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연구배경: 내독소로 유발된 급성폐손상의 발생기전에 산화스트레스가 중요한 역할은 한다. 본 실험은 LPS로 유발한 급성폐손상 모델에서 항산화제인 α-lipoic acid의 치료효과를 보고하였다.방 법: Sprague-Dawley 쥐를 대상으로 LPS (E.coli, 3mg/Kg)를 기도내 주입 후 α-lipoic acid를 복강 내 주입하였다. 2시간, 6시간 후에 폐포세척액에서 호중구수, CINC, 시토카인의 농도를 구하고 폐조직에서 MPO 를 측정하였다. 결 과: α-lipoic acid를 후처치한 군에서 LPS 단독군보다 2시간 뒤와 6시간 뒤에 총 세포수와 호중구의 수가 감소하였으나 단백질 농도는 차이가 없었다. 또한 염증성 인자인 TNF-α, IL-1ß, IL-6의 농도도 α-lipoic acid 처치군에서 유의한 감소를 보이지 못하였다.


Background: Oxidative stress may play an important role in the pathogenesis of endotoxin-induced acute lung injury (ALI). This study evaluated the therapeutic effect of α-lipoic acid, a nonenzymatic antioxidant, in a rat model of lipopolysaccharide (LPS) induced ALI. Materials and Methods: ALI was induced in Sprague-Dawley rats by instilling LPS (E.coli, 3mg/Kg) into the trachea. The rats were classified into the control, control+α-lipoic acid, LPS, and LPS+α-lipoic acid groups.The lung lavage neutrophil count, cytokine-induced neutrophil chemoattractant (CINC), lung myeloperoxidase (MPO), and cytokine concentrations (TNF-α, IL-1ß, IL-6 and IL-10) were measured at 2 h and 6 h after LPS administration. Results: The total cell and neutrophil counts of the LPS+α-lipoic acid groups were significantly lower than the LPS groups. The protein concentration in the BAL fluid was similar in the LPS groups and LPS+α-lipoic acid groups. The TNF-α, IL-1ß, and IL-6 concentrations in the BAL fluid were not decreased by the α-lipoic acid treatment in the LPS treated rats. Conclusions: Although α-lipoic acid decreased the level of LPS-induced neutrophil infiltration into the lung, it could not attenuate the LPS-induced ALI at the dose administered in this study. (Tuberc Respir Dis 2007; 62: 105-112)