通过细胞保护对5-甲诱导心脏毒性的甲福明的作用的评估
Nahlah Fahad Alreshidi1, Reham Abdullah Al-Dhelaan2, Amjad Yousuf3,4
1Department of Internal Medicine, University of Hail, Hail, Saudi Arabia.
概括
甲福明可能会保护心脏细胞免受5-Fluorouracil (5-FU) 化疗损伤. 这项研究表明,甲福明可以降低暴露于5-FU的人类心脏肌细胞中的氧化应激和亡.
科学领域:
- 心脏病学 心脏病学
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 5-甲 (5-FU) 是用于癌症治疗的重要化疗药物.
- 5-FU可以引起心脏毒性,治疗选择有限.
- 目前对5-FU心脏毒性的治疗依赖于标准的心力衰竭药物.
研究的目的:
- 调查甲福明在减轻5-FU诱导心脏毒性的潜力.
- 检查甲福明对人类心脏肌细胞 (HCM) 氧化应激,亡和线粒体功能障碍的影响.
主要方法:
- 通过MTT测定确定最佳的5-FU剂量.
- 用甲治疗了暴露于5-FU的HCM细胞.
- 评估了反应性氧物种 (ROS),谷氨酸 (GSH),超氧化脱酶 (SOD) 活性,细胞染色体c释放,线粒体膜潜力,BAX/Bcl-2表达和Caspase-3活性.
主要成果:
- 5-FU增加了ROS,降低了GSH,并降低了SOD活性.
- 甲胺可以逆转这些氧化应激标志物.
- 5-FU诱导了细胞亡和线粒体功能障碍,这使得甲福林剂量依赖性显著降低.
结论:
- 甲胺显示了对5-FU诱导的心脏毒性的治疗潜力.
- 甲胺可降低HCM细胞中的氧化应激,亡和线粒体功能障碍.
- 这些发现表明甲福明是5FU治疗患者的潜在保护剂.
更多相关视频
08:03Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation
Published on: October 20, 2022
2.0K
06:21Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
Published on: May 10, 2024
1.6K
相关概念视频
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
84
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
84
Oral Hypoglycemic Agents: Biguanides and Glitazones
998
Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
998
