CEBPD 调节氧化应激和炎症反应 在高血压心脏重塑中
Jinghong Zhao1, Jilin Hu, Rongyi Zhang
1Department of Cardiology, Nanchong Central Hospital, Nanchong, China.
Shock (Augusta, Ga.)
|September 26, 2023
概括
通过降低氧化应激和炎症,CCAAT/增强剂结合蛋白三角 (CEBPD) 的上调减轻高血压心脏重塑. CEBPD促进了miR-96-5p,它抑制了内醇1,4,5-三酸盐受体1 (IP3R),以保护心脏.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 细胞生理学 细胞生理学
背景情况:
- 高血压是心脏重塑和死亡的主要原因.
- 基础高血压心脏改造的分子机制,特别是氧化应激和炎症,需要进一步阐明.
研究的目的:
- 研究CCAAT/增强剂结合蛋白三角 (CEBPD) 在高血压心脏重塑中的作用.
- 探索涉及CEBPD,miR-96-5p和内醇1,4,5-三酸盐受体1 (IP3R) 调节氧化应激和炎症的分子途径.
主要方法:
- 通过注射 ангиотензин-II 建立了使用高血压的小鼠模型.
- 使用体内和体外模型与CEBPD过度表达来评估心脏功能,组织学变化,细胞活力,氧化应激标志物和炎症因素.
- 经过验证的分子相互作用使用促进剂丰富,化酶试验和基因沉默/过度表达实验.
主要成果:
- 在高血压心脏组织中,CEBPD水平下降.
- 对CEBPD的升调改善了心脏功能,减轻了心脏纤维化和缩,并减少了氧化应激和炎症标志物 (ROS,LDH,MDA,TNF-α,IL-1β,IL-6).
- CEBPD促进了miR-96-5p的表达,这反过来又对IP3R进行了负面调节. 沉默miR-96-5p或过度表达IP3R可以逆转CEBPD的保护作用.
结论:
- 在高血压心脏重塑过程中,CEBPD起着保护作用.
- CEBPD/miR-96-5p/IP3R轴抑制氧化应激和炎症,从而减轻心脏重塑.
- 针对CEBPD途径可能为高血压引起的心脏病提供治疗策略.
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