摘要
目的研究羧甲司坦对急性肺损伤小鼠气道黏蛋白的抑制作用。方法用脂多糖(LPS)刺激C57小鼠,建立急性肺损伤(ALI)的动物模型,同时用羧甲司坦进行干预,实验共分为4组:正常对照组、LPS组、羧甲司坦组和LPS+羧甲司坦组。采用细胞分类计数法观察各组小鼠BALF中炎性细胞的分布变化,酶联免疫吸附测定(ELISA)等方法检测羧甲司坦对ALI小鼠肺泡灌洗液(BALF)中黏蛋白Muc5AC、肿瘤坏死因子α(TNF-α)表达水平的影响。结果正常对照组小鼠BALF中淋巴细胞占绝大多数,单独给予羧甲司坦对BALF细胞分布无影响;LPS所致的ALI小鼠BALF中炎性细胞总数明显增加,且以中性粒细胞占多数,羧甲司坦能够明显抑制ALI小鼠BALF中炎性细胞总数及中性粒细胞数;羧甲司坦能够明显抑制ALI小鼠BALF中气道黏蛋白Muc5AC及TNF-α的表达水平。结论羧甲司坦能够明显抑制ALI小鼠气道炎性细胞及炎性因子TNF-α的表达水平,同时明显降低气道Muc5AC的表达水平。
Objective To study the inhibitory effect of Carbocisteine on airway Mucin 5AC. Methods Established acute lung injury mice model induced by Lipopolysaccharide (LPS). C57 mice were randomly divided into four groups (8 - 10 mice in each group) and given the following treatment:intranasal inhalation saline, intraperitoneal injection Carbocisteine, intranasal inhalation LPS and in- tranasal inhalation LPS + intraperitoneal injection Carbocisteine. Counting the inflammatory cell numbers in Bronchoalveolar Lavage Fluid (BALF) with HE staining method. Detecting the Mucin Muc5AC and tumor necrosis factor ot (TNF - α) levels in BALF. Results In BALF of the normal controls, the overwhelming majority of cells were lymphocyte, and Carbocisteine alone did not have effect to cellular distribution of normal mice. In BALF of acute lung injury (ALl) mice induced by LPS ,the number of inflammatory cells were marked in- creased, and most of them were neutrophils. Carbocisteine inhibited significantly the number of total inflammatory cells and neutriphils (P 〈0.05). In addition, Carbocisteine inhibited significantly the Muc5AC and TNF -α levels in BALF of ALI mice (P 〈 0.05 ). Conclusion Carboeisteine could inhibit significantly airway inflammation of ALI mice.
出处
《宁夏医学杂志》
CAS
2017年第7期594-596,共3页
Ningxia Medical Journal
基金
宁夏自然科学基金资助项目(NZ15166)