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Effects of cannabinoid receptor ligands on LPS-induced pulmonary inflammation in mice.

机译:大麻素受体配体对LPS诱导的小鼠肺部炎症的影响。

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The effects of cannabinoid receptor agonists WIN 55,212-2, delta9-tetrahydrocannabinol (delta9-THC), arachidonoylethanolamide (anandamide) and palmitoylethanolamide on lipopolysaccharide (LPS) -induced bronchopulmonary inflammation in mice were investigated. WIN 55,212-2 and delta9-THC induced a concentration-dependent decrease in TNF-alpha level in the bronchoalveolar lavage fluid (BALF) (maximum inhibition 52.7% and 36.9% for intranasal doses of 750 nmol x kg(-1) and 2.65 mmol x kg(-1), respectively). This effect was accompanied by moderately reduced neutrophil recruitment. Palmitoylethanolamide (750 nmol x kg(-1)) diminished the level of TNF-alpha in BALF by 31.5% but had no effect on neutrophil recruitment. Anandamide (7.5-750 nmol x kg(-1)) did not influence the inflammatory process but TNF-alpha level and neutrophil recruitment were decreased by 28.0% and 62.0%, respectively, with 0.075 nmol x kg(-1). These results demonstrate that the cannabinoid receptor ligands inhibited LPS-induced pulmonary inflammation and suggest that this effect could be at least in part mediated by the cannabinoid CB2 receptor.
机译:研究了大麻素受体激动剂WIN 55,212-2,delta9-四氢大麻酚(delta9-THC),花生四烯酰乙醇酰胺(anandamide)和棕榈酰乙醇酰胺对脂多糖(LPS)诱导的小鼠支气管肺炎症的影响。 WIN 55,212-2和delta9-THC引起支气管肺泡灌洗液(BALF)中TNF-α浓度的浓度依赖性降低(鼻内剂量750 nmol x kg(-1)和2.65 mmol时最大抑制率分别为52.7%和36.9% x kg(-1))。这种作用伴随着中性粒细胞募集的减少。棕榈酰乙醇酰胺(750 nmol x kg(-1))使BALF中的TNF-α水平降低了31.5%,但对中性粒细胞募集没有影响。 Anandamide(7.5-750 nmol x kg(-1))不影响炎症过程,但TNF-α水平和嗜中性白细胞募集分别降低了28.0%和62.0%,其中0.075 nmol x kg(-1)。这些结果表明,大麻素受体配体抑制了LPS诱导的肺部炎症,并表明这种作用可能至少部分由大麻素CB2受体介导。

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