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胆碱能抗炎通路是一条神经-免疫调节通路,其以迷走神经、乙酰胆碱及特异性乙酰胆碱受体为基础,可迅速对机体的炎症反应做出调控。研究发现,胆碱能抗炎通路的激活可有效抑制机体炎症的发生发展,近年来对其报道诸多,尤其是在中医药方面的研究,现就胆碱能抗炎通路的定义、抗炎机制及中医药治疗对其影响进行综述。 相似文献
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Objective
To observe the effect of electroacupuncture (EA) on the expressions of acetylcholine (ACh) and mucin 5AC (MUC5AC) in the lungs of rats with chronic obstructive pulmonary disease (COPD), and explore the mechanism of EA in treating COPD.Methods
Thirty Sprague-Dawley (SD) rats were randomly divided into a control group, a COPD group, and an EA group, with 10 rats in each group. The control group was a group of normal rats. The COPD rat model was induced by cigarette smoke combined with lipopolysaccharide (LPS). The COPD rats were treated with EA at bilateral Feishu (BL 13) and Zusanli (ST 36) in the EA group, 30 min each time, once a day, successively for 14 d. The lung function was tested. The contents of ACh and MUC5AC in lungs and bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Pearson method was used to analyze the correlation between pulmonary function and the content of MUC5AC in lungs. The mRNA and protein expressions of MUC5AC in lung tissues were detected by real-time polymerase chain reaction (RT-PCR) and Western blot (WB), respectively. The immune response of MUC5AC was observed by immunohistochemistry.Results
Eight rats were left in each group, and the other two died. Compared with the control group, the total airway resistance (Raw) increased significantly and dynamic compliance (Cdyn) decreased significantly in the COPD group (P<0.01); compared with the COPD group, the Raw level declined significantly and Cdyn increased significantly in the EA group (P<0.01). The contents of ACh and MUC5AC in the lungs and BALF were remarkably higher in the COPD group compared with those in the control group (P<0.01, P<0.001); compared with the COPD group, the contents of ACh and MUC5AC were significantly lower in the EA group (P<0.05, P<0.001). There was a negative correlation between MUC5AC content and lung function (P<0.001). The mRNA and protein expressions of MUC5AC in the lungs were significantly higher in the COPD group than in the control group (P<0.001); compared with the COPD group, the expressions were significantly lower in the EA group (P<0.01). Compared with the control group, the immune response of MUC5AC in the airway epithelium significantly increased in the COPD group (P<0.001); the immune response of MUC5AC was significantly lower in the EA group compared with that in the COPD group (P<0.001).Conclusion
EA treatment can improve the lung function of COPD rats, which may be related to its effect in the down-regulation of ACh and MUC5AC contents in the lungs as well as the inhibition of mucus hypersecretion.4.
目的:观察电针"足三里"对慢性阻塞性肺病(COPD)大鼠肺组织中表皮生长因子受体(EGFR)、肿瘤坏死因子α(TNF-α)、转化生长因子α(TGF-α)、白细胞介素-8(IL-8)、p38丝裂原活化蛋白激酶(p38MAPK)、黏蛋白5AC(MUC5AC)表达的影响,探讨电针治疗COPD大鼠气道黏液高分泌的作用机制。方法:SD大鼠随机分为正常组、模型组、电针组,每组10只。采用气管滴注脂多糖联合香烟烟熏的复合方法复制COPD大鼠模型。电针组取大鼠双侧"足三里"电针,每次30 min,连续2周。检测各组大鼠肺功能;HE染色法观察各组大鼠肺组织病理学变化;ELISA法检测血清、肺泡灌洗液(BALF)和肺组织内TNF-α、TGF-α和IL-8的含量;荧光定量PCR和Western blot法分别检测肺组织内EGFR、p38MAPK及MUC5AC mRNA和蛋白表达;免疫组织化学法检测肺组织中EGFR、p38MAPK及MUC5AC的表达。结果:与正常组比较,模型组大鼠肺组织及支气管有明显炎细胞浸润,管腔内出现大量黏液分泌物;用力肺活量(FVC)、第0.1秒用力呼气量(FEV0.1)、第0.3秒用力呼气量(FEV0.3)、FEV0.1/FVC、FEV0.3/FVC均明显下降(P<0.01);血清、BALF及肺组织内的TNF-α、TGF-α和IL-8的含量均显著升高(P<0.01),肺组织内的EGFR、p38MAPK及MUC5AC mRNA和蛋白表达水平及肺组织中的EGFR、p38MAPK和MUC5AC阳性表达水平均显著升高(P<0.01)。与模型组比较,电针组大鼠的炎细胞浸润和黏液高分泌有显著改善;FVC、FEV0.1、FEV0.3、FEV0.1/FVC和FEV0.3/FVC均明显上升(P<0.01,P<0.05);血清、BALF和肺组织内TNF-α、TGF-α和IL-8的含量和肺组织中的EGFR、p38MAPK及MUC5AC mRNA和蛋白表达水平含量及EGFR、p38MAPK和MUC5AC阳性表达水平均明显下降(P<0.01)。结论:电针"足三里"对COPD大鼠的气道黏液高分泌具有改善作用,其作用机制可能与抑制EGFR-p38MAPK信号通路介导的MUC5AC表达有关。 相似文献
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慢性阻塞性肺疾病(Chronic obstructive pulmonary disease,COPD)是一种十分复杂的全身性病变,其病因以及发病机制尚未完全清楚,但它是一种可以预防和治疗的肺部慢性炎症性疾病。COPD临床症状多表现为咳嗽、咳痰、喘息、气促等,而且病程长,常迁延不愈,极大地影响了COPD患者的生存质量。西医常规治疗可暂时缓解临床症状,但是常带有各种副作用,针灸疗法在治疗COPD稳定期有着独特的优势,笔者通过查阅文献研究针灸治疗COPD稳定期的研究进展,以期为临床寻找一种安全有效、毒副作用小的疗法。 相似文献
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目的:观察电针心经"神门"-"通里"段对急性心肌缺血(AMI)大鼠海马CA 1区去甲肾上腺素(NE)和白介素-6(IL-6)、IL-1β及肿瘤坏死因子-α(TNF-α)的影响,探讨电针心经改善AMI的作用机制。方法:SD大鼠分成伪手术组、模型组、心经组,每组6只。冠状动脉左前降支结扎法制备AMI模型。心经组电针刺激"神门"-"通里"段,每次30min,连续3d。用PowerLab 16导生理记录仪记录心电图(ECG);酶联免疫法检测血清肌酸激酶(CK)含量;微透析技术采集海马CA 1区细胞外液检测NE含量;酶联免疫法测定大鼠海马CA 1区IL-6、IL-1β及TNF-α的含量。结果:与伪手术组比较,模型组大鼠ECG-ST段抬高,血清CK含量升高(P0.001),海马CA 1区NE含量明显升高(P0.001),IL-6、IL-1β及TNF-α均显著升高(P0.001)。电针心经组血清CK含量下降(P0.05),海马CA 1区NE含量显著降低(P0.001),IL-6、IL-1β及TNF-α水平明显降低(P0.001),且IL-6、IL-1β及TNF-α含量与NE呈显著正相关(P0.001,P0.01)。结论:电针心经改善急性心肌缺血效应可能与下调CA 1区促炎因子,降低海马神经递质含量,从而抑制交感神经活动有关。 相似文献
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