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麻杏石甘汤对冷热循环诱导的大鼠肺损伤的治疗作用。

Post-treatment with Ma-Huang-Tang ameliorates cold-warm-cycles induced rat lung injury.

机构信息

Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.

Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing, 100191, China.

出版信息

Sci Rep. 2017 Mar 22;7(1):312. doi: 10.1038/s41598-017-00459-3.

Abstract

Frequent and drastic ambient temperature variation may cause respiratory diseases such as common cold and pneumonia, the mechanism for which is not fully understood, however, due to lack of appropriate animal models. Ma-Huang-Tang (MHT) is widely used in China for treatment of respiratory diseases. The present study aimed to investigate the effect of MHT on temperature alternation induced rat lung injury and explore underlying mechanisms. Male Sprague-Dawley rats were exposed to a cold environment for 1 h and then shifted to a warm environment for 30 min. This cold and warm alteration cycled 4 times. Rats were administrated with MHT (1.87 g/kg) by gavage 6 h after cold-warm-cycles. Cold-warm-cycles induced pulmonary microcirculatory disorders, lung edema and injury, decrease in the expression of tight junction proteins, increase in VE-cadherin activation, increase in the expression and activation of Caveolin-1, Src and NF-κB, and NADPH oxidase subunits p47, p40 and p67 membrane translocation and inflammatory cytokines production. All alterations were significantly ameliorated by post-treatment with MHT. This study showed that rats subjected to cold-warm-cycles may be used as an animal model to investigate ambient temperature variation-induced lung injury, and suggested MHT as a potential strategy to combat lung injury induced by temperature variation.

摘要

频繁而剧烈的环境温度变化可能导致感冒和肺炎等呼吸道疾病,但其机制尚不完全清楚,这主要是由于缺乏合适的动物模型。麻黄汤(MHT)在中国被广泛用于治疗呼吸道疾病。本研究旨在探讨 MHT 对温度交替诱导的大鼠肺损伤的作用及其机制。雄性 Sprague-Dawley 大鼠先暴露于寒冷环境 1 h,然后转移至温暖环境 30 min,这种冷-热交替循环进行 4 次。冷-热循环 6 h 后,大鼠通过灌胃给予 MHT(1.87 g/kg)。冷-热循环引起肺微循环障碍、肺水肿和损伤,降低紧密连接蛋白的表达,增加 VE-钙黏蛋白的激活,增加 Caveolin-1、Src 和 NF-κB 的表达和激活,以及 NADPH 氧化酶亚基 p47、p40 和 p67 的膜转位和炎症细胞因子的产生。MHT 后处理显著改善了所有改变。本研究表明,经历冷-热循环的大鼠可作为研究环境温度变化诱导肺损伤的动物模型,并提示 MHT 可能是一种对抗温度变化引起肺损伤的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1705/5428516/99f86a49bd08/41598_2017_459_Fig1_HTML.jpg

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