salvianolic b b通过影响糖尿病小鼠的骨形态发生蛋白4-ROS循环来改善血管内皮功能障碍。
摘要来源：
life sci。 2021年12月1日; 286：120039。 EPUB 2021 10月9日。PMID： 34637797 34637797 Zhang，Li Wang，Chi Wai Lau，Jing-Yan Han，Danzeng Pingcuo，Yu Huang，Limei Liu
文章隶属关系：Jian Liu
摘要：
and ROS in diabetic endothelial dysfunction and explored whether Salvianolic acid B (Sal B) improved endothelial function by affecting BMP4-ROS in diabetic mice.
MAIN METHODS: db/db mice were orally administrated with Sal B (10 mg/kg/day) for one week而db/m+小鼠注射腺病毒载体，提供BMP4（3×10pfu），然后接受了一周的B治疗。通过DHE染色测定ROS水平。通过蛋白质印迹评估蛋白质表达和磷酸化。主动脉环被悬挂在10片中以进行力测量。 Flow-mediated dilatations in the second-order mesenteric arteries were determined by pressure myograph.
KEY FINDINGS: We first revealed the existence of a BMP4-ROS cycle in db/db mice, which stimulated p38 MAPK/JNK/caspase 3 and thus participated in endothelial功能障碍。一周治疗或与SAL B的24 h融合破坏了周期，抑制了p38 mapk/jnk/caspase 3级联，并改善了DB/db小鼠主动脉的内皮依赖性松弛（EDRS）。重要的是，体内SAL B处理还改善了DB/DB小鼠二阶肠系膜动脉的流动介导的扩张。此外，体内BMP4过表达诱导氧化应激，stimulated p38 MAPK/JNK/caspase 3, and impaired EDRs in db/m + mouse aortas, which were all reversed by Sal B.
SIGNIFICANCE: The present study demonstrates that Sal B ameliorates endothelial dysfunction through breaking the BMP4-ROS cycle and subsequently在糖尿病小鼠中抑制p38 mapk/jnk/caspase 3，并为SAL B对糖尿病血管病的好处提供了其他新机制的证据。