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基于“风寒化肺热”病机探讨鼻渊合剂拆方对急性鼻窦炎大鼠鼻窦黏膜炎症的影响

Effects of Split Formulas of Biyuan Heji on Paranasal Sinus Mucosal Inflammation in ARS Rats Based on the Pathogenesis of“Wind-Cold Transforming into Lung-Heat”
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摘要 目的基于“风寒化肺热”病机,探讨鼻渊合剂拆方对急性鼻窦炎大鼠鼻窦黏膜炎症的影响。方法采用单侧鼻腔填塞联合鼻腔滴注金黄色葡萄球菌悬液的方法建立急性鼻窦炎大鼠模型。将SD大鼠随机分为空白组、模型组、鼻渊合剂(祛风寒+清肺热)组、清肺热组、祛风寒组、阳性药组,每组各6只,分别给予相应药物治疗7 d后取材。HE染色观察大鼠鼻窦黏膜组织病理性改变,ELISA测定血清中白细胞介素-1β(IL-1β)、IL-6、IL-8、IL-9、IL-10、IL-12水平,免疫组化检测鼻窦黏膜组织肿瘤坏死因子-α(TNF-α)和细胞间黏附分子(ICAM-1)的蛋白表达,Western blot检测鼻窦黏膜组织磷酸化p38丝裂原活化蛋白激酶(p38 MAPK)、核转录因子-κB(NF-κB)p50和NF-κB p65蛋白表达情况。结果急性鼻窦炎大鼠模型成功建立。与模型组比,鼻渊合剂组、清肺热组、祛风寒组及阳性药组大鼠饮水、饮食及体质量均明显改善,鼻窦黏膜组织中炎症细胞聚集减少,血清中IL-1β、IL-6、IL-8、IL-9、IL-12含量均明显降低(P<0.01),IL-10含量明显升高(P<0.01),鼻窦黏膜组织中TNF-α、ICAM-1、p38 MAPK、NF-κB p50和NF-κB p65蛋白表达均明显下降(P<0.01)。各中药组组间比较,鼻渊合剂组IL-1β、IL-6、IL-8、IL-9、IL-12、TNF-α、ICAM-1、p38 MAPK、NF-κB p50、NF-κB p65的降低及IL-10的升高均优于各拆方组(P<0.01),拆方组中清肺热组优于祛风寒组(P<0.01)。结论鼻渊合剂及其拆方均可有效抑制急性鼻窦炎大鼠炎症反应。 OBJECTIVE To investigate the effects of the split formulas of Biyuan Heji(BYHJ)on paranasal sinus mucosal inflammation in rats with acute rhinosinusitis(ARS)based on the pathogenesis of“wind-cold transforming into lung-heat”.METHODS Unilateral nasal cavity occlusion combined with nasal dripping of Staphylococcus aureus were performed to establish a rat model of ARS.SD rats were randomly divided into blank,model,BYHJ(wind-cold removal+lung-heat removal),lung-heat removal,wind-cold removal,and positive drug groups,with 6 rats in each group.The rats were treated with the corresponding drugs for 7 d and then the samples were collected.HE staining was used to observe the pathological changes of rat paranasal sinus mucosa tissues,ELISA was employed to determine the levels of interleukin-1β(IL-1β),IL-6,IL-8,IL-9,IL-10,and IL-12 in serum,immunohistochemistry(IHC)was adopted to measure the protein expression of tumor necrosis factor-α(TNF-α)and intercellular adhesion molecule(ICAM-1)in paranasal sinus mucosa tissues,and Western blot was used to detect the protein expression of phosphorylated p38 mitogen-activated protein kinase(p38 MAPK),nuclear transcription factor-κB p50(NF-κB p50),and NF-κB p65 in paranasal sinus mucosa tissues.RESULTS The acute sinusitis rat inflammation model was successfully established.Compared with the model group,the water drinking,diet eating,and body weight of rats in the BYHJ group,wind-cold removal,lung-heat removal,and positive drug groups were significantly improved,the aggregation of inflammatory cells in the paranasal sinus mucosal tissue was reduced,and the levels of IL-1β,IL-6,IL-8,IL-9,and IL-12 in the serum were significantly reduced(P<0.01),IL-10 content significantly increased(P<0.01),the protein expression of TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 in the paranasal sinus mucosa was significantly decreased(P<0.01).The comparison between various traditional Chinese medicine groups showed that the decrease of IL-1β,IL-6,IL-8,IL-9,IL-12,TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 and the increase of IL-10 in the BYHJ group were better than those in the split formula groups(P<0.01),and the lung-heat removal group was better than the wind-cold removal group(P<0.01).CONCLUSION BYHJ and its split formulas can effectively inhibit the inflammatory response in rats with ARS.
作者 周辉霞 薛珊珊 柏璐 方杨 孙炘宸 朱智媛 吴拥军 ZHOU Huixia;XUE Shanshan;BAI Lu;FANG Yang;SUN Xinchen;ZHU Zhiyuan;WU Yongjun(Affiliated Hospital of Nanjing University of Chinese Medicine,Nanjing 210029,China)
出处 《南京中医药大学学报》 北大核心 2025年第5期689-695,共7页 Journal of Nanjing University of Traditional Chinese Medicine
基金 国家自然科学基金面上项目(8217150577) 江苏省研究生科研创新计划(KYCX24_2225)。
关键词 鼻渊合剂 拆方 急性鼻窦炎 风寒化肺热 炎症 病机 鼻黏膜 大鼠 Biyuan Heji split formula acute rhinosinusitis wind-cold transforming into lung-heat inflammation pathogenesis nasal mucosa rats
作者简介 第一作者:周辉霞,女,硕士研究生,E-mail:zhouhx770517@163.com;通信作者:吴拥军,男,教授,主要从事中医耳鼻喉研究,E-mail:wooyongjun@163.com;通信作者:朱智媛,女,讲师,主治中医师,主要从事中医耳鼻喉研究,E-mail:260308@njucm.edu.cn。
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