摘要
目的:探讨青蒿琥酯通过调控M2巨噬细胞极化对香烟烟雾暴露小鼠气道重塑的影响。方法:小鼠随机分为5组:对照组、香烟烟雾诱导组和青蒿琥酯低、中、高剂量组。香烟烟雾诱导组和青蒿琥酯组小鼠进行烟熏处理,青蒿琥酯组小鼠分别腹腔注射25、50、100 mg/kg青蒿琥酯。生理数据采集检测肺功能;收集支气管肺泡灌洗液(BALF)检测炎症因子和氧化应激参数;HE和Masson三色染色评价肺组织病理学改变;免疫组化染色检测α-SMA和E-cadherin表达;Western blot检测蛋白表达。结果:香烟烟雾诱导组小鼠肺功能损伤、肺组织病理学损伤及胶原沉积增加;气道组织中α-SMA及M2巨噬细胞标志物清道夫受体(CD163)、甘露糖受体(CD206)和精氨酸酶-1(Arg-1)、转化生长因子-β1(TGF-β1)表达升高,E-cadherin表达减少;BALF中小鼠肿瘤坏死因子-α(TNF-α)、白细胞介素6(IL-6)、IL-1β、活性氧(ROS)和丙二醛(MDA)含量增加,还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活力降低。青蒿琥酯治疗可改善肺功能,减轻肺组织病理学损伤和胶原沉积;降低α-SMA及M2巨噬细胞标志物表达而增加E-cadherin表达;减少BALF中炎症因子和氧化应激。结论:青蒿琥酯可能部分通过抑制M2巨噬细胞极化改善香烟烟雾暴露小鼠的气道重塑。
Objective:To address the influence of artesunate on the airway remodeling in mice with obstructive pulmonary disease through regulating the polarization of M2 macrophages.Methods:Mice were randomized to 5 groups,namely,control group,cigarette smoke exposure group,low-,medium-and high-dose of artesunate groups.Mice in the cigarette smoke exposure group and artesunate treatment groups were exposed to smoke initially,and then artesunate was applied in dose of 25,50 and 100 mg/kg,respectively,to the mice in artesunate treatment groups via intraperitoneal injection.Physiological data were collected for evaluation of lung function.Bronchoalveolar lavage fluid(BALF)was harvested for detection of inflammatory factors and oxidative stress parameters.Histopathological changes of the lungs were detected by HE and Masson trichromatic staining.Immunohistochemistry was used to assessα-SMA and E-cadherin expression.The protein expressions were analyzed by Western blot.Results:Cigarette smoke exposure led to heightened pulmonary function impairment,lung tissue damage,and collagen accumulation in the model mice.Increased expressions ofα-SMA and M2 macrophage markers CD163,CD206,Arg1,and TGF-β1 were observed,whereas E-cadherin expression was reduced in the airway tissues.The contents of TNF-α,IL-6,IL-1β,ROS and MDA were enhanced,while GSH content and SOD activity were reduced in BALF.Artesunate administration improved the lung function,decreased lung tissue injury and collagen deposition.It also resulted in lower levels ofα-SMA and M2 macrophage markers,with an increase in E-cadherin expression,as well as reduction of inflammatory factors and oxidative stress in BALF.Conclusion:Artesunate might partially improve the airway remodeling in model mice exposed to the smoke by inhibiting M2 macrophage polarization.
作者
王洪高
杨小兰
田小平
岳小蓉
WANG Honggao;YANG Xiaolan;TIAN Xiaoping;YUE Xiaorong(Department of Pediatrics,Hospital of Traditional Chinese Medicine of Bazhong City(Bazhou District People′s Hospital),Bazhong 636000,Sichuan,China)
出处
《皖南医学院学报》
2025年第4期311-316,共6页
Journal of Wannan Medical College
基金
四川省医学(青年创新)科研课题项目(S211730)。
关键词
青蒿琥酯
巨噬细胞极化
阻塞性肺疾病
气道重塑
artesunate
macrophage polarization
obstructive pulmonary disease
airway remodeling
