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血小板在动脉巴罗反射功能障碍期间破坏血脑屏障的贡献
Bowen Shen1, Lili Yang1, Xiaoli Jia2
1Institute of Pharmacology, Shandong First Medical University & Shandong Academy of Medical Sciences, Tai'an 271016, China.
Microvascular research
|March 17, 2024
概括
血小板通过CD40L破坏动脉巴罗反射功能障碍中的血脑屏障,激活NF-kB信号,并增加矩阵金属蛋白酶-9. 向CD40L可能治疗相关的大脑疾病.
科学领域:
- 神经科学是一个神经科学.
- 心血管生理学心血管生理学
- 血管生物学 血管生物学
背景情况:
- 动脉巴罗反射 (ABR) 功能障碍与中枢神经系统疾病和血脑屏障 (BBB) 破坏有关.
- 导致ABR功能障碍中BBB干扰的确切机制尚不清楚.
- 这项研究调查了血小板在ABR功能障碍期间在BBB完整性中的作用.
研究的目的:
- 为了探索血小板在血脑屏障中与动脉巴罗反射功能障碍相关的破坏中的作用.
- 阐明涉及血小板CD40L和NF-kB信号传递在BBB损伤中的分子机制.
主要方法:
- 动脉巴罗反射功能障碍在老鼠中通过阴道动脉变性诱导.
- 使用埃文斯蓝色和FITC-dextran泄漏评估了血脑屏障的完整性.
- 血小板CD40L表达,聚合和对内皮细胞的影响使用免疫组织化学,西部抹杀和ELISA进行了分析.
主要成果:
- 阴道膜脱皮导致BBB的通透性和下调紧接口蛋白 (zonula occludens-1,occludin).
- 来自ABR功能障碍大鼠的血小板显示CD40L表达和聚合增加,导致健康大鼠和内皮细胞的BBB破坏.
- 这些效应是由NF-kB信号激活和矩阵金属蛋白酶-9上调调节的介导,部分由抗CD40L抗体或克洛皮多格雷尔抑制.
结论:
- 通过CD40L,血小板可以通过激活大脑微血管内皮细胞中的NF-kB信号来破坏ABR功能障碍中的BBB.
- 矩阵金属蛋白酶-9的升调是这种血小板介导的内皮细胞激活的关键结果.
- 向CD40L为与动脉巴罗反射功能障碍相关的大脑疾病提供了潜在的治疗策略.
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