
中文关键词: 痰热清 黄芩苷 心肌梗死 细胞凋亡 |
英文关键词:Tan-Re-Qing baicalin myocardial infarction apoptosis |
基金项目:湖南省自然科学基金(院校联合基金项目);痰热清吸收成分通过抗氧化途径发挥心脏保护作用的机理研究,基金号:2015JJ6099. |
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中文摘要: |
目的 探讨痰热清及其药效成分黄芩苷对小鼠心肌梗死后心肌细胞损伤的保护作用。方法将小鼠随机均分为假手术组、心梗模型组和痰热清高、中、低剂量组,以及高剂量组痰热清对应的黄芩苷含量100 mg/kg作为药效成分组。分别测定小鼠24 h心肌病理形态学检查、梗塞面积、心肌细胞凋亡数目比例、HMGB1、TLR4、NF-kB的表达活性、IL-6、TNF-α、MDA、caspase-3等指标。结果和心梗模型组相比,痰热清高剂量组与药效成分黄芩苷组均能显著改善心肌病理,降低梗死边缘区的心肌细胞凋亡率和梗死区面积,下调心梗小鼠心肌组织中HMGB1/TLR4/NF-kB信号通路以及IL-6、TNF-α、MDA、caspase-3的表达。结论痰热清与其药效成分黄芩苷具有类似的心脏保护药效,其机制涉及改善HMGB1/TLR4/NF-kB信号通路及下游炎性因子,氧化应激及凋亡因子的表达,从而降低小鼠心肌梗死后心肌细胞损伤。 |
英文摘要: |
Objective To investigate the protective effect of Tan-Re-Qing and its main absorption component,baicalin,on myocardial cell injury after myocardial infarction in mice.MethodsC57BL/6 mice were randomly divided into sham operation group,myocardial infarction model group,high,medium and low dose of Tan-Re-Qing group,and baicalin 100 mg/kg contents in high dose group Tan-Re-Qing as absorbed compounds group.24 h myocardial pathology,the number of myocardial infarct size and apoptosis ratio,expression of HMGB1,TLR4 and NF-kB activity,level of IL-6,TNF-α,MDA,caspase-3 were measured and the results were statistically analyzed.ResultsCompared with myocardial infarction model group,Tan-Re-Qing and its absorbed compound baicalin could significantly improve myocardial pathology,reduced infarct marginal zone and cell apoptosis rate of myocardial infarction area,down-regulated the HMGB1/TLR4/NF-kB signaling pathway and the expression of IL-6,TNF-α,MDA,caspase-3.ConclusionTan-Re-Qing and its absorbed compound baicalin has similar heart protection effect,its mechanism relates to the improvement of HMGB1/TLR4/NF-kB signaling pathway and expression of their downstream inflammatory factors,oxidative stress and apoptosis factors,thereby reducing myocardial cell injury after myocardial infarction in mice. |
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