卡达摩宁通过与KEAP1的分子相互作用激活巨细胞NRF2信号传递来保护糖尿病心肌病
Wenshan Nan1, Jialin Yin2, Wenhao Hao1,2
1Research Center of Translational Medicine, Jinan Central Hospital, Shandong University, 105 Jiefang Rd., Jinan, Shandong 250013, China. hwu@sdu.edu.cn.
Food & function
|October 21, 2024
概括
卡达摩宁 (CAD) 通过减少炎症和氧化应激,有效治疗糖尿病心肌病 (DCM). 这种黄胺激活NRF2通路,为糖尿病心脏病提供了潜在的新疗法.
科学领域:
- 心血管生物学 心血管生物学
- 药理学 药理学是指药理学的学科.
- 代谢疾病 代谢疾病
背景情况:
- 糖尿病心肌病 (DCM) 是糖尿病患者心力衰竭的主要原因.
- 目前DCM的治疗选择有限.
- 卡达摩宁 (CAD) 是一种黄类化合物,具有抗炎和抗氧化特性.
研究的目的:
- 调查卡达蒙因 (CAD) 对糖尿病心肌病 (DCM) 的保护作用.
- 探索CAD作用的潜在机制,重点关注巨细胞两极分化和NRF2激活.
主要方法:
- 在小鼠模型中,使用链毒素和高脂肪饮食,建立了2型糖尿病的模型.
- 通过 gavage,小鼠接受了CAD的治疗.
- 在体外研究中,M1极化巨细胞与CAD进行治疗,并与心肌细胞共同培养.
- 用分子对接和表面等离子体共振测试来确定CAD的分子标.
主要成果:
- 在糖尿病小鼠中,CAD治疗改善了高血糖症,葡萄糖不耐受性,并减轻了心脏功能障碍,增大和亡.
- CAD显著抑制了M1巨细胞的两极分化和随后的心肌细胞损伤.
- CAD激活了核因素红色素2相关因子2 (NRF2) 抗氧化剂信号通路.
- 凯尔奇样ECH相关蛋白1 (KEAP1) 被确定为CAD的分子标,CAD促进了NRF2核转位.
结论:
- 卡达摩宁 (CAD) 在临床前模型中显示出对糖尿病心肌病 (DCM) 的显著保护作用.
- CAD的机制涉及抑制M1巨细胞两极分化,并通过KEAP1.1激活NRF2抗氧化途径.
- 作为DCM治疗的新型治疗剂和NRF2激活剂,CAD具有前景.
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