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Original Research Article | OPEN ACCESS

Annexin A1 mimetic peptide Ac2-26 alleviates renal inflammatory injury in a diabetic mice model through the suppression of p38MAPK/NF-κB

Kangyi Zhang, Xiaochun Teng

Department of Nephrology and Department of Endocrinology, Chongqing Public Health Medical Center, Chongqing, China;

For correspondence:-  Xiaochun Teng   Email: tengxiaochun52@126.com   Tel:+8613452366285

Accepted: 25 August 2022        Published: 30 September 2022

Citation: Zhang K, Teng X. Annexin A1 mimetic peptide Ac2-26 alleviates renal inflammatory injury in a diabetic mice model through the suppression of p38MAPK/NF-κB. Trop J Pharm Res 2022; 21(9):1899-1905 doi: 10.4314/tjpr.v21i9.13

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To examine the protective effect of mimetic peptide Ac2-26 of Annexin A1 (ANXA1) against renal inflammatory injury in a diabetic mice model.
Methods: Twenty-four mice were randomized into three groups with eight mice per group. These included control group (CG), model group (MG) given intraperitoneal injection of streptozotocin (60 mg/kg), and AC2-26 group (AG) given AC2-26, 72 h after the induction of diabetes. Fasting blood glucose (FBG), blood lipids, and renal function in the mice were determined by Sysmex-180 Biochemistry Analyzer, while serum inflammatory factors in renal tissue were also determined.
Results: Compared with the model group, there was a significant decrease in the levels of FBG, triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), oxidized LDL (ox-LDL), as well as in 24 h urinary protein, creatinine (Cr) and blood urea nitrogen (BUN), but a significant increase in body weight in AC2-26 group (p < 0.001). There was a significant decrease in TNF-α, IL-6, IL-1β, and IL-18 levels, as well as in mRNA levels and protein expressions of p38MAPK, NF-κBP6, ANXA1 in AC2-26 group when compared with the model group (p < 0.001).
Conclusion: Annexin A1 is the target gene of p38MAPK. Annexin A1 mimetic peptide Ac2-26 alleviates renal inflammation by suppressing p38MAPK/NF-κB pathway, thus improving renal function in the diabetic mice model. Hence, the findings of this study provide a potential avenue for the development of an effective treatment for renal disease in diabetics.

Keywords: Diabetic mice model, Renal inflammatory injury, Annexin A1, p38 Mitogen-activated protein kinases, Nuclear factor-kappa β

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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