蒙特卢卡斯特改善2K1C-高血压诱导的内皮功能障碍和相关的血管痴呆症
Surbhi Gupta1, Prabhat Singh2, Bhupesh Sharma3
1Department of Pharmacology, School of Pharmacy, Bharat Institute of Technology, Partapur Bypass, Meerut, Uttar Pradesh, India.
Current hypertension reviews
|January 9, 2024
概括
在大鼠中,高血压诱导的血管痴呆症被CysLT1抗剂蒙特卢卡斯特逆转. 这种药物减少了认知缺陷,氧化应激和炎症,为治疗血管高血压相关的大脑损伤提供了潜力.
科学领域:
- 神经科学是一个神经科学.
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 功能下降和高血压与认知缺陷,痴呆症和脑损伤有关.
- 血管性痴呆症 (VaD) 构成了重大的公共卫生挑战,需要对其风险因素进行研究.
- 氨酸白血 (CysLT1) 受体在认知,炎症和神经发生过程中发挥作用.
研究的目的:
- 为了研究蒙特卢卡斯特的作用,一个CysLT1抗剂,在血管痴呆症 (VaD) 诱导的血管高血压在一个2-脏-1-剪辑 (2K1C) 鼠标模型.
- 评估蒙特卢卡斯特减轻认知衰退和相关的病理变化的潜力.
主要方法:
- 在使用2K1C模型的雄性大鼠中诱导了血管高血压.
- 用莫里斯水迷宫评估认知功能.
- 测量包括平均动脉压,氧化应激标志物,炎症性细胞因子,内皮功能和脑损伤.
主要成果:
- 2K1C大鼠表现出认知缺陷,血压升高,内皮功能障碍,大脑氧化应激,炎症和脑损伤.
- 蒙特卢卡斯特治疗 (5.0和10.0毫克/公斤-1) 剂量取决于改善认知行为和减少生化和病理标志物.
- 蒙特卢卡斯特治疗缓解了高血压引起的行为,生化,内皮功能和脑梗塞的损伤.
结论:
- 2K1C模型成功诱导了血管高血压和相关的血管痴呆症 (VaD).
- 蒙特卢卡斯特的使用有效地通过向CysLT1受体减轻了血管高血压诱导的VaD的影响.
- 蒙特卢卡斯特在治疗血管高血压诱导的VaD方面显示出进一步评估的希望.
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