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Ginkgo biloba extract improves brain uptake of ginsenosides by increasing blood-brain barrier permeability via activating A1 adenosine receptor signaling pathway.

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机构： [a]Guangdong Province Research Centre for Chinese Integrative Medicine Against Metabolic Disease, China [b]Key Unit of Modulating Liver to Treat Hyperlipemia SATCM (State Administration of Traditional Chinese Medicine), China [c]Guangdong TCM Key Laboratory for Metabolic Diseases, China [d]The Institute of Chinese Medicinal Sciences, Guangdong Pharmaceutical University, China [e]The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou,510515, China [f]College of Traditional Chinese Medicine (TCM), Guangdong Pharmaceutical University, Guangzhou, 510006, China

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Ginkgo biloba leaves and Panax ginseng are Chinese medicine commonly used in combination for cerebral disease. To investigate the effect of standard extract of Ginkgo biloba leaves (EGb) on facilitating brain uptake of ginsenoside and its underlying mechanisms. The increasing uptake of ginsenosides in the brain of rats by EGb were detected by LC-MS/MS analysis. Evans blue and FITC-dextran leakage were determined to evaluate blood-brain barrier (BBB) permeability in vivo. Transendothelial electrical resistance (TEER) and Na-F penetration rate were measured with a co-culture of the human cerebral microvascular endothelial cell line (hCMEC/D3) and human normal glial cell line (HEB) in vitro BBB model. WB were used to analyzed the expression of BBB tight junctions (TJs) related protein (ZO-1, Occludin, Claudin-3, p-ERM, and p-MLC), ultrastructure of TJs was determined by transmission electron microscope. LC-MS/MS analysis demonstrated that EGb could improve brain uptake of ginsenoside Rg1, Re, Rd and Rb1. In vivo study showed that, BBB permeability was significantly increased after EGb administration, evidenced by the markedly increased penetration of FITC-dextran and Evans Blue into the mice brain parenchyma. In the in vitro BBB model, reduced TEER and increased Na-F penetration rate was observed in EGb group, which was associated with alteration of TJs ultrastructure. Furthermore, the expression of p-ERM and p-MLC in hCMEC/D3 as well as mice brain microvessels were significantly upregulated, but no significant change on the expression of TJs proteins (ZO-1, Occludin and Claudin-3). Moreover, the effect of EGb on in vitro BBB permeability and ERM, MLC phosphorylation was counteracted by DPCPX, an A1 adenosine receptor (A1R) antagonist. EGb might induce ERM/MLC phosphorylation and increase the cell-cell junction gaps to cause a reversible increase of the BBB permeability via A1R signaling pathway. Our results may contribute to better use of EGb in the treatment of brain diseases. Copyright © 2019 Elsevier B.V. All rights reserved.

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出版当年[2019]版：

大类 | 3 区医学

小类 | 2 区全科医学与补充医学 2 区植物科学 3 区药物化学 3 区药学

最新[2025]版：

大类 | 2 区医学

小类 | 1 区全科医学与补充医学 1 区药学 2 区药物化学 2 区植物科学

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第一作者机构： [d]The Institute of Chinese Medicinal Sciences, Guangdong Pharmaceutical University, China

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通讯机构： [a]Guangdong Province Research Centre for Chinese Integrative Medicine Against Metabolic Disease, China [b]Key Unit of Modulating Liver to Treat Hyperlipemia SATCM (State Administration of Traditional Chinese Medicine), China [c]Guangdong TCM Key Laboratory for Metabolic Diseases, China [d]The Institute of Chinese Medicinal Sciences, Guangdong Pharmaceutical University, China [*1]Guangdong Province Research Centre for Chinese Integrative Medicine Against Metabolic Disease, China [*2]Guangdong Province Research Centre for Chinese Integrative Medicine Against Metabolic Disease, China.

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