Effect of aminoguanidine on pulmonary apoptosis in the lipopolysaccharide-induced acute lung injury in rats

Aim To investigate the effect and the possible mechanism of aminoguanidine (AG) on the lipopolysaccharide(LPS)-induced acute lung injury in rats. Methods Male SD rats were randomly divided into 3 groups: ① Control group; ② LPS group; ③ AG group. AG was administrated in AG group, saline was administrated in control group and LPS group. LPS group and AG group were further divided into 2 subgroups according to the duration of ALI:3 h+3 h group and 6 h+3 h group. In AG group and LPS group, LPS was administrated. Saline was administrated in control group. Expressions of NOS mRNA in the lung tissue were respectively measured with RT-PCR method;Apoptosis, the expression of Caspase-3 protein, Bcl-2 and bax were respectively detected with Flow Cytometry (FCM), Western blot analysis, and immunohistochemisty (IHC); the pathological changes of lung tissue were observed by light and electron microscope. Results Compared with that of the control group, the expression of iNOS mRNA was significantly increased; the eNOS mRNA was significantly decreased; apoptosis of pulmonary cells, the expression of Caspase-3 and Bax protein were significantly increased; the expression of Bcl-2 was decreased in alveolar and airway epithelial cells in LPS group respectively. Degree of ALI was gradually worsened after administration of LPS. In AG(3 h+3 h) group, the percentage of apoptotic cells, the expression of caspase-3 and Bax protein were decreased respectively, the expression of Bcl-2 and the ratio of Bcl-2 /Bax were increased and the lung damage was improved respectively compared with that of the LPS(3 h+3 h) group. Conclusion Relatively early administration of AG could ameliorate LPS-induced acute lung injury in rats. The possible mechanism is that AG could reduce the expression of iNOS mRNA,Caspase-3 and Bax protein,increase the expression of Bcl-2 protein, and regulate the balance between Bcl-2 and Bax protein.