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Updated: Feb 27, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy
Chun-Shan Han1, Kai Liu2, Ning Zhang3
1Department of Chest Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Abstract:
The present study investigated the effect of rutin on high glucose-induced actin, α2, smooth muscle, aorta (ACTA2) and p38 protein expression in diabetic nephropathy (DN). Human mesangial cells were divided into a control group, high glucose-induced mesangial cell group, high glucose + captopril group, and high glucose + rutin group (low, middle and high doses of rutin). Cell viability, adenosine 5'-triphosphate (ATP) content, cell cycle, and ACTA2 and p38 protein expression were examined using MTT assay, ATP assay kit, flow cytometry and immunofluorescence staining in cultured human mesangial cells, respectively. Cell viability, ATP content, and ACTA2 and p38 expression increased significantly in high glucose-induced mesangial cells (P<0.05). However, at concentrations of 0.2, 0.4 and 0.8 µmol/l rutin was able to inhibit high glucose-induced human mesangial cell viability, ATP content, and ACTA2 and p38 expression and improve the cell cycle progression of mesangial cells. In conclusion, ACTA2 and p38 proteins may have important roles in DN. Rutin may inhibit the expression of ACTA2 and p38 and may be utilized in the prevention and treatment of DN.
Insights
Rutin effectively inhibits high glucose-induced increases in actin, α2, smooth muscle, aorta (ACTA2) and p38 protein expression. This suggests rutin
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Diabetic nephropathy (DN) is a serious complication of diabetes.
- High glucose levels contribute to the pathogenesis of DN.
- Understanding molecular mechanisms in DN is crucial for developing treatments.
Purpose of the Study:
- To investigate the effect of rutin on high glucose-induced changes in human mesangial cells.
- To examine the role of actin, α2, smooth muscle, aorta (ACTA2) and p38 proteins in DN.
- To evaluate rutin's potential therapeutic effects in DN.
Main Methods:
- Human mesangial cells were cultured and exposed to high glucose conditions.
- Cells were treated with varying doses of rutin or captopril.
- Cell viability, ATP content, cell cycle, and protein expression (ACTA2, p38) were assessed using MTT assay, ATP assay kit, flow cytometry, and immunofluorescence staining.
Main Results:
- High glucose significantly increased cell viability, ATP content, and ACTA2 and p38 protein expression.
- Rutin treatment (0.2, 0.4, 0.8 µmol/l) inhibited these high glucose-induced effects.
- Rutin also improved the cell cycle progression in mesangial cells.
Conclusions:
- ACTA2 and p38 proteins play significant roles in the development of diabetic nephropathy.
- Rutin demonstrates inhibitory effects on ACTA2 and p38 expression.
- Rutin holds potential for the prevention and treatment of diabetic nephropathy.
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