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    ZHU Xianyi, ZHAO Yajie, WEN Xianli, LI Shanwen, ZHANG Aiqing, GAN Weihua. Effects of N-acetylcysteine on the expression of fibrosis related protein in renal proximal tubular epithelial cells induced by Ang Ⅱ[J]. Journal of Xuzhou Medical University, 2020, 40(3): 170-174. DOI: 10.3969/j.issn.2096-3882.2020.03.003
    Citation: ZHU Xianyi, ZHAO Yajie, WEN Xianli, LI Shanwen, ZHANG Aiqing, GAN Weihua. Effects of N-acetylcysteine on the expression of fibrosis related protein in renal proximal tubular epithelial cells induced by Ang Ⅱ[J]. Journal of Xuzhou Medical University, 2020, 40(3): 170-174. DOI: 10.3969/j.issn.2096-3882.2020.03.003

    Effects of N-acetylcysteine on the expression of fibrosis related protein in renal proximal tubular epithelial cells induced by Ang Ⅱ

    • Objective To investigate the effects of N-acetylcysteine (NAC) on the expression of fibrosis related protein in human renal proximal tubular epithelial cells induced by angiotensin Ⅱ (Ang Ⅱ). Methods HK2 cells were divided into four groups: a control group, an Ang Ⅱ group, an NAC group and an Ang Ⅱ+NAC group. The HK2 cells were treated with NAC (5 mmol/L) and Ang Ⅱ (1 mmol/L) for 48 h. Then, the expression of fibronectin (FN), collagen 1 and α-smooth muscle actin (α-SMA) were detected by Western blot. RT-PCR was adopted to determine the changes of FN, collage 1 and α-SMA mRNA levels. The expression of α-SAM in HK2 cells was observed by immunofluorescence. Results Compared with the control group, the Ang Ⅱgroup showed significantly up-regulated levels of FN, collagen 1 and α-SMA protein and mRNA (P<0.05). Compared with the NACl group, the Ang Ⅱ+NAC group showed remarkably reduced levels of FN, collagen 1 and α-SMA protein and mRNA (P<0.05). Furthermore, red immunofluorescence of α-SMA was found in the AngⅡgroup and remarkably reduced in the AngⅡ+NAC group, with no immunofluorescence staining of α-SMA in the control and NAC groups. Conclusions NAC can inhibit the expression of fibrosis related protein in renal proximal tubular epithelial cells induced by Ang Ⅱ, so as to play an important role in the prevention and treatment of chronic kidney disease.
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