博莱霉素
百里香醌
氧化应激
肺纤维化
乳酸脱氢酶
医学
支气管肺泡灌洗
羟脯氨酸
纤维化
药理学
超氧化物歧化酶
肺
化学
内科学
内分泌学
病理
抗氧化剂
生物化学
化疗
酶
作者
Dalia El-Khouly,Wesam M. El-Bakly,Azza S. Awad,Hala O. El-Mesallamy,Ebtehal El-Demerdash
出处
期刊:Toxicology
[Elsevier]
日期:2012-12-01
卷期号:302 (2-3): 106-113
被引量:64
标识
DOI:10.1016/j.tox.2012.09.001
摘要
Pulmonary fibrosis is one of the most common chronic interstitial lung diseases with high mortality rate after diagnosis and limited successful treatment. The present study was designed to assess the potential antifibrotic effect of thymoquinone (TQ) and whether TQ can attenuate the severity of oxidative stress and inflammatory response during bleomycin-induced pulmonary fibrosis. Male Wister rats were treated intraperitoneally with either bleomycin (15 mg/kg, 3 times a week for 4 weeks) and/or thymoquinone (5mg/kg/day, 1 week before and until the end of the experiment). Bleomycin significantly increased lung weight and the levels of Lactate dehydrogenase, total leucocytic count, total protein and mucin in bronchoalveolar lavage and these effects were significantly ameliorated by TQ treatment. As markers of oxidative stress, bleomycin caused a significant increase in the levels of lipid peroxides and nitric oxide accompanied with a significant decrease in the antioxidant enzyme activity of superoxide dismutase and glutathione transferase. TQ treatment restored these markers toward normal values. TQ also counteracted emphysema in air alveoli, inflammatory cell infiltration, lymphoid hyperplastic cells activation surrounding the bronchioles and the over expression of activated form of nuclear factor kappa-B (NF-B) in lung tissue that was induced by bleomycin. Fibrosis was assessed by measuring hydroxyproline content, which increased markedly in the bleomycin group and significantly reduced by concurrent treatment with TQ. Furthermore, histopathological examination confirmed the antifibrotic effect of TQ. Collectively these findings indicate that TQ has potential antifibrotic effect beside its antioxidant activity that could be through NF-κB inhibition.
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