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Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway

  • Authors:
    • Mei Tao
    • Danna Zheng
    • Xudong Liang
    • Diandian Wu
    • Kang Hu
    • Juan Jin
    • Qiang He
  • View Affiliations / Copyright

    Affiliations: Department of Nephrology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang 310015, P.R. China, Department of Nephrology, Zhejiang Provincial People's Hospital and Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China
    Copyright: © Tao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 592
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    Published online on: June 17, 2021
       https://doi.org/10.3892/mmr.2021.12231
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Abstract

Tripterygium glycoside (TG) is a traditional Chinese medicine extract with immunosuppressive, anti‑inflammatory and anti‑renal fibrosis effects. Epithelial‑mesenchymal transition (EMT) and cell apoptosis are considered to be the major cause of podocyte injury in diabetic kidney disease (DKD). However, it remains unknown as to whether TG is able to alleviate podocyte injury to prevent DKD progression. Therefore, the present study aimed to clarify the podocyte protective effects of TG on DKD. TG, Twist1 small interfering RNA (siRNA) and Twist1 overexpression vector were added to DKD mouse serum‑induced podocytes in vitro. Autophagic and EMT activities were evaluated by immunofluorescence staining and western blot analysis. Apoptotic activity was evaluated by Annexin V‑FITC/PI flow cytometric analysis. The results revealed that after treatment with DKD mouse serum, autophagy was decreased, whereas EMT and apoptotic rate were increased, in podocytes. In addition, Twist1 expression was increased in DKD‑induced podocytes. Furthermore, following Twist1‑small interfering RNA transfection, the DKD‑induced podocyte EMT and apoptotic rate were markedly reduced, indicating that Twist1 may be a promising therapeutic target for DKD. The present results also revealed that overexpression of Twist1 increased podocyte apoptosis, although this was decreased after TG treatment, indicating that TG may exhibit a protective effect on podocytes by inhibiting the Twist1 signaling pathway. After the addition of 3‑benzyl‑5‑((2‑nitrophenoxy) methyl)‑dihydrofuran‑2(3H)‑one, an activator of mTORC1, the effects of TG on podocyte EMT, apoptosis and the autophagy were reversed. These findings indicated that TG may alleviate EMT and apoptosis by upregulating autophagy through the mTOR/Twist1 signaling pathway in DKD.
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Copy and paste a formatted citation
Spandidos Publications style
Tao M, Zheng D, Liang X, Wu D, Hu K, Jin J and He Q: Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway. Mol Med Rep 24: 592, 2021.
APA
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., & He, Q. (2021). Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway. Molecular Medicine Reports, 24, 592. https://doi.org/10.3892/mmr.2021.12231
MLA
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., He, Q."Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway". Molecular Medicine Reports 24.2 (2021): 592.
Chicago
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., He, Q."Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway". Molecular Medicine Reports 24, no. 2 (2021): 592. https://doi.org/10.3892/mmr.2021.12231
Copy and paste a formatted citation
x
Spandidos Publications style
Tao M, Zheng D, Liang X, Wu D, Hu K, Jin J and He Q: Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway. Mol Med Rep 24: 592, 2021.
APA
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., & He, Q. (2021). Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway. Molecular Medicine Reports, 24, 592. https://doi.org/10.3892/mmr.2021.12231
MLA
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., He, Q."Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway". Molecular Medicine Reports 24.2 (2021): 592.
Chicago
Tao, M., Zheng, D., Liang, X., Wu, D., Hu, K., Jin, J., He, Q."Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway". Molecular Medicine Reports 24, no. 2 (2021): 592. https://doi.org/10.3892/mmr.2021.12231
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