阿斯特拉加洛西德IV通过通过HSF1/VEGF通路增强血管生成来改善压力过载引起的心力衰竭
Peizhao Du1, Linghao Xu2,3, Yuanqi Wang3
1Department of Cardiology, Baoshan District Hospital of Integrated Traditional Chinese and Western Medicine of Shanghai, Shanghai University of Traditional Chinese Medicine, Shanghai, 201999, China.
Heliyon
|September 19, 2024
概括
阿斯特拉加索酸IV (AS-IV) 通过激活热冲击转录因子1 (HSF1) / VEGF通路,促进血管生长和减少心脏损伤,改善心力衰竭.
科学领域:
- 心血管生物学 心血管生物学
- 药理学 药理学是指药理学的学科.
- 分子机制的分子机制
背景情况:
- 阿斯特拉加索酸IV (AS-IV) 是阿斯特拉加索的一个关键化合物,在治疗心力衰竭方面表现有前途.
- 针对AS-IV的精确分子通路仍然不完全理解.
研究的目的:
- 调查AS-IV在压力过载引起的心力衰竭中的作用.
- 阐明AS-IV治疗效果背后的分子机制,重点关注热冲击转录因子1 (HSF1) 途径.
主要方法:
- 利用网络药理学和分子对接来识别HSF1作为潜在的AS-IV目标.
- 使用心肌微血管内皮细胞 (MMVECs) 进行了体外研究,并在通过横向大动脉收缩 (TAC) 诱导的心力衰竭的小鼠模型中进行了体内实验.
- 评估基因和蛋白质表达,细胞管形成,心脏功能和心肌纤维化,使用包括PCR,西式涂抹,超声波和组织学在内的技术.
主要成果:
- 治疗AS-IV可以提高HSF1/VEGF信号通路中的关键分子的调节.
- 增强了MMVECs的管形成能力,并在体内增加了心肌毛细血管密度.
- 在TAC诱导的心力衰竭小鼠中减少心肌纤维化和改善心脏功能.
结论:
- AS-IV有效地改善了压力过载引起的心力衰竭.
- AS-IV的治疗效果通过调节HSF1/VEGF信号通路来促进血管生成.
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