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机构地区:[1]浙江大学医学院附属邵逸夫医院,浙江杭州310016 [2]浙江大学自家食品药品监督管理局浙江呼吸药物研究实验室,浙江杭州310058
出 处:《中草药》2009年第8期1254-1259,共6页Chinese Traditional and Herbal Drugs
基 金:国家自然科学基金资助项目(30671919,30772581);浙江省科技厅重点科研项目(2006C23009)
摘 要:目的研究甘草黄酮对抗内毒素脂多糖(LPS)诱导小鼠肺部炎症的作用机制。方法小鼠气管内滴入LPS或生理盐水,6或24 h后取支气管肺泡灌洗液(BALF)和肺组织,测定BALF中的白细胞总数和中性粒细胞以及超氧化物歧化酶(SOD)活性,测定肺组织的含水量和病理变化,测定肺组织匀浆和BALF中的髓过氧化物酶(MPO)活性、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的mRNA表达以及TNF-α蛋白水平。结果白细胞计数、肺含水量测定和肺组织病理检查等指标显示,小鼠气管内滴入LPS引起严重的肺部炎症。甘草黄酮给药后能预防LPS引起的这些变化。甘草黄酮能明显减少BALF中的总白细胞和中性粒细胞的数目,升高SOD活性。甘草黄酮能明显降低肺组织中的MPO活性,抑制TNF-α和IL-1βmRNA的表达,抑制TNF-α蛋白水平。结论甘草黄酮能改善LPS引起的小鼠肺部炎症,其抗炎作用可能与抑制细胞因子的表达和调节氧化/抗氧化反应有关。Objective To study the mechanism of anti-inflammatory effects of licorice flavonoids (LF) isolated from the roots of Glycyrrhiza uralensis (licorice) on lipopolysaccharide (LPS)-induced lung inflammation in mice. Methods Mice were intratracheally instillated with either LPS (4 mg/kg) or saline. At 6 or 24 h after LPS intratracheal instillation, pathological examination and bronchoalveolar lavage were performed and the lung wet/dry weight ratio as an index of acute lung injury was assessed. Then, the numbers of total leukocytes, neutrophils and the activity of superoxide dismutase (SOD) and TNF-α protein in bronchoalveolar lavage fluid (BALF) were measured. LPS-induced myeloporoxidase (MPO) activity and expressions of TNF-α and IL-1β at the mRNA levels and TNF-α at the protein level in lung tissues were determined by RT-PCR and ELISA. Results LPS caused a severe lung inflammation, as indicated by the pathological findings and the lung wet/dry weight ratio. However, oral LF could attenuate these LPS-induced abnormalities. LF could decrease the numbers of total leukocyte cells and neutrophils, and increase the levels of SOD and TNF-α BALF. In addition, LF significantly suppressed the MPO activity, TNF-α and IL-1β mRNA expression levels, and TNF-α protein level in the lung tissues. Conclusion Inhibition of inflammatory cytokines expressions and regulation of oxidation/antioxidation of LF may be its anti-inflammatory mechanism in LPS-induced lung inflammation in mice.
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