發(fā)布時(shí)間：2019-08-15 18:28

【摘要】：目的:研究蒙藥五味沙棘散(WSP)對(duì)吸煙所致小鼠肺部炎癥的改善作用及其機(jī)制。方法:將30只ICR小鼠隨機(jī)分為空白組(生理鹽水)、模型組(生理鹽水)和WSP組(2 g/kg)。模型組和WSP組小鼠采用被動(dòng)吸煙法復(fù)制肺部炎癥損傷模型,并于造模的同時(shí)每天ig相應(yīng)藥物1次,連續(xù)28 d。給藥結(jié)束后,采用酶聯(lián)免疫吸附法檢測(cè)小鼠肺泡灌洗液(BALF)中腫瘤壞死因子α(TNF-α)、白細(xì)胞介素1β(IL-1β)、IL-6和IL-10水平;蘇木精-伊紅染色后光鏡下觀察小鼠肺組織病理變化;Western blot法檢測(cè)小鼠肺組織中細(xì)胞外信號(hào)調(diào)節(jié)蛋白激酶1/2(ERK1/2)、磷酸化ERK1/2(p-ERK1/2)、p38絲裂原活化蛋白激酶(p38 MAPK)、磷酸化p38 MAPK(p-p38 MAPK)、核因子κB p65(NF-κB p65)和磷酸化NF-κB p65(p-NF-κB p65)蛋白表達(dá)。結(jié)果:與空白組比較,模型組小鼠BALF中TNF-α、IL-1β和IL-6水平明顯升高(P0.01),肺組織發(fā)生明顯炎癥病變,肺組織中p-ERK1/2、p-p38 MAPK、pNF-κB p65蛋白表達(dá)水平明顯升高(P0.01)。與模型組比較,WSP組大鼠BALF中TNF-α、IL-1β水平明顯降低(P0.05),肺組織炎癥損傷明顯改善,肺組織中p-p38 MAPK和p-NF-κB p65蛋白表達(dá)水平明顯降低(P0.05)。結(jié)論:WSP可能通過(guò)阻斷p38MAPK、NF-κB p65蛋白的磷酸化來(lái)抑制炎癥因子TNF-α和IL-6的高表達(dá),從而發(fā)揮其對(duì)吸煙所致小鼠肺部炎癥損傷的改善作用。
[Abstract]:Objective: to study the effect and mechanism of Mongolian medicine Wuwei Hippophae rhamnoides Powder (WSP) on pulmonary inflammation induced by smoking in mice. Methods: 30 ICR mice were randomly divided into blank group (saline), model group (saline) and WSP group (2 g/kg). The model group and WSP group were used to establish the model of pulmonary inflammatory injury by passive smoking, and the corresponding drugs of ig were made once a day for 28 days. After administration, the levels of tumor necrosis factor 偽 (TNF- 偽), IL 1 尾 (IL-1 尾), IL-6 and IL-10 in (BALF) of alveolar lavage fluid were detected by enzyme linked immunosorbent assay (Elisa), and the pathological changes of lung tissue were observed under light microscope after hematoxylin and eosin staining. The expression of extracellular signal-regulated protein kinase 1 鈮，

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