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.

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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