养肺通络方延缓感染后闭塞性细支气管炎模型大鼠气道重塑的作用机制研究 点击下载
| 论文标题： | 养肺通络方延缓感染后闭塞性细支气管炎模型大鼠气道重塑的作用机制研究 |
| 英文标题： | |
| 中文摘要： | 目的 探讨养肺通络方延缓感染后闭塞性细支气管炎（PIBO）模型大鼠气道重塑的作用机制。方法将48只2周龄SPF级雄性SD大鼠随机分为对照组（Control组）、PIBO模型组（Model组）、醋酸泼尼松片+阿奇霉素片组[阳性对照，醋酸泼尼松片0.0063g/（kg·d）+阿奇霉素片0.0315g/（kg·d）]和养肺通络方高、中、低剂量组[42.42、21.21、10.60g/（kg·d）]。通过气管内滴入二乙酰建立PIBO大鼠模型；造模结束后，各组大鼠灌胃相应药液或蒸馏水，每日1次，连续21d。通过苏木精-伊红染色评估大鼠肺组织病理改变，Masson染色评估大鼠肺组织纤维化程度；WesternBlot及实时荧光定量PCR检测大鼠肺组织中上皮-间充质转化（EMT）相关标志物[E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）、α-平滑肌肌动蛋白（α-SMA）、波形蛋白（Vimentin）]、转录因子[蜗牛同源物1（果蝇）样1蛋白（Snail1）、锌指E盒结合同源蛋白1（ZEB1）、Twist相关蛋白1（Twist1）]的蛋白及mRNA表达水平；ELISA法检测大鼠血液及肺泡灌洗液中转化生长因子-β（1TGF-β1）、血管内皮生长因子（VEGF）水平。结果与Control组比较，Model组大鼠肺组织可见肺泡结构大面积破坏，间质大量炎性细胞浸润；E-cadherin蛋白和mRNA表达水平显著降低，N-cadherin、Vimentin、α-SMA、Snail1、ZEB1、Twist1的蛋白和mRNA表达水平以及胶原阳性面积、TGF-β1和VEGF水平显著升高（P＜0.05）。与Model组比较，各给药组大鼠肺组织病理损伤显著改善，以上指标（胶原阳性面积除外）水平显著逆转（P＜0.05）。结论养肺通络方可能通过调控TGF-β1/VEGF介导的信号网络，抑制EMT相关转录因子激活，从而阻断EMT进程，延缓PIBO气道重塑。 |
| 英文摘要： | OBJECTIVE To investigate the mechanism of Yangfei tongluo formula in delaying airway remodeling in post-infectious bronchiolitis obliterans （PIBO） model rats.METHODS Forty-eight 2-week-old SPF male SD rats were randomly divided into control group （Control group）， PIBO model group （Model group）， Prednisone Acetate tablets+Azithromycin tablets group [positive control group， Prednisone Acetate tablets 0.006 3 g/（kg·d）+Azithromycin tablets 0.031 5 g/（kg·d）]， and high-， medium-， and low-dose Yangfei tongluo formula groups [42.42， 21.21， 10.60 g/（kg·d）]. The PIBO rat model was established by intratracheal instillation of diacetyl. After modeling， rats in each group were administered corresponding drug solution or distilled water by gavage once daily for 21 consecutive days. Hematoxylin-eosin staining was used to evaluate the pathological changes of lung tissue， and Masson staining was used to assess the degree of pulmonary fibrosis. Western blot and real-time quantitative PCR were performed to detect the protein and mRNA expression levels of epithelial-mesenchymal transition （EMT）-related markers [E-cadherin， N-cadherin， α -smooth muscle actin （ α -SMA）， Vimentin] and transcription factors [snail homolog 1（Drosophila）-like 1 protein （Snail1）， zinc finger E-box-binding homeobox protein 1 （ZEB1）， Twist-related protein 1 （Twist1）] in lung tissue. ELISA was used to detect the levels of transforming growth factor-β 1 （TGF-β 1 ） and vascular endothelial growth factor （VEGF） in blood and bronchoalveolar lavage fluid.RESULTS Compared with the Control group， the lung tissues of rats in the Model group showed extensive destruction of alveolar structure and massive inflammatory cell infiltration in the interstitium. The protein and mRNA expression levels of E-cadherin were significantly decreased， while the protein and mRNA expression levels of N-cadherin， Vimentin， α -SMA， Snail1， ZEB1， and Twist1， as well as the collagen-positive area and the levels of TGF-β 1 and VEGF， were significantly increased （ P ＜0.05）. Compared with the Model group， the pathological injury of lung tissue in each administration group was significantly improved， and the above indicators （except collagen-positive area） were significantly reversed （ P ＜0.05）.CONCLUSIONS Yangfei tongluo formula may delay airway remodeling in PIBO by regulating the TGF-β 1 /VEGF-mediated signaling network and inhibiting the activation of EMT-related transcription factors， thereby blocking the EMT process. |
| 期刊： | 2026年第37卷第16期 |
| 作者： | 赵转；陈文霞；王立彪；相恒杰；樊明会；岳淋帆 |
| 英文作者： | ZHAO Zhuan，CHEN Wenxia，WANG Libiao，XIANG Hengjie，FAN Minghui，YUE Linfan |
| 关键字： | 养肺通络方；感染后闭塞性细支气管炎；上皮-间充质转化；气道重塑 |
| KEYWORDS： | Yangfei tongluo formula;post-infectious bronchiolitis obliterans;epithelial-mesenchymal transition;airway remodeling |
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