Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2

Pingping Zhang, Jie Fang, Jianping Zhang, Shuxia Ding, Dongmei Gan Department of Endocrinology, Ningbo Women and Children’s Hospital, Ningbo City, Zhejiang Province, People’s Republic of ChinaCorrespondence: Dongmei GanNingbo Women and Children’s Hospital, 339 Liuting S...

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Autores principales:	Zhang P, Fang J, Zhang J, Ding S, Gan D
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2020
Materias:	curcumin diabetic nephropathy podocyte apoptosis autophagy beclin1/uvrag/bcl2 Specialties of internal medicine RC581-951
Acceso en línea:	https://doaj.org/article/960b7018ac224eaa99cfaa6d3a1049e9
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spelling	oai:doaj.org-article:960b7018ac224eaa99cfaa6d3a1049e92021-12-02T09:10:35ZCurcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl21178-7007https://doaj.org/article/960b7018ac224eaa99cfaa6d3a1049e92020-03-01T00:00:00Zhttps://www.dovepress.com/curcumin-inhibited-podocyte-cell-apoptosis-and-accelerated-cell-autoph-peer-reviewed-article-DMSOhttps://doaj.org/toc/1178-7007Pingping Zhang, Jie Fang, Jianping Zhang, Shuxia Ding, Dongmei Gan Department of Endocrinology, Ningbo Women and Children’s Hospital, Ningbo City, Zhejiang Province, People’s Republic of ChinaCorrespondence: Dongmei GanNingbo Women and Children’s Hospital, 339 Liuting Street, Haishu District, Ningbo City, Zhejiang Province 315000, People’s Republic of ChinaEmail DongmeiGan1@163.comIntroduction: Curcumin has various biological properties including being anti-inflammatory and antidiabetic. Podocyte apoptosis and autophagy dysfunction have been found to be responsible for the development of diabetic nephropathy (DN). Thus, the aim of the study was to investigate the effects of curcumin on the podocyte apoptosis and autophagy in DN and clarify its potential mechanisms.Methods: The mice with DN induced by injection of streptozotocin were treated with curcumin by gavage at a dose of 200 mg/kg/day for 8 weeks. The serum lipid levels were detected by total cholesterol (TC) and triglyceride (TG) kits at different time points. Renal damage was assessed by detecting urine albumin, serum creatinine (Scr), HE staining and PAS staining. The renal impairment was detected by immunohistochemical staining and TUNEL staining. Western blot assay tested the expression of autophagy-related and apoptotic-related proteins in vivo and vitro. The viabilities and apoptosis of MPC5 cells exposed to high glucose (HG) or curcumin were respectively detected by CCK-8 assay and flow cytometry.Results: The results showed that curcumin significantly decreased the progress of DN possibly via increasing autophagy and inhibiting apoptosis of renal cell in DN mice. Besides, podocyte marker proteins (podocalyxin and nephrin) were markedly increased in DN mice by curcumin treatment. The autophagy-related proteins LC3, p62, Beclin1, UVRAG and ATG5 were significantly affected in DN mice by curcumin, along with reducing expression of pro-apoptotic protein Bax and caspase-3 and increasing anti-apoptotic protein Bcl-2. In vitro, curcumin increased the viabilities and inhibited apoptosis of MPC5 cells exposed to high glucose (HG). In addition, the podocyte autophagy was enhanced partly via regulating beclin1/UVRAG.Discussion: Together, the results showed that curcumin inhibited podocyte apoptosis and accelerated cell autophagy via regulating Beclin1/UVRAG/Bcl2. Thus, the study showed that curcumin exerted significantly protective effects in DN.Keywords: curcumin, diabetic nephropathy, podocyte apoptosis, autophagy, Beclin1/UVRAG/Bcl2Zhang PFang JZhang JDing SGan DDove Medical Pressarticlecurcumindiabetic nephropathypodocyte apoptosisautophagybeclin1/uvrag/bcl2Specialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 13, Pp 641-652 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	curcumin diabetic nephropathy podocyte apoptosis autophagy beclin1/uvrag/bcl2 Specialties of internal medicine RC581-951
spellingShingle	curcumin diabetic nephropathy podocyte apoptosis autophagy beclin1/uvrag/bcl2 Specialties of internal medicine RC581-951 Zhang P Fang J Zhang J Ding S Gan D Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
description	Pingping Zhang, Jie Fang, Jianping Zhang, Shuxia Ding, Dongmei Gan Department of Endocrinology, Ningbo Women and Children’s Hospital, Ningbo City, Zhejiang Province, People’s Republic of ChinaCorrespondence: Dongmei GanNingbo Women and Children’s Hospital, 339 Liuting Street, Haishu District, Ningbo City, Zhejiang Province 315000, People’s Republic of ChinaEmail DongmeiGan1@163.comIntroduction: Curcumin has various biological properties including being anti-inflammatory and antidiabetic. Podocyte apoptosis and autophagy dysfunction have been found to be responsible for the development of diabetic nephropathy (DN). Thus, the aim of the study was to investigate the effects of curcumin on the podocyte apoptosis and autophagy in DN and clarify its potential mechanisms.Methods: The mice with DN induced by injection of streptozotocin were treated with curcumin by gavage at a dose of 200 mg/kg/day for 8 weeks. The serum lipid levels were detected by total cholesterol (TC) and triglyceride (TG) kits at different time points. Renal damage was assessed by detecting urine albumin, serum creatinine (Scr), HE staining and PAS staining. The renal impairment was detected by immunohistochemical staining and TUNEL staining. Western blot assay tested the expression of autophagy-related and apoptotic-related proteins in vivo and vitro. The viabilities and apoptosis of MPC5 cells exposed to high glucose (HG) or curcumin were respectively detected by CCK-8 assay and flow cytometry.Results: The results showed that curcumin significantly decreased the progress of DN possibly via increasing autophagy and inhibiting apoptosis of renal cell in DN mice. Besides, podocyte marker proteins (podocalyxin and nephrin) were markedly increased in DN mice by curcumin treatment. The autophagy-related proteins LC3, p62, Beclin1, UVRAG and ATG5 were significantly affected in DN mice by curcumin, along with reducing expression of pro-apoptotic protein Bax and caspase-3 and increasing anti-apoptotic protein Bcl-2. In vitro, curcumin increased the viabilities and inhibited apoptosis of MPC5 cells exposed to high glucose (HG). In addition, the podocyte autophagy was enhanced partly via regulating beclin1/UVRAG.Discussion: Together, the results showed that curcumin inhibited podocyte apoptosis and accelerated cell autophagy via regulating Beclin1/UVRAG/Bcl2. Thus, the study showed that curcumin exerted significantly protective effects in DN.Keywords: curcumin, diabetic nephropathy, podocyte apoptosis, autophagy, Beclin1/UVRAG/Bcl2
format	article
author	Zhang P Fang J Zhang J Ding S Gan D
author_facet	Zhang P Fang J Zhang J Ding S Gan D
author_sort	Zhang P
title	Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
title_short	Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
title_full	Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
title_fullStr	Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
title_full_unstemmed	Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2
title_sort	curcumin inhibited podocyte cell apoptosis and accelerated cell autophagy in diabetic nephropathy via regulating beclin1/uvrag/bcl2
publisher	Dove Medical Press
publishDate	2020
url	https://doaj.org/article/960b7018ac224eaa99cfaa6d3a1049e9
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Curcumin Inhibited Podocyte Cell Apoptosis and Accelerated Cell Autophagy in Diabetic Nephropathy via Regulating Beclin1/UVRAG/Bcl2

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