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Published:
Sep 22, 2022DOI:
10.4314/tjpr.v21i8.9Keywords:
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Main Article Content
Annexin A1 mimetic peptide Ac2 26 alleviates renal inflammatory injury in diabetic mouse model by suppressing p38MAPK/NF κB
Abstract
Purpose: To investigate the protective role of mimetic peptide Ac2-26 of annexin A1 (ANXA1) in regulating p38MAPK/NF-κB for renal inflammatory injury in a diabetic mouse model.
Methods: The mice were divided into three groups (control, model and Ac2-26; n = 8). Control was untreated, normal mice, while Ac2-26 was treated with mimetic peptide Ac2-26 after induction of type I diabetes with streptozotocin (60 mg/kg). The model group was not further treated after induction of diabetes. The fasting blood glucose (FBG), blood lipid, and renal function were evaluated. Serum inflammatory factors in renal tissue were also assessed.
Results: Compared with the model group, there was a significant decrease in the levels of FBG, blood lipids (TG, TC, LDL and ox-LDL), KI, 24 h urinary protein, Cr and BUN, and significant increase in body weight in AC2-26 group (p < 0.001). There was a marked decrease in TNF-α, IL-6, IL-1β, and IL-18 levels, as well as levels of mRNA and protein expressions of p38MAPK, NF-κBP6 and ANXA1 in AC2-26 group when compared with the model group (p < 0.001).
Conclusion: ANXA1 is the target gene of p38MAPK, and mimetic peptide Ac2-26 alleviates renal inflammation by suppressing p38MAPK/NF-κB pathway, thus improving renal function in diabetic mice models. This finding suggests a probable approach to developing an effective treatment for renal inflammation in diabetic renal injury.
