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KMID : 0383820120730010022
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Tuberculosis and Respiratory Diseases
2012 Volume.73 No. 1 p.22 ~ p.31
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The Effect of Post-Treatment N-Acetylcysteine in LPS-Induced Acute Lung Injury of Rats
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Choi Jae-Sung
Lee Ho-Sung
Seo Ki-Hyun
Na Ju-Ock
Kim Yong-Hoon
Uh Soo-Taek
Park Choon-Sik
Oh Mee-Hye
Lee Sang-Han
Kim Young-Tong
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Abstract
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Background: Oxidation plays an important role in acute lung injury. This study was conducted in order to elucidate the effect of repetitive post-treatment of N-acetylcysteine (NAC) in lipopolysaccaride (LPS)-induced acute lung injury (ALI) of rats.
Materials and Methods: Six-week-old male Sprague-Dawley rats were divided into 4 groups. LPS (Escherichia coli 5 mg/kg) was administered intravenously via the tail vein. NAC (20 mg/kg) was injected intraperitoneally 3, 6, and 12 hours after LPS injection. Broncho-alveolar lavage fluid (BALF) and lung tissues were obtained to evaluate the ALI at 24 hours after LPS injection. The concentration of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were measured in BALF. Nuclear factor κB (NF-κB), lipid peroxidation (LPO), and myeloperoxidase (MPO) were measured using lung tissues. Micro-computed tomography (micro-CT) images were examined in each group at 72 hours apart from the main experiments in order to observe the delayed effects of NAC.
Results: TNF-α and IL-1β concentration in BALF were not different between LPS and NAC treatment groups. The concentration of LPO in NAC treatment group was significantly lower than that of LPS group (5.5±2.8 nmol/mL vs. 16.5±1.6 nmol/mL) (p=0.001). The activity of MPO in NAC treatment group was significantly lower than that of LPS group (6.4±1.8 unit/g vs. 11.2±6.3 unit/g, tissue) (p＜0.048). The concentration of NF-κB in NAC treatment group was significantly lower than that of LPS group (0.3±0.1 ng/μL vs. 0.4±0.2 ng/μL) (p=0.0001). Micro-CT showed less extent of lung injury in NAC treatment than LPS group.
Conclusion: After induction of ALI with lipopolysaccharide, the therapeutic administration of NAC partially attenuated the extent of ALI through the inhibition of NF-κB activation.
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KEYWORD
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Acetylcysteine, Acute Lung Injury, Antioxidants
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