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Regulative effect of P38MAPK on release of TNF and NO from alveolar macrophages under endotoxin stimulation

Chinese Journal of Traumatology 2001年第2期4卷 75-77页

作者：卢家凯杨志焕蒋建新王正国朱佩芳

Objective:: To evaluate activation of P38 mitogen-activated protein kinase (P38MAPK) in alveolar macrophage (AM), release of TNFα and NO from cells, and their relationship following lipopolysacchride (LPS) stimulation. Methods: AM was isolated from branch alveolar lavage fluid (BALF). The activation of P38MAPK was assayed by Westernblot. SB203580, a specific inhibitor of P38MAPK, was used with gradient concentration to evaluate the regulative effect of P38MAPK on the release of TNFα and NO from AM. Results: P38MAPK was activated by LPS (100 ng/ml ) with peak activation at 30 minutes. The activation of P38MAPK was inhibited by SB203580. The secretion of TNFα and NO stimulated with LPS increased (P< 0.01 ) and was inhibited by SB203580 significantly. Conclusions: The results indicate that P38MAPK is involved in the secreting process of TNFα and NO following LPS stimulation. P38MAPK may be an important site for controlling the secretion of both inflammatory mediators during lung inflammatory disorders.

关键词： macrophages, alveolar Tumor necrosis factor Nitric oxide Lipopolysaccharides P38MAPK

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Cholecystokinin octapeptide inhibits the in vitro expression of CD14 in rat pulmonary interstitial macrophages induced by lipopolysaccharide

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Chinese Medical Journal 2002年第2期115卷 276-279页

作者：李淑瑾丛斌阎蕴力姚玉霞马春玲凌亦凌河北医科大学病理生理教研室河北石家庄050017 河北医科大学基础所细胞生物室河北石家庄050017 河北医科大学实验动物中心分子生物学研究室河北石家庄050017

OBJECTIVE: To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro. METHODS: PIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA. RESULTS: CCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide. CONCLUSION: CCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.

关键词： Animals Antigens, CD14 Cells, Cultured Culture Media, Conditioned Female Lipopolysaccharides macrophages, alveolar Rats Rats, Sprague-Dawley Research Support, Non-U.S. Gov't Sincalide Specific Pathogen-Free Organisms Tumor Necrosis Factor-alpha

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