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格玛克龙通过调节PI3K/AKT介导的氧化应激,炎症和亡来缓解心脏重塑

Zhao Fang¹, Feierkaiti Yushanjiang¹, Guangji Wang²

¹Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China; Hubei Key Laboratory of Cardiology, Wuhan 430060, China.

International immunopharmacology

|September 8, 2023

概括

格尔马克龙 (germacrone) 是一种来自草 (Rhizoma curcuma) 的化合物,通过减少氧化应激,炎症和亡来防止心脏重塑. 它抑制了氨基酸3-激酶 (PI3K) /蛋白激酶B (AKT) 途径,提供了一个潜在的治疗策略.

科学领域:

心血管研究研究心血管研究
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

心脏重塑是心血管疾病的重要后果,与氧化应激,炎症和亡密切相关.
格尔马克龙是一种来自Rhizoma curcuma的生物活性化合物,表现出已知的抗氧化,抗炎和抗丧性质.

研究的目的:

为了研究基马克龙对异二醇 (ISO) 诱导的心脏重塑的保护作用.
为了阐明基尔马克龙的心脏保护作用的潜在分子机制.

主要方法:

在体内研究使用C57BL/6小鼠接受ISO注射和germacrone治疗.
在体外研究使用新生小鼠心肌细胞 (NRCMs) 来评估ISO诱导的心脏损伤.
对氨基酸3-激酶 (PI3K) /蛋白激酶B (AKT) 路径激活的分析.

主要成果:

ISO的使用导致了显著的氧化应激,炎症和心脏组织和心肌细胞的亡.
格尔马克龙治疗显著减轻了这些ISO诱导的有害影响,减轻了心肌重塑和改善心脏功能.
格玛克隆抑制PI3K/AKT通路的激活,并且阻断该通路取消了格玛克隆的保护作用.

结论:

格尔马克龙通过减轻氧化应激,炎症和亡,显示出对心脏重塑的显著心脏保护作用.
该机制涉及PI3K/AKT信号通路的抑制.
格玛克龙代表了治疗心脏改造与心血管疾病相关的有前途的治疗候选者.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.进行心脏重塑.德玛克龙 (Germmacrone) 是一个微小的植物.炎症炎症是一种炎症.氧化应激是一种氧化应激.在PI3K/AKT中使用.

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