Diabetic kidney disease (DKD) is an inflammatory disease caused by metabolic disorder. As an important signaling pathway in the inflammatory response, the JNK signaling pathway plays an crucial role in kidney injury in DKD. Vitamin D3 can reduce the inflammatory reaction and delay or even reverse DKD progression. Unfortunately, the mechanism by which vitamin D3 regulates DKD pathogenesis is unclear. This research established a DKD rat model and vitamin D3 and irbesartan were used as interventions. Then, urine and blood biochemistry; and inflammatory cytokine (IL-1 and IL-6), phosphorylated JNK pathway protein (MEK-4 and JNK1/2/3) and downstream factor (AP-1 and ATF-2) expression were assessed. We found that the DKD group showed body weight and insulin secretion were significantly decreased; significantly increased FPG, HOMA-IR and blood lipids; and significantly increased 24-h urinary protein (UPro) compared with normal group. Additionally, the levels of IL-1 and IL-6 and phosphorylated JNK pathway proteins were significantly elevated. These changes were improved by vitamin D3, especially at a low dosage. These results suggest that active vitamin D3 protects against DKD in rats by reducing IL-6 and IL-1 release, downregulating the JNK inflammatory signaling pathway, and inhibiting downstream transcription factor AP-1- and ATF-2-mediated kidney damage. This research provides a new theoretical support for vitamin D3 treatment of diabetic nephropathy.
| Published in | International Journal of Diabetes and Endocrinology (Volume 6, Issue 3) |
| DOI | 10.11648/j.ijde.20210603.13 |
| Page(s) | 105-113 |
| 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 |
Diabetic Kidney Disease (DKD), Active Vitamin D3, IL-1, IL-6, JNK
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APA Style
Xiaoju Fan, Linlin Liu, Wenzhuo Zhu, Yumei Zhao, Haowei Zhang, et al. (2021). Active Vitamin D3 Protects Against Diabetic Kidney Disease by Regulating the JNK Signaling Pathway in Rats. International Journal of Diabetes and Endocrinology, 6(3), 105-113. https://doi.org/10.11648/j.ijde.20210603.13
ACS Style
Xiaoju Fan; Linlin Liu; Wenzhuo Zhu; Yumei Zhao; Haowei Zhang, et al. Active Vitamin D3 Protects Against Diabetic Kidney Disease by Regulating the JNK Signaling Pathway in Rats. Int. J. Diabetes Endocrinol. 2021, 6(3), 105-113. doi: 10.11648/j.ijde.20210603.13
AMA Style
Xiaoju Fan, Linlin Liu, Wenzhuo Zhu, Yumei Zhao, Haowei Zhang, et al. Active Vitamin D3 Protects Against Diabetic Kidney Disease by Regulating the JNK Signaling Pathway in Rats. Int J Diabetes Endocrinol. 2021;6(3):105-113. doi: 10.11648/j.ijde.20210603.13
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Download@article{10.11648/j.ijde.20210603.13,
author = {Xiaoju Fan and Linlin Liu and Wenzhuo Zhu and Yumei Zhao and Haowei Zhang and Yang Wu and Jia Fu and Hongmin Liang and Rui Han},
title = {Active Vitamin D3 Protects Against Diabetic Kidney Disease by Regulating the JNK Signaling Pathway in Rats},
journal = {International Journal of Diabetes and Endocrinology},
volume = {6},
number = {3},
pages = {105-113},
doi = {10.11648/j.ijde.20210603.13},
url = {https://doi.org/10.11648/j.ijde.20210603.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijde.20210603.13},
abstract = {Diabetic kidney disease (DKD) is an inflammatory disease caused by metabolic disorder. As an important signaling pathway in the inflammatory response, the JNK signaling pathway plays an crucial role in kidney injury in DKD. Vitamin D3 can reduce the inflammatory reaction and delay or even reverse DKD progression. Unfortunately, the mechanism by which vitamin D3 regulates DKD pathogenesis is unclear. This research established a DKD rat model and vitamin D3 and irbesartan were used as interventions. Then, urine and blood biochemistry; and inflammatory cytokine (IL-1 and IL-6), phosphorylated JNK pathway protein (MEK-4 and JNK1/2/3) and downstream factor (AP-1 and ATF-2) expression were assessed. We found that the DKD group showed body weight and insulin secretion were significantly decreased; significantly increased FPG, HOMA-IR and blood lipids; and significantly increased 24-h urinary protein (UPro) compared with normal group. Additionally, the levels of IL-1 and IL-6 and phosphorylated JNK pathway proteins were significantly elevated. These changes were improved by vitamin D3, especially at a low dosage. These results suggest that active vitamin D3 protects against DKD in rats by reducing IL-6 and IL-1 release, downregulating the JNK inflammatory signaling pathway, and inhibiting downstream transcription factor AP-1- and ATF-2-mediated kidney damage. This research provides a new theoretical support for vitamin D3 treatment of diabetic nephropathy.},
year = {2021}
}
TY - JOUR T1 - Active Vitamin D3 Protects Against Diabetic Kidney Disease by Regulating the JNK Signaling Pathway in Rats AU - Xiaoju Fan AU - Linlin Liu AU - Wenzhuo Zhu AU - Yumei Zhao AU - Haowei Zhang AU - Yang Wu AU - Jia Fu AU - Hongmin Liang AU - Rui Han Y1 - 2021/08/13 PY - 2021 N1 - https://doi.org/10.11648/j.ijde.20210603.13 DO - 10.11648/j.ijde.20210603.13 T2 - International Journal of Diabetes and Endocrinology JF - International Journal of Diabetes and Endocrinology JO - International Journal of Diabetes and Endocrinology SP - 105 EP - 113 PB - Science Publishing Group SN - 2640-1371 UR - https://doi.org/10.11648/j.ijde.20210603.13 AB - Diabetic kidney disease (DKD) is an inflammatory disease caused by metabolic disorder. As an important signaling pathway in the inflammatory response, the JNK signaling pathway plays an crucial role in kidney injury in DKD. Vitamin D3 can reduce the inflammatory reaction and delay or even reverse DKD progression. Unfortunately, the mechanism by which vitamin D3 regulates DKD pathogenesis is unclear. This research established a DKD rat model and vitamin D3 and irbesartan were used as interventions. Then, urine and blood biochemistry; and inflammatory cytokine (IL-1 and IL-6), phosphorylated JNK pathway protein (MEK-4 and JNK1/2/3) and downstream factor (AP-1 and ATF-2) expression were assessed. We found that the DKD group showed body weight and insulin secretion were significantly decreased; significantly increased FPG, HOMA-IR and blood lipids; and significantly increased 24-h urinary protein (UPro) compared with normal group. Additionally, the levels of IL-1 and IL-6 and phosphorylated JNK pathway proteins were significantly elevated. These changes were improved by vitamin D3, especially at a low dosage. These results suggest that active vitamin D3 protects against DKD in rats by reducing IL-6 and IL-1 release, downregulating the JNK inflammatory signaling pathway, and inhibiting downstream transcription factor AP-1- and ATF-2-mediated kidney damage. This research provides a new theoretical support for vitamin D3 treatment of diabetic nephropathy. VL - 6 IS - 3 ER -
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