Modified Citrus Pectin (MCP) Confers a Renoprotective Effect on Early‐Stage Nephropathy in Type‐2 Diabetic Mice

Author:

Mahmoud Hager M.1,Abdel‐Razik Abdel‐Razik H.2,Elrehany Mahmoud A.3,Othman Eman M.456ORCID,Bekhit Amany A.4

Affiliation:

1. Minia General Hospital 65111 Minia Egypt

2. Histology Department, Faculty of Veterinary Medicine Beni-Suef University 62511 Beni-Suef Egypt

3. Biochemistry Department, Faculty of Pharmacy Deraya University New Mina Egypt

4. Biochemistry Department, Faculty of Pharmacy Minia University 65111 Minia Egypt E-mail: amany

5. Cancer Therapy Research Center, Biochemistry Department -I, Biocenter University of Wuerzburg Am Hubland 97074 Würzburg Germany

6. Bioinformatics Department, Biocenter University of Wuerzburg Am Hubland 97074 Würzburg Germany

Abstract

AbstractDiabetic nephropathy (DN) is a significant global health concern with a high morbidity rate. Accumulating evidence reveals that Galectin‐3 (Gal‐3), a β‐galactoside‐binding lectin, is a biomarker in kidney diseases. Our study aimed to assess the advantageous impacts of modified citrus pectin (MCP) as an alternative therapeutic strategy for the initial and ongoing progression of DN in mice with type 2 diabetes mellitus (T2DM). The animal model has been split into four groups: control group, T2DM group (mice received intraperitoneal injections of nicotinamide (NA) and streptozotocin (STZ), T2DM+MCP group (mice received 100 mg/kg/day MCP following T2DM induction), and MCP group (mice received 100 mg/kg/day). After 4 weeks, kidney weight, blood glucose level, serum kidney function tests, histopathological structure alterations, oxidative stress, inflammation, apoptosis, and fibrosis parameters were determined in renal tissues. Our findings demonstrated that MCP treatment reduced blood glucose levels, renal histological damage, and restored kidney weight and kidney function tests. Additionally, MCP reduced malondialdehyde level and restored glutathione level, and catalase activity. MCP demonstrated a notable reduction in inflammatory and apoptosis mediators TNF‐α, iNOS, TGF‐βRII and caspase‐3. Overall, MCP could alleviate renal injury in an experimental model of DN by suppressing renal oxidative stress, inflammation, fibrosis, and apoptosis mediators.

Publisher

Wiley

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