ArticleExperimental and therapeutic medicine2017
Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 20 citations in OpenAlex.
- Oxidative Stress and NRF2/KEAP1/ARE Pathway in Diabetic Kidney Disease (DKD): New Perspectives.Biomolecules · 2022Review
- Flavonoids on diabetic nephropathy: advances and therapeutic opportunities.Chinese medicine · 2021Review
- Rutin ameliorates metabolic acidosis and fibrosis in alloxan induced diabetic nephropathy and cardiomyopathy in experimental rats.Molecular and cellular biochemistry · 2020Article
- Decoding the differentiation of mesenchymal stem cells into mesangial cells at the transcriptomic level.BMC genomics · 2020Article
- System Pharmacology-Based Dissection of the Synergistic Mechanism of Huangqi and Huanglian for Diabetes Mellitus.Frontiers in pharmacology · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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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.
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