■电针(EA),随着不同的刺激强度,已在动物和临床研究中证明了治疗慢性阻塞性肺疾病(COPD)的治疗潜力。然而,对强度相关效应的全面调查,特别是1mA和3mA的EA,基本机制仍然缺乏。
■通过长时间暴露于香烟烟雾和间歇性气管内滴注脂多糖建立COPD大鼠模型。EA治疗在BL13(肺舒)和ST36(足三里)穴位进行,每天20分钟,持续2周,强度为1mA和3mA。EA有效性通过肺功能评估,组织病理学改变,血清炎症细胞因子水平,血清和肺组织氧化应激标志物水平。进行转录组分析和加权基因共表达网络分析(WGCNA)以揭示基因表达模式并鉴定hub基因。实时定量PCR(RT-qPCR)和Westernblot(WB)检测mRNA和蛋白表达水平,分别。
■在1mA和3mA下的EA通过改善COPD大鼠的肺功能和减轻炎症和氧化应激而发挥不同的治疗作用。转录组分析显示两组之间不同的表达模式,功能上对应于共享和强度特异性(1mA和3mA)富集的途径。确定了八个候选基因,包括Aqp9,Trem1,Mrc1和Gpnmb,在COPD中被EA下调和上调。值得注意的是,Msr1和Slc26a4在EA-1mA中仅下调,而Pde3a和Bmp6仅在EA-3mA中上调。WGCNA构建了5个关键模块,并阐明了模块-特征关系,突出了上述8个基因。此外,通过RT-qPCR和WB验证其mRNA和蛋白水平。
■我们的结果表明,1mA和3mA强度在转录水平上诱导不同的基因表达模式,与共享和1mA和3mA特异性富集途径相关。基因Mrc1,Gpnmb,Trem1和Aqp9成为有希望的靶标,需要进一步的研究来阐明其在COPD中的功能后果。
UNASSIGNED: Electroacupuncture (EA), with varying stimulation intensities, has demonstrated therapeutic potentials in both animal and clinical studies for the treatment of chronic obstructive pulmonary disease (COPD). However, a comprehensive investigation of the intensity-related effects, particularly 1mA and 3mA of EA, and the underlying mechanisms remains lacking.
UNASSIGNED: A COPD rat model was established by prolonged exposure to cigarette smoke and intermittent intratracheal instillation of lipopolysaccharide. EA treatment was administered at acupoints BL13 (Feishu) and ST36 (Zusanli), 20 minutes daily for 2 weeks, with intensities of 1mA and 3mA. EA effectiveness was evaluated by pulmonary function, histopathological change, serum level of inflammatory cytokines, and level of oxidative stress markers in serum and lung tissues. Transcriptome profiling and weighted gene co-expression network analysis (WGCNA) were performed to reveal gene expression patterns and identify hub genes. Real-time quantitative PCR (RT-qPCR) and Western blot (WB) were performed to detect the mRNA and protein expression levels, respectively.
UNASSIGNED: EA at both 1mA and 3mA exerted differing therapeutic effects by improving lung function and reducing inflammation and oxidative stress in COPD rats. Transcriptome analysis revealed distinct expression patterns between the two groups, functionally corresponding to shared and intensity-specific (1mA and 3mA) enriched pathways. Eight candidate genes were identified, including Aqp9, Trem1, Mrc1, and Gpnmb that were downregulated by EA and upregulated in COPD. Notably, Msr1 and Slc26a4 exclusively downregulated in EA-1mA, while Pde3a and Bmp6 upregulated solely in EA-3mA. WGCNA constructed 5 key modules and elucidated the module-trait relationship, with the aforementioned 8 genes being highlighted. Additionally, their mRNA and protein levels were validated by RT-qPCR and WB.
UNASSIGNED: Our results demonstrated that 1mA and 3mA intensities induce distinct gene expression patterns at the transcriptional level, associated with shared and 1mA vs 3mA-specific enriched pathways. Genes Mrc1, Gpnmb, Trem1, and Aqp9 emerge as promising targets, and further studies are needed to elucidate their functional consequences in COPD.