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Salvianolic Acid B Reducing Portal Hypertension Depends on Macrophages in Isolated Portal Perfused Rat Livers with Chronic Hepatitis

This study is aimed to investigate the effects of Sal B on portal hypertension (PH). PH with chronic hepatitis was induced by carbon tetrachloride (CCl(4)) in rats. The model was confirmed with elevated portal pressures and increased serum CD163 levels. The inducible nitric oxide synthase (iNOS) or...

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Detalles Bibliográficos
Autores principales: Zhao, Xin, Jia, Hongmei, Yang, Shijun, Liu, Yuetao, Deng, Bo, Xu, Xueyan, Zhang, Tao, Zhou, Hang, Zu, Chengzhe, Yin, He, Li, Ting, Song, Yijun, Wang, Yueqi, Li, Pengtao, Zou, Zhongmei, Cai, Dayong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3480689/
https://www.ncbi.nlm.nih.gov/pubmed/23118797
http://dx.doi.org/10.1155/2012/786365
Descripción
Sumario:This study is aimed to investigate the effects of Sal B on portal hypertension (PH). PH with chronic hepatitis was induced by carbon tetrachloride (CCl(4)) in rats. The model was confirmed with elevated portal pressures and increased serum CD163 levels. The inducible nitric oxide synthase (iNOS) or heme oxygenase-1 (HO-1) in portal triads was assessed. The isolated portal perfused rat liver (IPPRL) was performed at d (0), d (28), d (56) , and d (84) in the progression of chronic hepatitis. After constricting with phenylephrine, the portal veins were relaxed with Sal B. The EC(50) of Sal B for relaxing portal veins was −2.04 × 10(−9), 7.28 × 10(−11), 1.52 × 10(−11), and 8.44 × 10(−11) mol/L at d (0), d (28), d (56), and d (84), respectively. More macrophages infiltrated in portal triads and expressed more iNOS or HO-1 as PH advanced. The areas under the curve (AUCs) of Sal B for reducing PH were positively correlated with the levels of iNOS or HO-1 in portal triads, and so did with serum CD163 levels. Sal B reduces PH in IPPRL with chronic hepatitis, via promoting portal relaxation due to macrophage-originated NO or CO in portal triads, partly at least.