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Bleomycin-induced oxidative stress and lung injury in rats: Inhibition by curcumin

机译:博来霉素诱导的大鼠氧化应激和肺损伤:姜黄素的抑制作用

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摘要

In this study, we investigated whether oxidant/antioxidant imbalance in bleomycin (BLM)-instilled lungs would be prevented by curcumin. A single intratracheal injection of bleomycin (5 mg/kg body weight) to rats induced acute lung injury accompanied by significant increases in biochemical markers and inflammatory cell accumulation in bronchoalveolar lavage fluid and increased lung levels of myeloperoxidase (MPO) and intercellular adhesion molecule-1 (ICAM-1) 7 days after bleomycin administration. Also, bleomycin instillation led to leukocytes accumulation and fibrotic changes in the lung interstitium. Lung levels of thiobarbituric acid reactive substances (TBARS), conjugated dienes and protein carbonyls were increased at 7 and 14 days after bleomycin administration. In addition, increases in lung antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, glutathione reductase and glutamate cysteine ligase were noticed 7 and 14 days after BLM administration. Curcumin (300 mg/kg body weight, one week before and daily thereafter for 14 days) treatment significantly inhibited bleomycin-induced increases in lung lavage fluid biomarkers, histopathological changes, lung lipid peroxidation products and restored the levels of antioxidant enzymes to normal values. These findings indicate that curcumin is capable of inhibiting bleomycin-induced lung injury through inhibition of oxidative stress and perturbations in pulmonary antioxidant defense mechanisms. 2006 Bentham Science Publishers Ltd.
机译:在这项研究中,我们研究了姜黄素是否可以预防博莱霉素(BLM)注入的肺中的氧化剂/抗氧化剂失衡。向大鼠单次气管内注射博来霉素(5 mg / kg体重)诱发急性肺损伤,并伴有生化标志物和支气管肺泡灌洗液中炎性细胞积聚的显着增加,以及肺过氧化物酶(MPO)和细胞间粘附分子-1的水平升高(ICAM-1)博来霉素给药后7天。同样,博来霉素滴注导致肺间质中白细胞积聚和纤维化改变。博来霉素给药后7天和14天,肺巴中的硫代巴比妥酸反应性物质(TBARS),共轭二烯和蛋白质羰基的含量增加。另外,在BLM给药后7天和14天,发现肺抗氧化剂酶例如超氧化物歧化酶,谷胱甘肽过氧化物酶,谷胱甘肽还原酶和谷氨酸半胱氨酸连接酶增加。姜黄素(300 mg / kg体重,在治疗前1周和治疗后每天1天,持续14天)可显着抑制博来霉素诱导的肺灌洗液生物标志物增加,组织病理学变化,肺脂质过氧化产物并将抗氧化酶水平恢复至正常值。这些发现表明姜黄素能够通过抑制氧化应激和肺抗氧化防御机制中的扰动来抑制博来霉素诱导的肺损伤。 2006边沁科学出版有限公司。

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