高脂肪饮食诱导的LCN2通过增强血小板激活来加剧心肌缺血-再输血损伤
Peng Li1, Juhai Chen2, Mingdong Wang3
1Department of Pathology and Pathophysiology, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou 561113, P.R. China.
Molecular medicine reports
|September 20, 2024
概括
高脂肪饮食增加了利波卡林2 (LCN2),这是一种分子,通过促进血小板激活和聚合,使心肌缺血-再输液 (MI/R) 损伤恶化. 淘汰LCN2可以减少MI/R损伤和炎症细胞的招募.
科学领域:
- 心血管生物学 心血管生物学
- 炎症研究 炎症研究
- 代谢综合征是代谢综合征的一种.
背景情况:
- 心肌缺血-反 (MI/R) 损伤涉及炎症,氧化应激和微血管阻塞.
- 血小板通过反应性氧物种,炎症因素和血栓形成加剧MI / R损伤.
- 与代谢风险因素相关的利波卡林2 (LCN2) 对MI/R中血小板功能有未知的影响.
研究的目的:
- 调查LCN2在高脂肪饮食 (HFD) 引起的MI/R损伤中的作用.
- 为了确定LCN2是否影响血小板功能和炎症细胞招募.
- 评估针对MI/R的LCN2的治疗潜力.
主要方法:
- 使用RT-qPCR和ELISA评估了HFD食小鼠的肝脏和血清中的LCN2表达.
- 评估了LCN2对血小板激活,聚合,粘附和P-选择素表达的影响.
- 使用野生型和LCN2淘汰赛小鼠遭受MI/R损伤,随后进行组织学分析和细胞标志物检测.
主要成果:
- 在小鼠中,HFD上调了LCN2表达.
- LCN2加速了血小板的激活,聚合和粘附.
- LCN2淘汰赛减轻了MI/R损伤,并减少了心脏中的血小板和炎症细胞透.
结论:
- 由HFD诱导的LCN2会加剧MI/R损伤,至少部分是通过促进血小板功能.
- 在血小板介导的MI/R损伤中,LCN2起着重要作用.
- 准LCN2可能为MI/R损伤在代谢性疾病环境中提供治疗策略.
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