Protective effect of umbilical cord mesenchymal stem cells combined with resveratrol against renal podocyte damage in NOD mice.


Journal

Diabetes research and clinical practice
ISSN: 1872-8227
Titre abrégé: Diabetes Res Clin Pract
Pays: Ireland
ID NLM: 8508335

Informations de publication

Date de publication:
Oct 2019
Historique:
received: 16 03 2019
revised: 28 04 2019
accepted: 23 05 2019
pubmed: 1 6 2019
medline: 6 2 2020
entrez: 1 6 2019
Statut: ppublish

Résumé

The role of chronic inflammation initiated by persistent hyperglycemia in podocyte injury has attracted increasing attention. The advanced glycation end products (RAGE) receptor- nuclear factor-kappa B (NF-кB) signaling pathway is involved in the occurrence of inflammation. We speculate that treatment with human umbilical cord mesenchymal stem cells (hUCMSCs) combined with resveratrol can block this signaling pathway and protect podocyte function. Non obesity diabetes(NOD) mice were randomly divided into 5 groups: NOD-T1DM, Res, hUCMSCs, hUCMSCs + Res and insulin (INS)groups. Mice without diabetes were classified as NOD control group(NOD group). Blood glucose(BG), blood urea nitrogen(BUN), serum creatinine(SCr), 24-h urine albumin excretion rate (UAER) were measured. The expression of nephrin, WT1 and RAGE, MCP-1 in renal tissues were detected by Western blot, expression of NF-кB protein(P65) was determined by immunohistochemistry. The combined treatment of hUCMSCs and Resveratrol can reduce BG, BUN, SCr, 24-h UAER, and the expression of the inflammatory factors MCP-1, RAGE and NF-кB; increase the number of podocytes and the expression of the podocyte-related proteins nephrin and WT1 in type 1 diabetes mellitus, and improve renal pathological structure. Combining of hUCMSCs and resveratrol can better protect renal podocyte function, and the effects on the reduction of blood glucose and renal injury are better than those obtained by insulin treatment. This indicated that the combination of Res and hUCMSCs may be a novel therapeutic method for the treatment of DN.

Sections du résumé

BACKGROUND BACKGROUND
The role of chronic inflammation initiated by persistent hyperglycemia in podocyte injury has attracted increasing attention. The advanced glycation end products (RAGE) receptor- nuclear factor-kappa B (NF-кB) signaling pathway is involved in the occurrence of inflammation. We speculate that treatment with human umbilical cord mesenchymal stem cells (hUCMSCs) combined with resveratrol can block this signaling pathway and protect podocyte function.
METHODS METHODS
Non obesity diabetes(NOD) mice were randomly divided into 5 groups: NOD-T1DM, Res, hUCMSCs, hUCMSCs + Res and insulin (INS)groups. Mice without diabetes were classified as NOD control group(NOD group). Blood glucose(BG), blood urea nitrogen(BUN), serum creatinine(SCr), 24-h urine albumin excretion rate (UAER) were measured. The expression of nephrin, WT1 and RAGE, MCP-1 in renal tissues were detected by Western blot, expression of NF-кB protein(P65) was determined by immunohistochemistry.
RESULTS RESULTS
The combined treatment of hUCMSCs and Resveratrol can reduce BG, BUN, SCr, 24-h UAER, and the expression of the inflammatory factors MCP-1, RAGE and NF-кB; increase the number of podocytes and the expression of the podocyte-related proteins nephrin and WT1 in type 1 diabetes mellitus, and improve renal pathological structure.
CONCLUSIONS CONCLUSIONS
Combining of hUCMSCs and resveratrol can better protect renal podocyte function, and the effects on the reduction of blood glucose and renal injury are better than those obtained by insulin treatment. This indicated that the combination of Res and hUCMSCs may be a novel therapeutic method for the treatment of DN.

Identifiants

pubmed: 31150720
pii: S0168-8227(19)30381-X
doi: 10.1016/j.diabres.2019.05.034
pii:
doi:

Substances chimiques

Resveratrol Q369O8926L

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107755

Informations de copyright

Copyright © 2019. Published by Elsevier B.V.

Auteurs

Yuxin Xian (Y)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yi Lin (Y)

Department of Pediatric, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Caixia Cao (C)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Li Li (L)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Jing Wang (J)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Jiapeng Niu (J)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yunlei Guo (Y)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yanan Sun (Y)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Yangang Wang (Y)

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China. Electronic address: wangyg1966@icloud.com.

Wei Wang (W)

Department of Hematology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China. Electronic address: 18661807392@163.com.

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