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新优化的Sheng-Mai-San公式的机制通过NMDAR途径调节心肌细胞亡

Yazhu Hou¹, Zixun He^1,2, Yixiao Han³

¹Department of Cardiovascular Diseases, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300381, China.

|July 7, 2023

概括

在心力衰竭模型中,新的优化Sheng-Mai-San (NO-SMS) 改善了心脏功能,并减少了心肌细胞亡. 这种草药配方可以通过调节NMDAR信号通路并降低和ROS水平来起作用.

科学领域:

心血管医学心血管医学
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:

缺血性心力衰竭 (HF) 构成严重的健康风险.
新优化的Sheng-Mai-San (NO-SMS) 是一种草药配方,有效改善心脏功能,减缓HF患者的纤维化.
NO-SMS在治疗高血压时的精确机制,特别是其对心肌细胞亡的影响,需要进一步研究.

研究的目的:

研究NO-SMS在治疗心力衰竭中的作用机制,重点关注其与心肌细胞亡的关系.
评估NO-SMS在改善心脏功能和抑制心肌纤维化中的疗效,在HF的体内大鼠模型中.
评估NO-SMS在H9c2心肌细胞中对亡的保护作用,这些心肌细胞在体外受到氧化和刺激性压力.

主要方法:

在体内:雄性SD大鼠诱导心力衰竭 (EF ≤ 50%) 被用NO-SMS,伊芬产或埃纳拉普利尔治疗了4周. 评估了心脏功能,结构变化和亡标志物.
在体外:使用H2O2和NMDA损伤了H9c2心肌细胞. 细胞被用NO-SMS和含有Ifenprodil的血清治疗,并使用Annexin V-FITC/PI染色测量了细胞亡.
用西方斑点,qRT-PCR,ELISA和流式细胞计量来评估亡.

主要成果:

与模型组相比,NO-SMS显著改善了HF大鼠的心脏功能,并延迟了心肌纤维化.
在体外和体外模型中,NO-SMS和Ifenprodil降低了亲细胞亡蛋白,mRNA和细胞内Ca2+和ROS水平的表达.
受损心肌细胞的亡率显著降低,心肌细胞亡被NO-SMS有效抑制.

结论:

在HF大鼠中,NO-SMS配方有效地改善了心脏功能,并抑制了心室重塑和心肌细胞亡.
NO-SMS的机制可能涉及NMDAR信号通路的调节.
NO-SMS在抑制心肌细胞中过度的细胞内Ca2+流入和ROS产生方面表现出潜力,从而保护心肌细胞免受亡.

关键词:

心肌细胞的亡是心肌细胞的亡.心血管疾病是什么心血管疾病在NMDAR路径上.没有-SMS.

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