Chrysin Alleviates Monocrotaline-Induced Pulmonary Hypertension in Rats Through Regulation of Intracellular Calcium Homeostasis in Pulmonary Arterial Smooth Muscle Cells
| Autor: | Xiuqing Chen, Jun Zhang, Zhiping Guo, Yufei Peng, Licheng Zhu, Fang Dong, Suya Zhang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Hypertension Pulmonary 030204 cardiovascular system & hematology Pharmacology Pulmonary Artery Vascular Remodeling TRPC4 Muscle Smooth Vascular TRPC6 TRPC1 Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Right ventricular hypertrophy medicine Ventricular Pressure Animals Arterial Pressure Chrysin Calcium Signaling Antihypertensive Agents TRPC Cation Channels Flavonoids Monocrotaline biology Hypertrophy Right Ventricular Ventricular Remodeling Chemistry medicine.disease Pulmonary hypertension Proliferating cell nuclear antigen Disease Models Animal 030104 developmental biology biology.protein Ventricular pressure Ventricular Function Right Cardiology and Cardiovascular Medicine |
| Zdroj: | Journal of cardiovascular pharmacology. 75(6) |
| ISSN: | 1533-4023 |
| Popis: | Chrysin (CH) is the main ingredient of many medicinal plants. Our previous study showed that CH could suppress hypoxia-induced pulmonary arterial smooth muscle cells proliferation and alleviate chronic hypoxia-induced pulmonary hypertension by targeting store-operated Ca entry (SOCE)-[Ca]i pathway. In this study, we investigated the effect of CH on monocrotaline-induced pulmonary hypertension (MCTPH) and the mechanism behind it. Results show that, in MCTPH model rats, (1) CH significantly reduced the enhancement of right ventricular pressure, right ventricular hypertrophy, and pulmonary vascular remodeling; (2) CH markedly suppressed the promotion of SOCE and [Ca]i in pulmonary arterial smooth muscle cells; and (3) CH obviously inhibited the MCT-upregulated proliferating cell nuclear antigen, TRPC1, TRPC4, and TRPC6 expression in distal pulmonary arteries. These results demonstrate that CH likely alleviates MCTPH by targeting TRPC1,4,6-SOCE-[Ca]i pathway. |
| Databáze: | OpenAIRE |
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