
Protective Effect of Adalimumab on Diabetic Nephropathy by Regulating TNF-α Signal Pathway
Author(s) -
Zhiying Ding,
Hongxia Jiang,
Yongsong Fan,
Guo Ping Sun
Publication year - 2021
Publication title -
iranian journal of public health
Language(s) - English
Resource type - Journals
eISSN - 2251-6093
pISSN - 2251-6085
DOI - 10.18502/ijph.v50i12.7936
Subject(s) - adalimumab , diabetic nephropathy , medicine , tumor necrosis factor alpha , kidney , streptozotocin , nephropathy , endocrinology , pharmacology , diabetes mellitus
Background: To evaluate the inhibitory effect of adalimumab on diabetic nephropathyDN) through animal models.
Methods: We carried out the study in Weifang People’s Hospital, Weifang 261041, China in December 2020. Streptozotocin was used to induce DN in model animal Sprague-Dawley (SD) rats. The DN animal model was given treatment with adalimumab, and the inhibitory effect of adalimumab on the development process of DN was evaluated by detecting changes in blood glucose and urinary albumin levels. Meanwhile, the content of UN, Cr and CysC of the blood in different experimental groups was tested by weighing the ratio of kidney and performing ELISA to evaluate the protective effect of adalimumab on kidney of DN animal model. In addition, the changes in the transcription and translation levels of tumor necrosis factor α (TNF-α) and its downstream regulatory factors MCP-1 and NF-kB in kidney of different experimental groups were detected by fluorescence quantitative PCR and Western blot tests to further reveal the molecular mechanism of adalimumab inhibiting the diabetic nephropathy.
Results: adalimumab could significantly downregulate blood glucose and urinary albumin levels (P <0.05). The renal body weight ratio and the contents of UN, Cr and Cysc in blood in the adalimumab group were significantly lower than those in the placebo group (P <0.05). Meanwhile, adalimumab could significantly downregulate the expression of these molecules (P <0.05).
Conclusion: adalimumab could exert its therapeutic effect on diabetic nephropathy through its specific targeting TNF-α signaling pathways.