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KMID : 0603520020070020087
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Journal of Korean Association of Cancer Prevention
2002 Volume.7 No. 2 p.87 ~ p.93
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The Aqueous Extract from Plapcodi radix Attenuates Lipopolysaccharide-Induced NF-кB Activation in RAW 264.7 Cell and Acute Lung Injury in Rats
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Lee Jun-Hyuk
Choi Yung-Hyun
Choi Byung-Tae
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Abstract
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We examined the effects of the aquous extract from Platycodi radix (AEPR), a traditional drug for respiratory infIammation, on the process of lipopolysaccharide (LPS)-induced nuclear factor (NF)-кBp65 activation in RAW 264.7 cell and anima1 model for acute lung injury. Immunoblot anaIysis Showed that the level of NF-KBp65 was rapidly up-regulated and inhibitory (I)-кBα was down-regulated by LPS challenge. While AEPR inhibitory an increase of NF-кBp65 and degradation of I-кBαin RAW 264.7 celI, an increase of tumor necrosis factor (TNF)-αactivation was observed. The total cells and protein content of the bronchoalveolar lavage f1uid by LPS challenge markedly decreased in the AEPR Pretreated rats. AEPR pretreatment caused aIso a decline in neutrophils infiltration into interstitium of the lllng. The immunoreation of NF-κBp65, I-кBα, inducible nitric oxide synthase (iNOS) and TNF-α was strongly localized at the alveolar and interstitial acrophages, but weak reaction also detected in neutrophils. The decrease of these immunoreactive cells in number were observed in AEPR pretreated rats. It may be concluded that AEPR attenuates the progress of LPS-induced inflammation by reduction of NF-кBp65 activation and neutrophil influx to lung. AEPR would be useful as a therapeutic agent for endotoxin-induced lung disease.
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KEYWORD
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Plapcodi radix, Lipopolysaccharide, Lung, Inflmmation, NF-кBp65
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