目的 探討川芎嗪調(diào)節(jié)TGF-β/Smad信號(hào)通路對(duì)哮喘小鼠的氣道炎癥和氣道重塑的影響及其作用機(jī)制。方法 選取40只健康雌性BALB/c小鼠，隨機(jī)分為對(duì)照、模型、川芎嗪、地塞米松組，每組各10只。采用卵清白蛋白（OVA）＋氫氧化鋁混合液腹腔注射致敏、OVA滴鼻激發(fā)構(gòu)建小鼠慢性哮喘模型，在激發(fā)同時(shí)川芎嗪、地塞米松組小鼠分別于每日滴鼻激發(fā)前30 min ip川芎嗪注射液80 mg/kg或地塞米松注射液2 mg/kg，模型組小鼠ip等量生理鹽水。小鼠處死后取肺組織行HE染色觀察評(píng)估肺組織病理變化，Masson染色觀察評(píng)估小鼠肺組織氣道重塑，ELISA法檢測(cè)血清中免疫球蛋白E（IgE）、白細(xì)胞介素-5（IL-5）、轉(zhuǎn)錄因子GATA-3及轉(zhuǎn)化生長因子-β（TGF-β）表達(dá)水平，免疫印跡法檢測(cè)小鼠肺組織中TGF-β1和Smad2、Smad7表達(dá)水平。結(jié)果 與模型組比較，川芎嗪組小鼠氣道改變明顯減輕，氣管壁炎性細(xì)胞浸潤減少，氣道壁、平滑肌層和基底膜層增厚減輕。川芎嗪組氣道周圍炎癥和肺泡炎癥評(píng)分顯著降低（P<0.05）。川芎嗪組基底膜層、平滑肌層厚度明顯降低，氣道壁內(nèi)外徑比值明顯升高（P<0.05）。川芎嗪組小鼠血清中IgE、IL-5、GATA-3和TGF-β1水平明顯降低（P<0.05）。川芎嗪組小鼠肺組織中TGF-β1、Smad2表達(dá)均降低，而Smad7表達(dá)增加（P<0.05）。結(jié)論 川芎嗪可改善哮喘小鼠氣道重塑，其機(jī)制是通過調(diào)節(jié)TGF-β/Smad信號(hào)通路來實(shí)現(xiàn)的。

Objective To investigate the effect of ligustrazine on airway inflammation and airway remodeling in mice asthma models by regulating TGF-β/Smad signaling pathway and explore its mechanism. Methods Healthy female BALB/c mice were randomly divided into control group, model group, ligustrazine group, and dexamethasone group, and each group had 10 mice. The model was established by ip OVA + Al₂(OH)₃ mixture, and nasal instillation of OVA. Mice in the ligustrazine and dexamethasone groups were ip administered with Ligustrazine Injection 80 mg/kg, or Dexamethasone Injection 2 mg/kg 30 min before nasal instillation. Mice in model group were ip with the same amount of saline. Pathological changes of lung tissue in mice were observed by HE staining, airway remodeling in lung tissue of mice were observed by Masson staining, the levels of IgE, IL-5, GATA-3, and TGF-β1 in serum were detected by ELISA, and the expression levels of TGF-β1, Smad2, and Smad7 in lung tissue of mice were detected by Western blotting method. Results Compared with the model group, the airway changes were significantly relieved, the infiltration of inflammatory cells in tracheal wall of mice in the ligustrazine group were reduced, and the thickening of airway wall, smooth muscle layer, and basement membrane were decreased. Compared with the model group, the scores of airway inflammation and alveolar inflammation of mice in the ligustrazine group were significantly reduced (P<0.05). Compared with the model group, the ratio of inner and outer diameter of the airway wall of mice in the ligustrazine group was significantly increased (P<0.05). Compared with the model group, serum IgE, IL-5, GATA-3 and TGF-β1 levels in the ligustrazine and dexamethasone groups were significantly reduced (P<0.05). Compared with the model group, the expressions of TGF-β1 and Smad2 in lung tissues of mice in the ligustrazine group were decreased, but the expressions of Smad7 were increased (P<0.05). Conclusions Ligustrazine can improve airway remodeling in asthma by regulating the TGF-β/Smad signaling pathway.