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. 2017 Jul;14(1):181-186.
doi: 10.3892/etm.2017.4509. Epub 2017 May 23.

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

Affiliations

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

Chun-Shan Han et al. Exp Ther Med. 2017 Jul.

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.

Keywords: actin; aorta; diabetic nephropathy; human mesangial cells; p38; rutin; smooth muscle; α2.

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Figures

Figure 1.
Figure 1.
Mesangial cell viability. Data are presented as the mean ± standard error of the mean. **P<0.01 and *P<0.05 vs. M. C, control group; M, high glucose-induced group; P, captopril group; Low, group treated with 0.2 µmol/l rutin; Middle, group treated with 0.4 µmol/l rutin; High, group treated with and 0.8 µmol/l rutin.
Figure 2.
Figure 2.
ATP content of mesangial cells. Data are presented as the mean ± standard error of the mean. **P<0.01. ATP, adenosine 5′-triphosphate; C, control group; M, high glucose-induced group; P, captopril group; Low, group treated with 0.2 µmol/l rutin; Middle, group treated with 0.4 µmol/l rutin; High, group treated with and 0.8 µmol/l rutin.
Figure 3.
Figure 3.
Cell cycle analysis in each group of mesangial cells. Cell cycle analysis of the (A) control, (B) high glucose-induced, (C) captopril group and (D) 0.2 (low), (E) 0.4 (middle) and (F) 0.8 µmol/l (high) rutin treatment groups.
Figure 4.
Figure 4.
Immunofluorescence staining with DAPI. Immunofluorescence images from the (A) control, (B) high glucose-induced, (C) captopril group and (D) 0.2, (E) 0.4 and (F) 0.8 µmol/l rutin treatment groups. Magnification, ×200.
Figure 5.
Figure 5.
ACTA2 protein expression in the different mesangial cell groups. ACTA2 protein expression in the (A) control, (B) high glucose-induced, (C) captopril group and (D) 0.2, (E) 0.4 and (F) 0.8 µmol/l rutin treatment groups. ACTA2, actin, α2, smooth muscle, aorta. Magnification, ×200.
Figure 6.
Figure 6.
p38 protein expression in the different mesangial cell groups. p38 protein expression in the (A) control, (B) high glucose-induced, (C) captopril group and (D) 0.2, (E) 0.4 and (F) 0.8 µmol/l rutin treatment groups. Magnification, ×200.

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