This research was conducted to investigate possible protective influences of
levocetirizine, a nonsedating H1
antihistamine, against
lipopolysaccharide (LPS)-induced
lung injury in rats. Male Sprague Dawley rats received either
levocetirizine (1 mg/kg/day, orally) or the vehicle of the drug (2 ml/kg/day, orally) for 1 week before a single IP injection of LPS (7.5 mg/kg). A group of normal rats served as control. The experiments were terminated 18 h after the LPS challenge. Serum
C-reactive protein levels were determined. Moreover, total cell count,
lactate dehydrogenase (LDH) activity,
protein levels, and total NOx were evaluated in bronchoalveolar lavage fluid (BALF).
Pulmonary edema was evaluated as the wet/dry lung weight ratio. Lung tissue homogenate was assessed for
antioxidant/
pro-oxidant status. BALF and lung tissue levels of
tumor necrosis factor-α (TNF-α) were assessed. Lungs were examined for histological alterations. LPS-mediated
lung injury was manifested by
pulmonary edema, leukocyte infiltration, oxidative stress, and
inflammation.
Levocetirizine attenuated lung
edema and mitigated the increases in BALF
protein levels, LDH activity, and lung leukocyte recruitment in LPS-challenged rats. Additionally, TNF-α
protein levels in BALF and lung tissue were diminished by
levocetirizine administration.
Levocetirizine also exhibited a potent
antioxidant activity as indicated by a decrease in lung tissue levels of
malondialdehyde and an enhancement of
superoxide dismutase activity. Histological examination of lung tissues confirmed the beneficial effect of
levocetirizine against LPS-induced histopathological alterations. In conclusion,
levocetirizine may offer protection against lung tissue damage and
inflammation in LPS-challenged rats.