克利斯坦丁A在孤立的组织制剂中引起外周血管收缩和心肌抑郁
Kawin Padmaja1, Roshni Parameswaran1, G Srisangeetha2
1Department of Physiology, Christian Medical College, Vellore, India.
Toxicology mechanisms and methods
|July 18, 2023
概括
克利斯坦丁A是一种来自Cleistanthus collinus的毒素,会引起心脏毒性,而不是血管扩张,导致中毒病例的低血压. 粉碎的叶子提取物含有较高的克莱斯坦丁A水平.
科学领域:
- 毒理学 毒理学 毒理学
- 药理学 药理学是指药理学的学科.
- 植物化学 植物化学
背景情况:
- 科林斯 (Cleistanthus collinus) 是一种有毒的植物,在南印度被用来自伤.
- 克利斯坦索化A和克利斯坦丁A是主要的毒素.
- 对于C. collinus毒性的确切机制仍然不完全理解.
研究的目的:
- 为了阐明克莱斯坦丁A毒性的机制.
- 在各种C. collinus提取物中量化Cleistanthoside A和Cleistanthin A.
主要方法:
- 隔离的山羊腿动脉和老鼠后肢制剂被用于评估血管效应.
- 孤立的老鼠心脏实验评估了心肌收缩性.
- 分析高性能液体染色学 (HPLC) 量化了五种不同的叶子提取物中的毒素度.
主要成果:
- 克利斯坦丁 增加了血管张力和大动脉压力,表明血管收缩.
- 心肌研究显示心室压力增加和脉冲压力下降,表明心脏毒性.
- 量化结果显示,煮熟的提取物富含克利斯坦胺A,而碎碎的叶子提取物含克利斯坦胺A较高.
结论:
- 在Cleistanthus collinus中毒的低血压可能是由于心脏毒性,挑战了当前的血管扩张理论.
- 粉碎的叶子制剂是心脏毒剂克莱斯坦丁A的更强有力的来源.
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