| Peer-Reviewed

Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy

Received: 5 December 2018    Accepted:     Published: 6 December 2018
Views:       Downloads:
Abstract

To investigate the mechanism of valsartan protecting podocytes and inhibiting renal injury in diabetic rats. The rat model of diabetic nephropathy was induced by combination of valsartan and high-sugar and high-fat diet. The urinary protein content, renal index, inflammatory and antioxidant indexes in the kidney, renal pathological changes and podocyte holes were investigated. Membrane WT1 and P-Cadherin protein expression levels. Compared with the model group, the 24h urine protein content of valsartan was significantly decreased (P<0.05). Valsartan significantly inhibited the body weight of the model group (P<0.01), and significantly inhibited The increase of renal index (P<0.05); the high and middle doses of valsartan could significantly reduce the levels of IL-β, TNF-α and IL-6 in rat kidney (P<0.05-0.01). The valsartan high and middle dose groups significantly reduced MDA content in rat kidney (P<0.05), and significantly increased SOD activity (P<0.05). HE and PAS staining showed that valsartan was used in model group rats. The pathological changes were alleviated, and the glomerular morphology returned to normal. The protein expression of WT1 and P-Cadherin in the kidney of DN rats by Western blot showed that P- in the kidney tissue of valsartan rats. The expression levels of Cadherin and WT1 protein were significantly increased (P<0.05). Valsartan can regulate the expression of podocyte membrane proteins WT1 and P-Cadherin to protect podocytes, and then repair renal function and anti-diabetic nephropathy.

Published in American Journal of Life Sciences (Volume 6, Issue 3)
DOI 10.11648/j.ajls.20180603.12
Page(s) 47-51
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Valsartan, Diabetic Nephropathy, Podocyte, P-Cadherin, WT1 Protein

References
[1] Wadie W, El-Tanbouly DM. Vinpocetine mitigates proteinuria and podocytes injury in a rat model of diabetic nephropathy. European journal of pharmacology. 2017; 814: 187-95.
[2] Peng T, Chang X, Wang J, Zhen J, Yang X, Hu Z. Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats. Molecular medicine reports. 2017; 15 (5): 3172-8.
[3] Mukhi D, Nishad R, Menon RK, Pasupulati AK. Novel Actions of Growth Hormone in Podocytes: Implications for Diabetic Nephropathy. Frontiers in medicine. 2017; 4: 102.
[4] Liu Y, Zhang J, Wang Y, Zeng X. Apelin involved in progression of diabetic nephropathy by inhibiting autophagy in podocytes. Cell death & disease. 2017; 8 (8): e3006.
[5] Huang SS, Ding DF, Chen S, Dong CL, Ye XL, Yuan YG, et al. Resveratrol protects podocytes against apoptosis via stimulation of autophagy in a mouse model of diabetic nephropathy. Scientific reports. 2017; 7: 45692.
[6] Hsu YH, Li HH, Sung JM, Chen WY, Hou YC, Weng YH, et al. Interleukin-20 targets podocytes and is upregulated in experimental murine diabetic nephropathy. Experimental & molecular medicine. 2017; 49 (3): e310.
[7] Guo Y, Song Z, Zhou M, Yang Y, Zhao Y, Liu B, et al. Infiltrating macrophages in diabetic nephropathy promote podocytes apoptosis via TNF-alpha-ROS-p38MAPK pathway. Oncotarget. 2017; 8 (32): 53276-87.
[8] Zhang H, Luo W, Sun Y, Qiao Y, Zhang L, Zhao Z, et al. Wnt/beta-Catenin Signaling Mediated-UCH-L1 Expression in Podocytes of Diabetic Nephropathy. International journal of molecular sciences. 2016; 17 (9).
[9] Tharaux PL, Huber TB. How Is Proteinuric Diabetic Nephropathy Caused by Disturbed Proteostasis and Autophagy in Podocytes? Diabetes. 2016; 65 (3): 539-41.
[10] Sawada K, Toyoda M, Kaneyama N, Shiraiwa S, Moriya H, Miyatake H, et al. Upregulation of alpha3beta1-Integrin in Podocytes in Early-Stage Diabetic Nephropathy. Journal of diabetes research. 2016; 2016: 9265074.
[11] Liu F, Zong M, Wen X, Li X, Wang J, Wang Y, et al. Silencing of Histone Deacetylase 9 Expression in Podocytes Attenuates Kidney Injury in Diabetic Nephropathy. Scientific reports. 2016; 6: 33676.
[12] Ji ZZ, Xu YC. Melatonin protects podocytes from angiotensin II-induced injury in an in vitro diabetic nephropathy model. Molecular medicine reports. 2016; 14 (1): 920-6.
[13] He Y, Zhang M, Wu Y, Jiang H, Fu H, Cai Y, et al. Aberrant activation of Notch-1 signaling inhibits podocyte restoration after islet transplantation in a rat model of diabetic nephropathy. Cell death & disease. 2018; 9 (10): 950.
[14] Zhang Y, Chen X, Yuan L, Wu J, Guo N, Liu J. Down-regulation of IRAK1 attenuates podocyte apoptosis in diabetic nephropathy through PI3K/Akt signaling pathway. Biochemical and biophysical research communications. 2018; 506 (3): 529-35.
[15] Lei X, Zhang L, Li Z, Ren J. Astragaloside IV/lncRNA-TUG1/TRAF5 signaling pathway participates in podocyte apoptosis of diabetic nephropathy rats. Drug design, development and therapy. 2018; 12: 2785-93.
[16] Wang Y, Li H, Song SP. beta-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/beta-Catenin Pathway. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 1724-32.
[17] Pan Y, Jiang S, Hou Q, Qiu D, Shi J, Wang L, et al. Dissection of Glomerular Transcriptional Profile in Patients With Diabetic Nephropathy: SRGAP2a Protects Podocyte Structure and Function. Diabetes. 2018; 67 (4): 717-30.
[18] Wang XB, Zhu H, Song W, Su JH. Gremlin Regulates Podocyte Apoptosis via Transforming Growth Factor-beta (TGF-beta) Pathway in Diabetic Nephropathy. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 183-9.
[19] Lv Z, Hu M, Fan M, Li X, Lin J, Zhen J, et al. Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice. Cell death & disease. 2018; 9 (3): 342.
Cite This Article
  • APA Style

    Qingfen Wang, Rui Li, Weiwei Li, Lei Wang. (2018). Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy. American Journal of Life Sciences, 6(3), 47-51. https://doi.org/10.11648/j.ajls.20180603.12

    Copy | Download

    ACS Style

    Qingfen Wang; Rui Li; Weiwei Li; Lei Wang. Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy. Am. J. Life Sci. 2018, 6(3), 47-51. doi: 10.11648/j.ajls.20180603.12

    Copy | Download

    AMA Style

    Qingfen Wang, Rui Li, Weiwei Li, Lei Wang. Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy. Am J Life Sci. 2018;6(3):47-51. doi: 10.11648/j.ajls.20180603.12

    Copy | Download

  • @article{10.11648/j.ajls.20180603.12,
      author = {Qingfen Wang and Rui Li and Weiwei Li and Lei Wang},
      title = {Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy},
      journal = {American Journal of Life Sciences},
      volume = {6},
      number = {3},
      pages = {47-51},
      doi = {10.11648/j.ajls.20180603.12},
      url = {https://doi.org/10.11648/j.ajls.20180603.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajls.20180603.12},
      abstract = {To investigate the mechanism of valsartan protecting podocytes and inhibiting renal injury in diabetic rats. The rat model of diabetic nephropathy was induced by combination of valsartan and high-sugar and high-fat diet. The urinary protein content, renal index, inflammatory and antioxidant indexes in the kidney, renal pathological changes and podocyte holes were investigated. Membrane WT1 and P-Cadherin protein expression levels. Compared with the model group, the 24h urine protein content of valsartan was significantly decreased (P<0.05). Valsartan significantly inhibited the body weight of the model group (P<0.01), and significantly inhibited The increase of renal index (P<0.05); the high and middle doses of valsartan could significantly reduce the levels of IL-β, TNF-α and IL-6 in rat kidney (P<0.05-0.01). The valsartan high and middle dose groups significantly reduced MDA content in rat kidney (P<0.05), and significantly increased SOD activity (P<0.05). HE and PAS staining showed that valsartan was used in model group rats. The pathological changes were alleviated, and the glomerular morphology returned to normal. The protein expression of WT1 and P-Cadherin in the kidney of DN rats by Western blot showed that P- in the kidney tissue of valsartan rats. The expression levels of Cadherin and WT1 protein were significantly increased (P<0.05). Valsartan can regulate the expression of podocyte membrane proteins WT1 and P-Cadherin to protect podocytes, and then repair renal function and anti-diabetic nephropathy.},
     year = {2018}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy
    AU  - Qingfen Wang
    AU  - Rui Li
    AU  - Weiwei Li
    AU  - Lei Wang
    Y1  - 2018/12/06
    PY  - 2018
    N1  - https://doi.org/10.11648/j.ajls.20180603.12
    DO  - 10.11648/j.ajls.20180603.12
    T2  - American Journal of Life Sciences
    JF  - American Journal of Life Sciences
    JO  - American Journal of Life Sciences
    SP  - 47
    EP  - 51
    PB  - Science Publishing Group
    SN  - 2328-5737
    UR  - https://doi.org/10.11648/j.ajls.20180603.12
    AB  - To investigate the mechanism of valsartan protecting podocytes and inhibiting renal injury in diabetic rats. The rat model of diabetic nephropathy was induced by combination of valsartan and high-sugar and high-fat diet. The urinary protein content, renal index, inflammatory and antioxidant indexes in the kidney, renal pathological changes and podocyte holes were investigated. Membrane WT1 and P-Cadherin protein expression levels. Compared with the model group, the 24h urine protein content of valsartan was significantly decreased (P<0.05). Valsartan significantly inhibited the body weight of the model group (P<0.01), and significantly inhibited The increase of renal index (P<0.05); the high and middle doses of valsartan could significantly reduce the levels of IL-β, TNF-α and IL-6 in rat kidney (P<0.05-0.01). The valsartan high and middle dose groups significantly reduced MDA content in rat kidney (P<0.05), and significantly increased SOD activity (P<0.05). HE and PAS staining showed that valsartan was used in model group rats. The pathological changes were alleviated, and the glomerular morphology returned to normal. The protein expression of WT1 and P-Cadherin in the kidney of DN rats by Western blot showed that P- in the kidney tissue of valsartan rats. The expression levels of Cadherin and WT1 protein were significantly increased (P<0.05). Valsartan can regulate the expression of podocyte membrane proteins WT1 and P-Cadherin to protect podocytes, and then repair renal function and anti-diabetic nephropathy.
    VL  - 6
    IS  - 3
    ER  - 

    Copy | Download

Author Information
  • Department of Nephrology, Binzhou People's Hospital, Binzhou, China

  • Department of Nephrology, Binzhou People's Hospital, Binzhou, China

  • Department of Nephrology, Binzhou People's Hospital, Binzhou, China

  • Department of Urology, Binzhou People's Hospital, Binzhou, China

  • Sections