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柏柏林通过通过RAGE-NF-κB通路调节自和炎症来缓解动脉样硬化

Peng Zhang¹, Meiying Jin², Lei Zhang³

¹College of traditional Chinese medicine, Binzhou Medical University, Yantai, China.

Frontiers in pharmacology

|April 15, 2025

概括

柏柏林 (BBR) 通过激活自和调节炎症来缓解动脉样硬化. 这项研究澄清了BBR减少脂质沉积和斑块面积的机制,提供了新的治疗见解.

科学领域:

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

背景情况:

动脉样硬化 (AS) 的进展与脂质积累和泡细胞形成有关.
异常的自在AS发展中起着关键作用.
柏柏林 (BBR) 已知会影响AS,但其在自调节和减轻炎症方面的确切作用尚不清楚.

研究的目的:

通过激活自和减少炎症来研究BBR在缓解AS中的作用和机制.
通过自调节来探索BBR对AS的治疗潜力.

主要方法:

网络药理学被用来预测AS中BBR的机制.
为了验证预测的机制,进行了体内 (ApoE-/-小鼠) 和体外实验.
分析了主要的脂质特征,组织学变化 (HE,油红 O) 和蛋白质表达 (RAGE,p-NF-κB,自标志物).

主要成果:

在体内,BBR治疗减少了大动脉脂沉积和动脉样硬化斑块区域.
BBR调节了与炎症相关的信号通路,降低了RAGE,p-NF-κB,TNF-α和P62,同时增加了IL-10,CD31,VEGF,LC3B和Beclin1.
试验室结果证实了体内发现,NF-κB激活剂1减弱了BBR的影响.

结论:

BBR有效地缓解了动脉样硬化的进展.
BBR通过调节RAGE和p-NF-κB信号通路并激活自来发挥其治疗作用.
这些发现为BBR作为AS的潜在治疗剂提供了机制基础.

关键词:

在RAGE-NF-κB信号通路中.动脉样硬化动脉样硬化自自是自的过程.柏柏林氨酸是什么柏柏林氨酸是什么网络药理学网络药理学

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