宣肺健脾方对慢性阻塞性肺疾病大鼠肺组织病理、气道杯状细胞及黏蛋白5AC的影响

doi:10.20047/j.issn1673-7210.2022.34.02

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摘要目的观察宣肺健脾方对慢性阻塞性肺疾病（COPD）大鼠肺组织病理、气道杯状细胞及黏蛋白5AC（MUC5AC）的影响。方法将鼠龄10～12周，体重（230±20）g的40只Wistar雄性大鼠，按随机数字表法分为空白组、模型组、中药组、西药组，每组10只。除空白组正常饲养外，其余各组采用注入脂多糖加熏香烟方法制备COPD大鼠模型。造模完成后中药组给予宣肺健脾方（1 ml/100 g），西药组给予沐舒坦（1 ml/100 g），空白组及模型组给予等量0.9%生理盐水，连续14 d。各组进行苏木精-伊红（HE）染色观察肺组织病理，检测支气管肺泡灌洗液（BALF）中白细胞总数及分类，进行阿尔辛蓝-过碘酸希夫（AB-PAS）染色观察杯状细胞，行免疫组织化学法检测MUC5AC。结果空白组肺组织结构完整，未见炎症细胞浸润，模型组肺组织结构破坏及炎症反应明显，中药组肺组织结构及炎症反应较模型组改善。模型组BALF中白细胞总数、中性粒细胞数、淋巴细胞数高于空白组，差异有统计学意义（P＜0.05）；中药组BALF中白细胞总数、中性粒细胞数、淋巴细胞数低于模型组，差异有统计学意义（P＜0.05）。空白组偶有少量杯状细胞，模型组杯状细胞增生高于空白组；中药组、西药组杯状细胞增生低于模型组。模型组相对着色面积高于空白组，差异有统计学意义（P＜0.05）；中药组相对着色面积低于模型组，差异有统计学意义（P＜0.05）。模型组肺组织MUC5AC蛋白表达高于空白组，差异有统计学意义（P＜0.05）；中药组MUC5AC蛋白表达低于模型组，差异有统计学意义（P＜0.05）。结论宣肺健脾方可能通过抑制杯状细胞化生，下调MUC5AC的表达，减少气道黏液高分泌；同时可减轻肺组织病理损害。

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	李先莉1 史利卿2 马建岭2 季坤2 温绍惠2 王梁敏2 李渊2 魏双颖2

关键词 ：慢性阻塞性肺疾病, 气道黏液高分泌, 宣肺健脾方, 杯状细胞, 黏蛋白5AC

Abstract：Objective To observe the effects of Xuanfei Jianpi Formula on the lung tissue pathology, airway goblet cells and Mucin5AC (MUC5AC) in rats with chronic obstructive pulmonary disease (COPD). Methods Forty Wistar male rats aged 10 to 12 weeks and weighing (230±20) g were divided into blank group, model group, traditional Chinese medicine group, and western medicine group according to random number table method, with ten rats in each group. Except the normal feeding of the blank group, the other groups were treated with lipopolysaccharide injection and smoked cigarettes to prepare COPD rat models. After the modeling, the traditional Chinese medicine group was given Xuanfei Jianpi Formula (1 ml/ 100 g), the western medicine group was given Mucosolvan (1 ml/100 g), and the blank and the model groups were given 0.9% normal saline for 14 consecutive days. Hematoxylin and eosin (HE) staining was performed to observe lung tissue pathology, and the total number and classification of white blood cells in bronchoalveolar lavage fluid (BALF) were detected. Goblet cells were observed by Alcian blue periodic acid-Schiff (AB-PAS) staining, and MUC5AC was detected by immunohistochemistry. Results The lung structure of blank group was complete, no inflammatory cell infiltration was observed, the lung structure destruction and inflammatory reaction were obvious in the model group, and the lung structure and inflammatory reaction were improved in the traditional Chinese medicine group compared with the model group. The total number of white blood cells, neutrophils and lymphocytes in BALF in model group were higher than those in blank group, and the differences were statistically significant (P＜0.05). The total number of white blood cells, neutrophils and lymphocytes in BALF in traditional Chinese medicine group were lower than those in model group, and the differences were statistically significant (P＜0.05). There were a few goblet cells occasionally in blank group, and the goblet cell proliferation in model group was higher than that in blank group. The goblet cell proliferation in the traditional Chinese medicine group and the western medicine group was lower than that in model group. The relative coloring area of model group was higher than that of the blank group, and the difference was statistically significant (P＜0.05). The relative coloring area of the traditional Chinese medicine group was lower than that of model group, and the difference was statistically significant (P＜0.05). The expression of MUC5AC protein in lung tissue of model group was higher than that of the blank group, and the difference was statistically significant (P＜0.05). The protein expression of MUC5AC in the traditional Chinese medicine group group was lower than that in the model group, and the difference was statistically significant (P＜0.05). Conclusion Xuanfei Jianpi Formula may down-regulate the expression of MUC5AC and reduce airway mucus hypersecretion by inhibiting goblet cell metaplasia. At the same time, it can reduce the pathological damage of lung tissue.

Key words： Chronic obstructive pulmonary disease Airway mucus hypersecretion Xuanfei Jianpi Formula Goblet cells Mucin5AC

基金资助:国家自然科学基金资助项目（81903987）；
北京中医药大学东方医院“1166”人才培养项目（0402040010010 02012）。

通讯作者: 马建岭（1982-），男，博士，主任医师，北京中医药大学东方医院呼吸热病科副主任；研究方向：呼吸系统疾病的中西医诊疗。李渊（1981-），女，博士，副主任医师；研究方向：慢性阻塞性肺疾病的中西医诊疗。

作者简介: 李先莉（1995-），女，北京中医药大学第二临床医学院2019级中医内科学专业在读硕士研究生；研究方向：呼吸系统疾病的中西医诊疗。

引用本文:

李先莉1 史利卿2 马建岭2 季坤2 温绍惠2 王梁敏2 李渊2 魏双颖2. 宣肺健脾方对慢性阻塞性肺疾病大鼠肺组织病理、气道杯状细胞及黏蛋白5AC的影响[J]. 中国医药导报, 2022, 19(34): 8-12.
LI Xianli1 SHI Liqing2 MA Jianling2 JI Kun2 WEN Shaohui2 WANG Liangmin2 LI Yuan2 WEI Shuangyin2. Effects of Xuanfei Jianpi Formula on lung tissue pathology, airway goblet cells and Mucin5AC in rats with chronic obstructive pulmonary disease. 中国医药导报, 2022, 19(34): 8-12.

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[1] 周玲凤，何庆华，唐海，等.慢性阻塞性肺疾病流行病学调查及防控分析[J].中国医学创新，2021，18（6）：84-87.
[2] Szalontai K，Gémes N，Furák J，et al. Chronic Obstructive Pulmonary Disease：Epidemiology，Biomarkers，and Paving the Way to Lung Cancer [J]. J Clin Med，2021，10（13）：2889.
[3] Wang C，Xu J，Yang L，et al. Prevalence and risk factors of chronic obstructive pulmonary disease in China（the China Pulmonary Health [CPH] study）：a national cross-sectional study [J]. Lancet，2018，391（10131）：1706-1717.
[4] 林展增.中国慢性阻塞性肺疾病流行病学研究进展[J].河北北方学院学报（自然科学版），2020，36（8）：49-51.
[5] 廖清，陶玉坚.慢性阻塞性肺疾病流行病学及危险因素研究现状[J].中华临床医师杂志（电子版），2018，12（8）：468-471.
[6] Stylianou P，Clark K，Gooptu B，et al. Tensin1 expression and function in chronic obstructive pulmonary disease [J]. Sci Rep，2019，9（1）：18942.
[7] 中华医学会呼吸病学分会慢性阻塞性肺疾病学组，中国医师协会呼吸医师分会慢性阻塞性肺疾病工作委员会.慢性阻塞性肺疾病诊治指南（2021年修订版）[J].中华结核和呼吸杂志，2021，44（3）：170-205.
[8] Boucher RC. Muco-Obstructive Lung Diseases [J]. N Engl J Med，2019，380（20）：1941-1953.
[9] 张晶，王彬，高峰.中医药干预慢性阻塞性肺疾病气道黏液高分泌作用机制研究进展[J].国际中医中药杂志，2020， 42（10）：1040-1043.
[10] 吕明圣，张沂，张迪，等.中医药多靶点干预慢性阻塞性肺疾病机制研究概述[J].中医杂志，2019，60（19）：1697- 1700.
[11] 范英兰，朱竟赫，甘雨，等.慢性阻塞性肺疾病大鼠模型的建立与评价[J].实用中医内科杂志，2021，36（10）：27-29， 158-159.
[12] 何转霞，齐鑫鑫，刘涛.慢性阻塞性肺疾病的体内外实验模型研究进展[J].毒理学杂志，2022，36（1）：80-85.
[13] 马建岭，季坤，董尚娟，等.宣肺健脾方治疗COPD稳定期气道黏液高分泌的临床疗效观察[J].世界中医药，2020， 15（4）：578-581.
[14] 唐欣，万南生，杨夏，等.慢性气道黏液高分泌与慢性阻塞性肺疾病的研究进展[J].中华结核和呼吸杂志，2021， 44（6）：574-578.
[15] 蔡霜，邹文静，王婷，等.Brg1通过STAT6促进哮喘气道黏液高分泌[J].南方医科大学学报，2018，38（1）：42-47.
[16] 蔺林，戴飞，任国强，等.嗜中性粒细胞弹性蛋白酶体外促进嗜中性粒细胞型鼻息肉中MUC5AC合成和释放[J].中国免疫学杂志，2020，36（15）：1873-1876.
[17] Kim MD，Baumlin N，Dennis JS，et al. Losartan reduces cigarette smoke-induced airway inflammation and mucus hypersecretion [J]. ERJ Open Res，2021，7（1）：00394- 2020.
[18] 钟秀君，高丹丹，顾文燕，等.蠲饮泄肺方对脂多糖诱导的气道黏液高分泌MUC5AC表达的影响[J].国际呼吸杂志，2018，38（16）：1256-1260.
[19] 伍清华，陈瑞坤，彭芳，等.气道炎症在COPD发生发展中的研究进展[J].中国医药科学，2020，10（17）：48-52.
[20] Radicioni G，Ceppe A，Ford AA，et al. Airway mucin MUC5AC and MUC5B concentrations and the initiation and progression of chronic obstructive pulmonary disease：an analysis of the SPIROMICS cohort [J]. Lancet Respir Med，2021，9（11）：1241-1254.
[21] Singanayagam A，Footitt J，Marczynski M，et al. Airway mucins promote immunopathology in virus-exacerbated chronic obstructive pulmonary disease [J]. J Clin Invest，2022，132（8）：e120901.
[22] 陈翠仪，吴雷，吕嘉春，等.黏蛋白在哮喘-慢性阻塞性肺疾病重叠中的表达与临床意义[J].现代医学与健康研究电子杂志，2021，5（10）：23-25.
[23] Lin XG，Li W，Xiang SY，et al. Electroacupuncture improves lung function by suppressing mucin-5AC mediated EGFR-p38MAPK signaling and inflammation reaction in chronic obstructive pulmonary disease rats [J]. Zhen Ci Yan Jiu，2021，46（3）：180-186.
[24] Cheon YH，Kim MS，Kim JY，et al. Eupatilin downregulates phorbol 12-myristate 13-acetate-induced MUC5AC expression via inhibition of p38/ERK/JNK MAPKs signal pathway in human airway epithelial cells [J]. Korean J Physiol Pharmacol，2020，24（2）：157-163.
[25] Li J, Ye Z. The Potential Role and Regulatory Mechanisms of MUC5AC in Chronic Obstructive Pulmonary Disease [J]. Molecules，2020，25（19）：4437.
[26] Lee SU，Kim MO，Kang MJ，et al. Transforming Growth Factor beta Inhibits MUC5AC Expression by Smad3/ HDAC2 Complex Formation and NF-kappaB Deacetylation at K310 in NCI-H292 Cells [J]. Mol Cells，2021，44（1）：38-49.