基于斑马鱼模型和网络药理学探究金露梅抗心肌缺血作用机制
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1.青海师范大学 生命科学学院 青海省药用动植物资源重点实验室;2.1.青海师范大学 生命科学学院 青海省药用动植物资源重点实验室 2.高原科学与可持续发展研究院

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Q501

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(2020-ZJ-918);


Based on zebrafish model and network pharmacology to invesetigate the mechanism of anti-myocardial ischemia action of Potentilla fruticosa L
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Qinghai Normal University

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    摘要:

    基于盐酸异丙肾上腺素诱导斑马鱼心肌细胞凋亡模型探究金露梅水提物对其的影响机制。前期试验确定最大耐受浓度(MTC)为15.63 μg?mL-1,并依据MTC划分高中低剂量组分别为7.81 μg?mL-1(1/2 MTC)、2.60 μg?mL-1(1/6 MTC)、0.868 μg?mL-1(1/18 MTC),阳性药物组为N-乙酰半胱氨酸(125 μg?mL-1)。心肌细胞凋亡荧光强度作为实验后期的测量指标。金露梅水提物高中低剂量组抗心肌缺血的功效分别为:36%、40%、49%,借助斑马鱼心脏荧光强度表型图发现金露梅水提物与阳性药物组对比具有明显的防治心肌缺血功效。最后使用网络药理学及分子对接技术预测金露梅有效成分抑制心肌细胞凋亡,减缓心肌缺血的可能作用机制。Rap1信号通路、癌症通路、癌症中的蛋白巨糖、PI3K-Akt信号通路、脂质和动脉粥样硬化5条通路有关。

    Abstract:

    Based on the model of zebrafish cardiomyocyte apoptosis induced by isoproterenol hydrochloride, studied the effect of water extract of Potentilla fruticosa on zebrafish cardiomyocyte apoptosis.The maximum tolerance concentration (MTC) was determined to be 15.63 μg?mL-1, and was divided into high, middle and low dose groups of 7.81 μg?mL-1 (1/2 MTC), 2.60 μg?mL-1 (1/6 MTC) and 0.868 μg?mL-1 (1/18 MTC) according to MTC. The positive drug group was N-acetylcysteine (125 μg?mL-1). In the later stage, using the fluorescence intensity of cardiomyocytes apoptosis as the measurement index, getted the efficacy of the high, middle and low dose group of Potentilla fruticosa water extract was 36%, 40% and 49%, respectively. Moreover, the phenotype of zebrafish heart fluorescence intensity showed that Potentilla fruticosa water extract had obvious prevention and treatment effect on myocardial ischemia compared with the positive drug group. Finally, according to the network pharmacological research method, the mechanism of Potentilla fruticosa inhibiting the apoptosis of cardiomyocytes and slowing myocardial ischemia may be related to Rap1 signaling pathway, cancer pathway, protein megalose in cancer, PI3K-Akt signaling pathway, lipid and atherosclerosis.

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田雪花,左文明,刘力宽,等. 基于斑马鱼模型和网络药理学探究金露梅抗心肌缺血作用机制[J]. 科学技术与工程, , ():

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  • 收稿日期:2024-01-04
  • 最后修改日期:2024-04-12
  • 录用日期:2024-04-25
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