二甲素I通过调节AKT和MAPK信号通路来减少H9c2细胞损伤
Ya-Chao Wang1,2, Yi-da Shao1,2, Chang-le Shao1,2
1School of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
In vitro cellular & developmental biology. Animal
|January 22, 2024
概括
二坦辛I (DHT) 通过减少亡和氧化应激,保护心脏细胞免受损伤. 这种化合物可以通过调节关键信号通路来提供心血管疾病的治疗策略.
科学领域:
- 心血管研究的心血管研究.
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 心血管疾病仍然是全球主要的死亡原因.
- 二坦辛I (DHT) 已显示出改善心肌损伤后心脏功能的潜力.
- 了解心脏细胞中DHT的保护机制对于治疗的发展至关重要.
研究的目的:
- 为了研究二中素I (DHT) 对受到氧气-葡萄糖剥夺/氧化恢复 (OGD/R) 损伤的H9c2细胞的保护作用.
- 阐明DHT心脏保护作用的潜在机制,重点关注氧化应激和细胞亡.
- 评估DHT对涉及心脏损伤的关键细胞信号通路的影响.
主要方法:
- 在H9c2心脏细胞中建立氧气-葡萄糖剥夺/再氧化 (OGD/R) 损伤模型.
- 治疗OGD/R受伤的细胞,使用不同度的Dihydrotanshinone I (DHT).
- 评估细胞活力,细胞亡,氧化应激标志物 (MDA,SOD,ROS,超氧化物) 和蛋白质酸化 (AKT,ERK,P38MAPK).
主要成果:
- 在0.1μmol/L的Dihydrotanshinone I (DHT) 时,在24,48,72小时没有影响H9c2细胞的增殖.
- 在H9c2细胞中,DHT显著降低了OGD/R诱导的亡和氧化应激,降低了MDA和增加了SOD水平.
- DHT减轻了线粒体的活性氧物种 (ROS) 和超氧化物水平,并调节了AKT,ERK和P38MAPK信号通路的酸化.
结论:
- 二坦辛I (DHT) 对H9c2细胞中OGD/R诱导的损伤具有显著的心脏保护作用.
- DHT减少了亡和氧化应激,可能通过调节AKT,ERK和P38MAPK信号通路.
- DHT代表了一种有前途的治疗药物,可以缓解心肌损伤和心血管疾病.
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