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Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy

  • Authors:
    • Chun‑Shan Han
    • Kai Liu
    • Ning Zhang
    • Shi‑Wen Li
    • Hai‑Cheng Gao
  • View Affiliations / Copyright

    Affiliations: Department of Chest Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Department of Pathology and Pathophysiology, Chengde Medical College, Chengde, Hebei 300000, P.R. China, Department of Clinical Pharmacy, Jilin University School of Pharmaceutical Sciences, Changchun, Jilin 130021, P.R. China
    Copyright: © Han et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 181-186
    |
    Published online on: May 23, 2017
       https://doi.org/10.3892/etm.2017.4509
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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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Copy and paste a formatted citation
Spandidos Publications style
Han CS, Liu K, Zhang N, Li SW and Gao HC: Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy. Exp Ther Med 14: 181-186, 2017.
APA
Han, C., Liu, K., Zhang, N., Li, S., & Gao, H. (2017). Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy. Experimental and Therapeutic Medicine, 14, 181-186. https://doi.org/10.3892/etm.2017.4509
MLA
Han, C., Liu, K., Zhang, N., Li, S., Gao, H."Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy". Experimental and Therapeutic Medicine 14.1 (2017): 181-186.
Chicago
Han, C., Liu, K., Zhang, N., Li, S., Gao, H."Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy". Experimental and Therapeutic Medicine 14, no. 1 (2017): 181-186. https://doi.org/10.3892/etm.2017.4509
Copy and paste a formatted citation
x
Spandidos Publications style
Han CS, Liu K, Zhang N, Li SW and Gao HC: Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy. Exp Ther Med 14: 181-186, 2017.
APA
Han, C., Liu, K., Zhang, N., Li, S., & Gao, H. (2017). Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy. Experimental and Therapeutic Medicine, 14, 181-186. https://doi.org/10.3892/etm.2017.4509
MLA
Han, C., Liu, K., Zhang, N., Li, S., Gao, H."Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy". Experimental and Therapeutic Medicine 14.1 (2017): 181-186.
Chicago
Han, C., Liu, K., Zhang, N., Li, S., Gao, H."Rutin suppresses high glucose-induced ACTA2 and p38 protein expression in diabetic nephropathy". Experimental and Therapeutic Medicine 14, no. 1 (2017): 181-186. https://doi.org/10.3892/etm.2017.4509
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