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Cited by 71Chronic Kidney Disease and DiabetesDiabetes Treatment and ManagementAcute Kidney Injury Research

Exendin-4 attenuates renal tubular injury by decreasing oxidative stress and inflammation in streptozotocin-induced diabetic mice

Sancar-Bas, Serap, Gezginci-Oktayoglu, Selda, Bolkent, Sehnaz·2015·Growth Factors
DOI 10.3109/08977194.2015.1125349
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Abstract

In this study, we aimed to research the restorative effects of exendin-4, a GLP-1 analog, on renal tubular injury in streptozotocin-induced diabetes model. BALB/c male mice were divided into four groups: non-diabetic, non-diabetic + exendin-4 (3 μg/kg), diabetic and diabetic + exendin-4. In our diabetic model, we observed renal injury mainly in tubular area rather than glomeruli and exendin-4 decreased tubular injury with its glucose lowering effect. Besides, PCNA positive tubular cells, activities of LDH and Na(+)-K(+)-ATPase were also significantly declined by the administration of exendin-4. Furthermore, exendin-4 attenuated the levels of ROS, MDA, 8-OHdG, proinflammatory cytokines (TNF-α, IL-1β), chemokine MCP-1, ICAM-1, and fibrosis-related molecules (transforming growth factor β1 and fibronectin). In consistent with reducing tubular injury, macrophage infiltration and both MCP-1 and ICAM-1 production in tubular cells were decreased. These results indicate that exendin-4 may decrease renal tubular injury seen in the beginning of diabetic nephropathy by decreasing ROS production and inflammation.

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Crossref · 10.3109/08977194.2015.1125349

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  • Exendin-4 (3 and 10 μg/kg/day) treatment significantly downregulated the gene expression of CD14, ICAM-1, and TGFβ1 in the renal cortex, prevented glomerular macrophage infiltration in glomeruli, and reduced oxidative stress and inflammation in tubular cells in STZ-induced diabetic animals.

    “Exendin-4 (3 and 10 μg/kg/day) treatment significantly downregulated the gene expression of CD14, ICAM-1, and TGFβ1 in the renal cortex, prevented glomerular macrophage infiltration in glomeruli, and reduced oxidative stress and inflammation in tubular cells in STZ-induced diabetic animals [101, 103].”

    From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [103]

  • In mice, NOX4 expression can be attenuated by treatment with exendin-4.

    “The pro-oxidant enzyme NAD(P)H oxidase 4 (NOX4) has been shown to promote kidney injury (60), and in mice its expression can be attenuated by treatment with exendin-4 (61).”

    From GLP-1 agonists in the treatment of chronic kidney disease in type 2 diabetes and obesity (2025) · cites this paper as [61]

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Authors
Sancar-Bas, S., Gezginci-Oktayoglu, S., & Bolkent, S.
Venue
Growth Factors
Publisher
Informa UK Limited
Published
2015-09-03
Volume
33
Issue
5-6
Pages
419-429
ISSN
  • 0897-7194 (ISSN-L)
  • 1029-2292
DOI
10.3109/08977194.2015.1125349
OpenAlex
W2338607841
Cited by
71
References
72
Citations by year
2026: 2 · 2025: 7 · 2024: 5 · 2023: 9 · 2022: 10 · 2021: 10 · 2020: 7 · 2019: 8 · 2018: 7 · 2017: 3 · 2016: 3
FWCI
3.76
Type
journal article
Language
en
Open access
closed
Locations
  • Growth Factors (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Keywords
exendin-4, GLP-1 analogues, diabetic nephropathy, renal tubular injury, oxidative stress, inflammation, streptozotocin-induced diabetes, macrophage infiltration, MCP-1, ICAM-1, TNF-α, IL-1β, TGF-β1, fibronectin, renal fibrosis, Na+/K+-ATPase, lipid peroxidation, DNA damage
MeSH terms
Exenatide, Sodium-Potassium-Exchanging ATPase, Animals, Diabetes Mellitus, Experimental, Diabetic Nephropathies, Inflammation, Kidney Tubules, L-Lactate Dehydrogenase, Macrophages, Male, Mice, Inbred BALB C, Peptides, Streptozocin, Tumor Necrosis Factor-alpha, Venoms, Reactive Oxygen Species, Oxidative Stress, Intercellular Adhesion Molecule-1, Proliferating Cell Nuclear Antigen, Chemokine CCL2, Mice

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