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

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-alpha, IL-6, IL-1 beta, and IL-18 levels, as well as in mRNA levels and protein expressions of p38MAPK, NF-kappa BP6, 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-kappa B 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.

Automated summary

This study examined the protective effect of the mimetic peptide AC2-26 of Annexin A1 against renal inflammatory injury in a diabetic mice model. The results showed that AC2-26 significantly decreased blood glucose and lipids levels, improved renal function, and reduced inflammatory factors. Furthermore, AC2-26 suppressed the p38MAPK/NF-kappa B pathway and alleviated renal inflammation. These findings suggest that AC2-26 may be a potential treatment for renal disease in diabetics.