Minocycline Attenuates Kidney Injury in a Rat Model Of Streptozotocin-Induced Diabetic Nephropathy
- 10.2991/bbe-16.2016.41How to use a DOI?
- Minocycline, Kidney injury, Rat model, Diabetic nephropathy.
The effects of minocycline on the development of diabetic nephropathy (DN) in streptozotocin (STZ) induced diabetic rats were evaluated in this study. The diabetes rats with diabetic nephropathy (DN) were induced by STZ (55 mg/kg) injection. The experiment included 5 groups 1) normal, 2) normal plus minocucline for 16 weeks, 3) DN plus vehicle, 4) DN plus minocucline 16 weeks and 5) DN plus minocucline for 8 weeks. The pathological changes were analyzed by H.E. staining and the apoptotic cells were stained by TUNEL staining. The mRNA expression of caspase-3, bax and bcl-2 in the kidney tissues was detected by quantitative RT-PCR. The biochemical parameters of blood and urine were determined by biochemical analyzer. Treatment with minocycline reduced the urine volume, 24-hour urine protein, serum creatinine, blood urea nitrogen but not blood ALT in the DN rats. Furthermore, treatment with minocycline improved the pathological score of STZ-injured kidney and reduced the numbers of apoptotic cells in the kidney of DN rats. Moreover, minocycline mitigated the expression of caspase-3 and bax mRNA, but increased Bcl-2 expression in the kidney of DN rats. These data indicated that minocycline improved the STZ-induced kidney damages, at least partially by protection form long-term hyperglycemia-induced kidney cell apoptosis.
- © 2016, the Authors. Published by Atlantis Press.
- Open Access
- This is an open access article distributed under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/).
Cite this article
TY - CONF AU - Hongping Yuan AU - Dongxu Zhao AU - Boyin Zhang PY - 2016/07 DA - 2016/07 TI - Minocycline Attenuates Kidney Injury in a Rat Model Of Streptozotocin-Induced Diabetic Nephropathy BT - Proceedings of the 2016 International Conference on Biomedical and Biological Engineering PB - Atlantis Press SP - 247 EP - 257 SN - 2468-5747 UR - https://doi.org/10.2991/bbe-16.2016.41 DO - 10.2991/bbe-16.2016.41 ID - Yuan2016/07 ER -