Protective effect of aminoguanidine against acute lung injury induced by influenza A(H1N1)pdm09 (mouse-adapted) virus in mice with diabetes mellitus

Advanced glycation end products (AGEs) formation is a reason for protein dysfunction and inflammatory response during acute lung injury (ALI) and diabetes mellitus (DM). Previous studies showed the efficacy of AGEs blockers against inflammatory response and protein dysfunction. But the efficacy of AGEs blockers against ALI with combined pathology stays unclear. This study was performed on albino female mice with DM. Virus-induced ALI was induced by the pandemic strain of influenza virus A(H1N1)pdm09. Experimental DM was induced by a single subcutaneous injection of alloxan monohydrate (180 mg/kg). Aminoguanidine bicarbonate (25 mg/kg, subcutaneously) was administered during 7 days post-infection. In our research, we evaluated parameters of ALI during influenza infection such as survival rate, blood-oxygen saturation, levels of cytokines in lung tissue, specific hematological parameters, lung tissue morphology, and AGEs level in the lungs. The protective effect of aminoguanidine was confirmed by reduction mortality, decreasing of hypoxia and limitation of lung damage(p<0.05). At the same time, a reduction of inflammation response and AGEs level in the lung was observed in treated infected mice with DM (p<0.05). Based on obtained results, aminoguanidine showed efficacy against virus-induced ALI with DM.