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Effect of baicalin on gestational hypertension-induced vascular endothelial cell damage

OBJECTIVE: Baicalin is a compound extracted from the dried root of Scutellaria baicalensis Georgi. Studies have shown that baicalin has a protective effect on vascular endothelial cells, but whether baicalin could alleviate ascular endothelial cell damage in pregnancy-induced hypertensive patients r...

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Detalles Bibliográficos
Autores principales: Liu, Yang, Xiong, Miao, Zhou, Fangfang, Shi, Nana, Jia, Yunbin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588769/
https://www.ncbi.nlm.nih.gov/pubmed/33081553
http://dx.doi.org/10.1177/0300060520934288
Descripción
Sumario:OBJECTIVE: Baicalin is a compound extracted from the dried root of Scutellaria baicalensis Georgi. Studies have shown that baicalin has a protective effect on vascular endothelial cells, but whether baicalin could alleviate ascular endothelial cell damage in pregnancy-induced hypertensive patients remains unknown. MATERIALS AND METHODS: We established a hypertensive pregnant rat model to study vascular endothelial injury during pregnancy-induced hypertension. Plasma epoprostenol (PGI-2), thromboxane A2 (Txa-2), β-human chorionic gonadotropin (β-HCG), and estrogen levels in rats were detected using ELISA. Vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and C-reactive protein (CRP) expression were detected using western blotting and quantitative PCR (q-PCR). RESULTS: Results showed that baicalin alleviated symptoms of pregnancy-induced hypertension. CRP, Txa-2, and β-HCG expression were significantly upregulated, while VEGF, eNOS, PGI-2, and estrogen expression was decreased in plasma and placental tissues of hypertensive rats. However, the levels of these injury indicators were significantly decreased after baicalin therapy, while the expression of protective indicators was significantly increased. CONCLUSION: Baicalin reversed vascular endothelial cell injury in pregnant hypertensive rats by promoting VEGF, eNOS, PGI-2, and estrogen expression.