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骆驼奶可抑制香烟烟雾暴露诱导的慢性阻塞性肺疾病大鼠模型中的肺部氧化应激和炎症反应。

Camel milk inhibits pulmonary oxidative stress and inflammation in a rat model of COPD induced by cigarette smoke exposure.

作者信息

Behrouz Sepide, Mohammadi Mahla, Sarir Hadi, Mohammadian Roshan Nema, Boskabady Mohammad Hossein

机构信息

Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

Heliyon. 2024 Oct 16;10(20):e39416. doi: 10.1016/j.heliyon.2024.e39416. eCollection 2024 Oct 30.

DOI:10.1016/j.heliyon.2024.e39416
PMID:39497967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11532301/
Abstract

BACKGROUND

One of the main causes of death in the world is chronic obstructive pulmonary disease (COPD) with partially reversible airflow limitation, which is defined as a preventable and treatable pathological condition. Anti-inflammatory and antioxidant properties of camel milk (CM) were indicated previously. The effect of CM in cigarette smoke induced-COPD in rats was evaluated in this study.

METHODS

Five groups of rats including a) control, b) chronic obstructive pulmonary diseases (COPD, cigarette smoke exposed), c) COPD group treated with dexamethasone, d) COPD group treated with low dose of camel milk (CM) and e) COPD group treated with high dose of CM by gavage during the cigarette smoke exposure period (n = 7) were studied.

RESULTS

In the COPD group, total and differential white blood cells (WBC) count in the bronchoalveolar fluid (BALF), tumor necrosis factor-alpha (TNF-α) level in the lung tissue and malondialdehyde (MDA) level in the BALF and lung tissue, lung pathological changes and tracheal responsiveness to methacholine were significantly increased, but catalase (CAT) and superoxide dismutase (SOD) activities and the level of thiol in the BALF and lung tissue were significantly decreased compared to the control group (all,  < 0.001). However, in the COPD groups treated with both doses of CM and dexamethasone, most variable did not achieved to the control levels and were significantly different with the control group ( < 0.05 to  < 0.001). In the COPD group treated with both doses of CM (dose dependently) and dexamethasone, almost all measured variables were significantly improved ( < 0.05 to  < 0.001).

CONCLUSION

The potential effect of CM on lung inflammation and oxidative stress in a rat model of COPD comparable to dexamethasone was demonstrated.

摘要

背景

世界上主要的死亡原因之一是慢性阻塞性肺疾病(COPD),其气流受限部分可逆,这被定义为一种可预防和可治疗的病理状况。先前已表明骆驼奶(CM)具有抗炎和抗氧化特性。本研究评估了CM对香烟烟雾诱导的大鼠COPD的影响。

方法

研究了五组大鼠,包括a)对照组,b)慢性阻塞性肺疾病(COPD,暴露于香烟烟雾)组,c)用 dexamethasone治疗的COPD组,d)在香烟烟雾暴露期间通过灌胃给予低剂量骆驼奶(CM)的COPD组,以及e)在香烟烟雾暴露期间通过灌胃给予高剂量CM的COPD组(n = 7)。

结果

在COPD组中,支气管肺泡灌洗液(BALF)中的白细胞总数和分类计数、肺组织中的肿瘤坏死因子-α(TNF-α)水平以及BALF和肺组织中的丙二醛(MDA)水平、肺部病理变化以及气管对乙酰甲胆碱的反应性均显著增加,但与对照组相比,BALF和肺组织中的过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性以及巯基水平显著降低(所有P均<0.001)。然而,在接受两种剂量CM和dexamethasone治疗的COPD组中,大多数变量未达到对照水平,且与对照组有显著差异(P<0.05至P<0.001)。在接受两种剂量CM(剂量依赖性)和dexamethasone治疗的COPD组中,几乎所有测量变量均得到显著改善(P<0.05至P<0.001)。

结论

证明了CM对COPD大鼠模型中肺部炎症和氧化应激的潜在作用与dexamethasone相当。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/4383307264b1/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/1e24afc5dd53/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/2c97c2ab7d94/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/0ee918212094/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/3864341f4fdc/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/90a1d8a01149/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/76ac6cf9b1de/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/2e667590a411/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/4383307264b1/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/1e24afc5dd53/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/2c97c2ab7d94/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/0ee918212094/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/3864341f4fdc/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/90a1d8a01149/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/76ac6cf9b1de/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/2e667590a411/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db81/11532301/4383307264b1/gr8.jpg

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