金色化物Rb1 减少由高葡萄糖和内皮功能障碍诱导的超血管收缩在老鼠大动脉中
Jubin Park1,2, You Kyoung Shin1, Uihwan Kim1,2
1Department of Basic Nursing Science, College of Nursing, Korea University, Seoul 02841, Republic of Korea.
Pharmaceuticals (Basel, Switzerland)
|September 28, 2023
概括
金色化物Rb1有效地减少高葡萄糖诱导的高收缩和大鼠大动脉内皮功能障碍. 这种化合物通过受体操作和电压控制的通道抑制的流入,这表明糖尿病相关的血管问题的治疗潜力.
科学领域:
- 药理学 药理学是指药理学的学科.
- 血管生物学 血管生物学
- 内分泌学 在内分泌学.
背景情况:
- 急性高血糖会导致氧化损伤,炎症和血管功能障碍.
- 红人参成分的金色诺化物Rb1 (Rb1) 具有抗糖尿病,抗氧化和抗炎性质.
- 内皮功能障碍 (ED) 是糖尿病的一个关键并发症.
研究的目的:
- 调查Rb1对高葡萄糖 (HG) 诱导的超收缩和ED的有益影响.
- 阐明Rb1在血管光滑肌收缩中的作用的基本机制.
主要方法:
- 鼠类大动脉环的同度张力是使用肌肉学测量.
- 使用N-G-nitro-L-arginine甲基 (L-NAME) 和高葡萄糖 (HG50) 诱导了内皮功能障碍.
- 评估了Rb1对激动剂诱导的血管收缩,细胞外Ca2+流入和从肉质细胞网膜释放的Ca2+的影响.
主要成果:
- 与单独使用HG50或L-NAME相比,L-NAME + HG50显著增加了激动剂诱导的血管收缩.
- 在用L-NAME + HG50.0.治疗的大动脉环中,Rb1显著降低了超收缩.
- Rb1通过受体操作的Ca2+通道 (ROCC) 和电压关闭的Ca2+通道 (VGCC) 抑制了细胞外Ca2+的流入,但没有影响来自肉质细胞网膜的Ca2+释放.
结论:
- 通过抑制ROCC和VGCC,Rb1可以减轻大鼠大动脉中HG诱导的过度收缩和ED.
- 对ATP敏感的K+通道 (KATP) 的激活也可能导致Rb1的作用.
- 在糖尿病中,Rb1显示出作为内皮功能障碍治疗剂的潜力.
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