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Protective effect of catalpolon destruction of tight junctions of high glucose induced BMECs / 中国中药杂志
China Journal of Chinese Materia Medica ; (24): 4118-4124, 2018.
Artigo em Chinês | WPRIM | ID: wpr-775369
ABSTRACT
This paper aimed to observe the protective effect of catalpol on the high glucose induced destruction of tight junctions of rat primary brain microvascular endothelial cells (BMECs). Catalpol co-administrated with high glucose increased BMECs survival, decreased its ET-1 secretion, and improved transmembrane electrical resistance in a time-dependent manner. Furthermore, transmission electron microscopy was used to observe catalpol's protective effect on tight junction. Fluorescence staining displayed that catalpol reversed the rearrangement of the cytoskeleton protein F-actin and up-regulated the tight junction proteins claudin-5 and ZO-1, which were further demonstrated by the mRNA expression levels of claudin-5, occludin, ZO-1, ZO-2, ZO-3, -actintin, vinculin and cateinins. This study indicated that catalpol reverses the disaggregation of cytoskeleton actin in BMECs and up-regulates the expression of tight junction proteins, such as claudin-5, occludin, and ZO-1, and finally alleviates the increase in high glucose-induced BMECs injury.
Assuntos

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Fosfoproteínas / Encéfalo / Citoesqueleto de Actina / Células Cultivadas / Actinas / Junções Íntimas / Biologia Celular / Células Endoteliais / Glucosídeos Iridoides Limite: Animais Idioma: Chinês Revista: China Journal of Chinese Materia Medica Ano de publicação: 2018 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Fosfoproteínas / Encéfalo / Citoesqueleto de Actina / Células Cultivadas / Actinas / Junções Íntimas / Biologia Celular / Células Endoteliais / Glucosídeos Iridoides Limite: Animais Idioma: Chinês Revista: China Journal of Chinese Materia Medica Ano de publicação: 2018 Tipo de documento: Artigo