伊诺斯
安普克
肺动脉高压
山奈酚
信号转导
医学
药理学
心脏病学
内科学
化学
一氧化氮
蛋白激酶A
激酶
生物化学
槲皮素
一氧化氮合酶
抗氧化剂
作者
Xin Xie,Huiru Li,Liangqi Wang,Xiaonan Zhang,Dianxiang Lu,Zhanqiang Li
标识
DOI:10.1177/1934578x241274896
摘要
Background Previous studies have found that kaempferol can relieve pulmonary hypertension (PH). Objective Explore the protective impact of kaempferol on pulmonary vascular endothelium in rats with high altitude pulmonary hypertension (HAPH). Materials and methods In a simulated altitude of 5000 m environment, rats were induced to develop HAPH after continuous intragastric administration of kaempferol (25, 50 and 100 mg·kg −1 ) and Sildenafil (30 mg·kg −1 ) for 28 days. Assessment of isolated pulmonary arterial rings in rats and relevant indicators in lung tissue was performed, with the mechanism of action investigated using Western blotting. Results Kaempferol effectively dilates rat pulmonary arterial rings, with an EC 50 of 55.75 μmol/L. L-NAME can effectively counteract the vasodilatory effect of kaempferol. Acetylcholine demonstrated better relaxation of pulmonary arterial rings in HAPH rats after kaempferol intervention. Elastic Van Gieson staining (EVG) and immunohistochemistry (CD31) results indicate that kaempferol can partially protect pulmonary vascular endothelial function in HAPH rats. Western blotting reveals that kaempferol has the ability to regulate the Renin-Angiotensin System (RAS). This leads to a compensatory increase in eNOS expression, upregulation of AMPK activity, and downregulation of eNOS monomer/dimer levels. Conclusions Kaempferol can improve pulmonary vascular endothelial dysfunction caused by chronic hypoxia by upregulating the phosphorylation level of AMPK, regulating the RAS system, and inhibiting eNOS uncoupling, thereby achieving vasodilation and endothelial protection.
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