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Tripterygium glycoside protects diabetic kidney disease mouse serum-induced podocyte injury by upregulating autophagy and downregulating β-arrestin-1

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dc.contributor.authorZhan, Huifang
dc.contributor.authorJin, Juan
dc.contributor.authorLiang, Shikai
dc.contributor.authorZhao, Li
dc.contributor.authorGong, Jianguang
dc.contributor.authorHe, Qiang
dc.date.accessioned2022-07-07T08:13:29Z
dc.date.available2022-07-07T08:13:29Z
dc.date.issued2019
dc.description.abstractBackground. Diabetic kidney disease (DKD), one of the most common causes of end-stage renal disease (ESRD), remains prevalent in many populations. Podocyte loss and apoptosis play a crucial role in the progression of DKD. Tripterygium glycoside (TG), a widely used Chinese herb, exerted comprehensive protective effects on preventing DKD progression. This study was performed to assess the podocyte protective effect of tripterygium glycoside on DKD by the potential role of activation of autophagy and downregulating βarrestin-1. Methods. Tripterygium glycoside and small interfering RNA (siRNA) of β-arrestin-1 were added to 10% db/db mice high-glucose serum induced podocytes in vitro. Autophagic activity was evaluated by transmission electronic microscopy, immunofluorescence staining and western blot analysis. Apoptotic activity was evaluated by Annexin V-FITC/PI flow cytometric analysis. The levels of nephrin and podocin, a marker protein of podocytes, were examined using western blot analysis. Results. Significantly ameliorated podocyte apoptosis, increased nephrin and podocin levels and inhibited expression of β-arrestin-1 were observed after pretreatment of tripterygium glycoside in DKD mouse serum treated podocytes. Significantly higher levels of autophagic activity were also observed. Silencing βarrestin-1 upregulated autophagic activity and ameliorated podocyte apoptosis. Silencing β-arrestin-1 in combination with tripterygium glycoside enhanced the levels of LC3-II and LC3-II/LC3-I ratios and reduced the expression of p62. Finally, we observed a notable reduction in podocyte apoptotic rate in DKD serum + siRNA-β-arrestin-1 + TG group compared to DKD serum + siRNA-β-arrestin-1 group, and upregulated protein levels of nephrin and podocin compared to treatment with siRNA-β-arrestin-1 only. Conclusions. This study demonstrated that tripterygium glycoside provided protection against podocyte injury induced by high-glucose serum, and that this effect was mediated by the concomitant activation of autophagy and downregulation of β-arrestin-1.es
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dc.format.extent10es
dc.identifier.citationHistology and Histopathology, Vol.34, nº8, (2019)
dc.identifier.doiDOI: 10.14670/HH-18-097
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/122186
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectTripterygium glycosidees
dc.subjectAutophagyes
dc.subjectApoptosises
dc.subjectβ-arrestin-1es
dc.subjectPodocytees
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleTripterygium glycoside protects diabetic kidney disease mouse serum-induced podocyte injury by upregulating autophagy and downregulating β-arrestin-1es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.34, nº8 (2019)