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Sericin ameliorates epithelial -mesenchymal transition of podocytes induced by high glucose / 安徽医科大学学报
Article em Zh | WPRIM | ID: wpr-1038692
Biblioteca responsável: WPRO
ABSTRACT
Objective @#To explore the effect of sericin on podocyte epithelial-mesenchymal transition induced by high glucose.@*Methods @#Conditional immortalized mouse podocytes were used as the research object to construct podocyte injury model by high glucose stimulation.The podocytes were divided into normal (NG) group ,hyperton- ic control (MG) group ,high glucose injury ( HG) group ,low ,medium and high dose sericin ( LS ,MS ,HS) group.CCK-8 method was used to determine the viability of podocytes in each group ; the morphological structure of podocytes in each group was observed by ordinary optical inverted microscope.The migration ability was detected by Transwell and cell scratch test.Western blot was used to detect the expression levels of EMT-related mesenchy- mal phenotype factors Snai1,α-SMA,FSP-1,MMP-9 and epithelial phenotype factors Nephrin,E-cadherin,and WT-1 in podocytes of each group. @*Results @#Compared with NG group,HG group showed lower podocyte activity (P<0. 01) ,worse podocyte status and enhanced podocyte migration ability,up-regulated Snai1,α-SMA,FSP-1 and MMP-9 protein expressions (P <0. 01) ,and down-regulated Nephrin,E-cadherin and WT-1 protein expres- sions (P<0. 01) .Compared with HG group,the viability of podocytes in sericin group increased (P<0. 05) ,the state of podocytes was improved ,the migration ability of podocytes was weakened ,the expression of Snai1 ,α - SMA,FSP-1 and MMP-9 was down-regulated (P<0. 05) ,and the expression of Nephrin,E-cadherin and WT-1 was up-regulated (P <0. 05 ) .@*Conclusion @#Sericin can alleviate podocyte epithelial-mesenchymal transition in- duced by high glucose.
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Índice: WPRIM Idioma: Zh Revista: Acta Universitatis Medicinalis Anhui Ano de publicação: 2022 Tipo de documento: Article
Buscar no Google
Índice: WPRIM Idioma: Zh Revista: Acta Universitatis Medicinalis Anhui Ano de publicação: 2022 Tipo de documento: Article