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孟鲁司特对实验性糖尿病肺部的影响。

Montelukast Influence on Lung in Experimental Diabetes.

机构信息

Department of Histology, "Gr T Popa" University of Medicine and Pharmacy, Universitatii 16, 700115 Iasi, Romania.

Department of Biochemistry, "Gr T Popa" University of Medicine and Pharmacy, Universitatii 16, 700115 Iasi, Romania.

出版信息

Medicina (Kaunas). 2024 Apr 30;60(5):749. doi: 10.3390/medicina60050749.

Abstract

: The influence of montelukast (MK), an antagonist of cysLT1 leukotriene receptors, on lung lesions caused by experimental diabetes was studied. : The study was conducted on four groups of six adult male Wistar rats. Diabetes was produced by administration of streptozotocin 65 mg/kg ip. in a single dose. Before the administration of streptozotocin, after 72 h, and after 8 weeks, the serum values of glucose, SOD, MDA, and total antioxidant capacity (TAS) were determined. After 8 weeks, the animals were anesthetized and sacrificed, and the lungs were harvested and examined by optical microscopy. Pulmonary fibrosis, the extent of lung lesions, and the lung wet-weight/dry-weight ratio were evaluated. : The obtained results showed that MK significantly reduced pulmonary fibrosis (3.34 ± 0.41 in the STZ group vs. 1.73 ± 0.24 in the STZ+MK group < 0.01) and lung lesion scores and also decreased the lung wet-weight/dry-weight (W/D) ratio. SOD and TAS values increased significantly when MK was administered to animals with diabetes (77.2 ± 11 U/mL in the STZ group vs. 95.7 ± 13.3 U/mL in the STZ+MK group, < 0.05, and 25.52 ± 2.09 Trolox units in the STZ group vs. 33.29 ± 1.64 Trolox units in the STZ+MK group, respectively, < 0.01), and MDA values decreased. MK administered alone did not significantly alter any of these parameters in normal animals. : The obtained data showed that by blocking the action of peptide leukotrienes on cysLT1 receptors, montelukast significantly reduced the lung lesions caused by diabetes. The involvement of these leukotrienes in the pathogenesis of fibrosis and other lung diabetic lesions was also demonstrated.

摘要

: 本研究旨在探讨孟鲁司特(MK)——半胱氨酰白三烯受体 1 拮抗剂对实验性糖尿病所致肺部病变的影响。 : 研究共纳入四组 6 只成年雄性 Wistar 大鼠,采用链脲佐菌素(65mg/kg,腹腔注射)单次给药建立糖尿病模型。在给予链脲佐菌素前、72 小时后和 8 周后,测定血清中葡萄糖、SOD、MDA 和总抗氧化能力(TAS)的含量。8 周后,动物麻醉处死,取肺脏,行光镜检查。观察肺纤维化程度、肺损伤评分和肺湿重/干重比值。 : 结果显示,MK 可显著减轻肺纤维化(STZ 组 3.34±0.41,STZ+MK 组 1.73±0.24, < 0.01)和肺损伤评分,降低肺湿重/干重比值。糖尿病动物给予 MK 治疗后 SOD 和 TAS 显著升高(STZ 组 77.2±11U/ml,STZ+MK 组 95.7±13.3U/ml, < 0.05;STZ 组 25.52±2.09Trolox 单位,STZ+MK 组 33.29±1.64Trolox 单位, < 0.01),MDA 降低。MK 单独给药对正常动物的上述参数无显著影响。 : 上述结果表明,通过阻断半胱氨酰白三烯受体 1 上的肽类白三烯的作用,孟鲁司特可显著减轻糖尿病引起的肺部病变,提示这些白三烯参与了纤维化等糖尿病肺部病变的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/130f/11123472/88f2b2687c82/medicina-60-00749-g001.jpg

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