TITLE:
Protective Effect of Liraglutide on Early Renal Fibrosis in Diabetes Mice
AUTHORS:
Xiaolan Ke, Te’an Ma
KEYWORDS:
Liraglutide, Diabetes, Renal fibrosis, TGF-β1, E-Cadherin
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.13 No.1,
January
14,
2025
ABSTRACT: Background: In recent years, studies have shown that liraglutide may delay the progression of renal fibrosis by inhibiting renal fibrosis signaling pathways and reducing collagen deposition. TGF-β1 and E-Cadherin play crucial roles in renal fibrosis. Objective: To explore the protective effect of liraglutide on early renal fibrosis in diabetes mice. Methods: Twenty-four 8-week-old healthy male C57BL/6J mice were randomly divided into a normal diet feeding group (NG, n = 8) and a high-fat diet feeding group (HG, n = 16) using a simple random sampling method. Four weeks later, the high-fat diet feeding group received a one-time intraperitoneal injection of STZ diluted with 0.1 mol/L sodium citrate buffer (50 mg/Kg). The diabetes model was established after 7 days of continuous injection. The diabetes model mice were randomly divided into 2 groups, each containing 8 mice. One group received liraglutide (400 ug per kilogram per day, subcutaneous injection), named Liraglutide Intervention Group (LDG); the other group received an equal dose of saline subcutaneously, named the Diabetes Model Non-intervention Group (NDG). NG also received an equal dose of saline subcutaneously, named Normal Control Group (NCG). Renal tissue pathological changes were observed by HE and Masson staining; TGF-βl and E-Cadherin protein expressions were detected by immunohistochemistry; E-Cadherin protein expression was detected by Western blotting. Results: The degree of kidney tissue damage and fibrosis in liraglutide intervention group was milder than that in non-intervention group, and the expression of TGF-β1 and E-Cadherin protein tended to be similar to that in normal control group. Conclusion: Liraglutide can significantly reduce early renal fibrosis in diabetes mice, and its mechanism may be related to the reduction of TGF-β1 expression to induce EMT changes in epithelial cells (for example, up regulation of E-Cadherin).