Fig 1: Illustration summarizes the study design, methods, and major findings.Acute kidney injury (AKI) in rats was induced by intramuscular (i.m) injection of 50% glycerol (5 ml/kg). Rats were then divided into four groups (n = 6 rats/group): untreated AKI, AKI+saline( received 1.5 mL of normal saline subcutaneous injection), AKI+vildagliptin (treated with oral vildagliptin 10 mg/kg), and AKI+saline+vildagliptin: received saline and vildagliptin. The study compared the protective effect of saline and vildagliptin DPP-4 inhibitor. There was an insignificant difference regarding the relative expression of AP-1, JUN, c-fos, MAPK, and HMGB1between the AKI+saline group and AKI+vildagliptin group. Even the hepatic content of the M1 marker (iNOS) and M2 marker (Arg-1) showed insignificant differences between both groups. However, combined therapy produced more pronounced changes in these markers, as the difference in their relative expression between the AKI+saline+vildagliptin group and both the AKI+saline group and AKI+vildagliptin group was significant. We suggest that the vildagliptin hepatoprotective effect involves the downregulation of the MAPK/AP-1 signaling pathway.
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