Basyigit Ilknur, Sahin Murat, Sahin Deniz, Yildiz Fusun, Boyaci Hasim, Sirvanci Serap, Ercan Feriha
Department of Pulmonary Diseases, School of Medicine, Kocaeli University, Kocaeli, Turkey.
Multidiscip Respir Med. 2010 Apr 30;5(2):92-8. doi: 10.1186/2049-6958-5-2-92.
To evaluate the effects of montelukast in smoke-induced lung injury.
28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg) dissolved in Na2CO3 was given in one group (MON), Na2CO3 only was given in another group (MON control) and placebo was injected in the third group (COPD control) intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analyses were performed on the lung tissues of sacrificed rats.
Serum TNF-α levels in the MON group were significantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p < 0.05). Furthermore there was no statistically significant difference between the MON group and healthy controls with respect to serum TNF-α levels (38.84 ± 4.9 pg/ml vs. 29.5 ± 3.6 pg/ml, p > 0.05). Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respectively, p < 0.05), while there was no significant difference between the MON group and healthy controls (5.1 ± 0.6 vs 2.3 ± 0.2, p > 0.05).
These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view.
评估孟鲁司特对烟雾诱导的肺损伤的影响。
将28只Wistar - 白化大鼠分为4组，每组7只。健康对照组暴露于新鲜空气中，而3个实验组的所有大鼠每天暴露于香烟烟雾中2小时，持续20周。在通过组织病理学验证烟雾诱导的肺损伤后，一组（MON组）腹腔注射溶解于碳酸钠的孟鲁司特（0.1 mg/kg），另一组（MON对照组）仅注射碳酸钠，第三组（慢性阻塞性肺疾病对照组）注射安慰剂，持续21天。在此期间结束时，采集血样进行血清肿瘤坏死因子 -α（TNF-α）评估，并对处死大鼠的肺组织进行光镜和电镜分析。
MON组的血清TNF-α水平显著低于MON对照组和慢性阻塞性肺疾病对照组（分别为38.84±4.9 pg/ml、77.5±5.8 pg/ml和79.2±6.9 pg/ml，p<0.05）。此外，MON组与健康对照组在血清TNF-α水平方面无统计学显著差异（38.84±4.9 pg/ml对29.5±3.6 pg/ml，p>0.05）。肺组织的光镜和电镜评估表明，MON组肺样本的总组织病理学损伤评分显著低于MON对照组和慢性阻塞性肺疾病对照组（分别为5.14±0.5、8.4±0.6和8.7±0.4，p<0.05），而MON组与健康对照组之间无显著差异（5.1±0.6对2.3±0.2，p>0.05）。
这些发现表明，从组织病理学和炎症角度来看，孟鲁司特可能对大鼠烟雾诱导的肺损伤具有保护作用。
