Abstract
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.
Highlights
Acute lung injury (ALI) is a critical pathological event that causes acute pulmonary failure and death
The term ALI has been widely replaced with the acute respiratory distress syndrome (ARDS), which is currently defined based on several diagnostic criteria [1]
Serum C-reactive protein (CRP) levels were significantly higher in LPS-treated rats than control group (P < 0.0001), indicating an acute inflammation
Summary
Acute lung injury (ALI) is a critical pathological event that causes acute pulmonary failure and death. The ALI/ARDS may arise due to a diverse set of inciting insults such as major trauma, burns, pneumonia, aspiration, and sepsis [1]. Of these factors, sepsis related to bacterial infection garners special interest since it remains the most common etiology of postsurgery and posttrauma deaths [3]. LPS is robustly used to elicit experimental ALI, which exhibits major features of lung tissue injury in human ARDS, including leukocyte infiltration, lung edema, abnormal gas exchange, and mortality [7, 8]. Apoptosis takes place in several cell types that are located in the inflammatory lung milieu [7]
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