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Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling

  • Authors:
    • Jun Yin
    • Ke Wang
    • Xue Zhu
    • Guoyuan Lu
    • Donghua Jin
    • Junsi Qiu
    • Fanfan Zhou
  • View Affiliations / Copyright

    Affiliations: Department of Nephrology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China, NHC Key Laboratory of Nuclear Medicine, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu 214063, P.R. China, Department of Nephrology, People's Hospital of Suzhou New District, Suzhou, Jiangsu 215129, P.R. China, Department of Nephrology, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China, Sydney Pharmacy School, The University of Sydney, Sydney, New South Wales A-2006, Australia
    Copyright: © Yin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 496
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    Published online on: June 7, 2022
       https://doi.org/10.3892/etm.2022.11423
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Abstract

The dysfunction of renal mesangial cells (MCs) is a hallmark of diabetic kidney disease (DKD), which triggers glomerulosclerosis leading to end‑stage renal disease. Procyanidin B2 (PB2), the main component of proanthocyanidin, is well known for its antioxidant and anti‑inflammatory effects; however, it remains unclear as to whether it has protective effects on DKD. The present study investigated the protective effect of PB2 against hyperglycemia‑induced renal MC dysfunction in mouse SV40‑Mes13 (Mes13) cells. The Mes13 cells were treated with or without PB2 under HG conditions. Cell proliferation was assessed using an MTT assay and oxidative stress was assessed by examining intracellular ROS generation and H2O2 production. The changes in extracellular matrix accumulation‑ and cellular inflammation‑related proteins were measured by western blot analysis, ELISA and immunofluorescence analysis. The results showed that PB2 treatment markedly attenuated hyperglycemia‑induced cell proliferation, oxidative stress, extracellular matrix accumulation and cellular inflammation in Mes13 cells, which was accompanied by an inactivation of redoxosomes, TGF‑β1/SMAD and IL‑1β/TNF‑α/NF‑κB signaling pathways. The present study also demonstrated that hyperglycemia upregulated and activated caveolin‑1 (CAV‑1), whereas PB2 treatment potently reversed this effect. In accordance, CAV‑1 overexpression abolished the protective effects of PB2 against hyperglycemia in Mes13 cells, indicating that the cytoprotective effect of PB2 was CAV‑1‑dependent. These findings form the basis of the potential clinical applications of PB2 in the treatment of DKD.
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Copy and paste a formatted citation
Spandidos Publications style
Yin J, Wang K, Zhu X, Lu G, Jin D, Qiu J and Zhou F: Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling. Exp Ther Med 24: 496, 2022.
APA
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., & Zhou, F. (2022). Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling. Experimental and Therapeutic Medicine, 24, 496. https://doi.org/10.3892/etm.2022.11423
MLA
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., Zhou, F."Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling". Experimental and Therapeutic Medicine 24.2 (2022): 496.
Chicago
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., Zhou, F."Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling". Experimental and Therapeutic Medicine 24, no. 2 (2022): 496. https://doi.org/10.3892/etm.2022.11423
Copy and paste a formatted citation
x
Spandidos Publications style
Yin J, Wang K, Zhu X, Lu G, Jin D, Qiu J and Zhou F: Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling. Exp Ther Med 24: 496, 2022.
APA
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., & Zhou, F. (2022). Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling. Experimental and Therapeutic Medicine, 24, 496. https://doi.org/10.3892/etm.2022.11423
MLA
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., Zhou, F."Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling". Experimental and Therapeutic Medicine 24.2 (2022): 496.
Chicago
Yin, J., Wang, K., Zhu, X., Lu, G., Jin, D., Qiu, J., Zhou, F."Procyanidin B2 suppresses hyperglycemia‑induced renal mesangial cell dysfunction by modulating CAV‑1‑dependent signaling". Experimental and Therapeutic Medicine 24, no. 2 (2022): 496. https://doi.org/10.3892/etm.2022.11423
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