Objective: To observe the effect of enalapril on airway inflammation in rat models induced by inhaling acrolein and to explore its mechanism.
Methods: Twenty-four Sprague-Dawley rats were randomly divided into 4 groups (n = 6): 1) control group (inhaled 0.9% normal saline for 3 hours, twice every day); 2) enalapril self-control group [intragastrically administrated enalapril 0.5 mg/(kg x d) only]; 3) model group (stimulated with 4 mg/L acrolein for 3 hours, twice every day); 4) enalapril interventive group [inhaled acrolein and intragastrically administrated enalapril 0.5 mg/(kg x d)]. Lung tissue was acquired after the rats were sacrificed on the 21st day. Histopathology examination of lung tissue section stained with HE. Nuclear factor-kappa B and angiotensin II were assayed by immunohistochemistry. Nuclear factor-kappa B were also detected by Western blot. IL-8 and TNF-alpha in BALF were estimated by ELISA.
Results: Compared with the control group and the enalapril interventive group, the expression of Ang II and NF-kappa B in the model group was significantly increased (all P < 0.05). Compared with the control group and the enalapril interventive group, the ratio of NF-kappa B nuclear translocation in the model group was remarkably increased. Neutrophils and the level of IL-8 and TNF-alpha in BALF were higher in model group than those in control group. Enalapril can suppress them significantly.
Conclusion: Acrolein inhalation could upregulate the expression of Ang II and NF-kappa B and also increase nuclear translocation ratio of NF-kappa B. Enalapril can suppress the airway inflammation induced by acrolein.