吴茱萸碱对哮喘模型大鼠炎症及上皮细胞凋亡的影响及机制 点击下载
| 论文标题： | 吴茱萸碱对哮喘模型大鼠炎症及上皮细胞凋亡的影响及机制 |
| 英文标题： | |
| 中文摘要： | 目的 探究吴茱萸碱对哮喘模型大鼠炎症反应及上皮细胞凋亡的影响及潜在机制。方法将SD大鼠分为对照组、模型组、吴茱萸碱低剂量组（10mg/kg）、吴茱萸碱高剂量组（20mg/kg）、地塞米松组（阳性对照，0.5mg/kg）、表皮细胞生长因子（EGF）组[丝裂原活化蛋白激酶（MAPK）激活剂，10μg]、吴茱萸碱高剂量+EGF组（20mg/kg吴茱萸碱+10μgEGF），每组10只。除对照组外，其余各组大鼠以10%卵白蛋白（OVA）-氢氧化铝混合液3点注射致敏联合2%OVA雾化液吸入激发的方式建立哮喘模型。检测各组大鼠支气管肺泡灌洗液（BALF）中的炎症细胞（巨噬细胞、淋巴细胞）数，观察大鼠肺组织的病理变化，检测大鼠肺组织中气道上皮细胞凋亡情况、血清炎症因子（肿瘤坏死因子α、白细胞介素6、白细胞介素4）水平、通路相关蛋白[p38MAPK、磷酸化p38MAPK（p-p38MAPK）、信号转导及转录激活因子1（STAT1）]及凋亡相关蛋白[B细胞淋巴瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）]的表达水平。结果与对照组比较，模型组大鼠肺组织可见支气管黏膜水肿、肺泡间隔增厚和大量炎症细胞浸润，炎症细胞数显著增多；气道上皮细胞凋亡率、炎症因子水平、p-38MAPK/p-38MAPK和Bax、STAT1蛋白表达水平均显著升高，Bcl-2蛋白表达水平和Bcl-2/Bax均显著降低（P＜0.05）。与模型组比较，吴茱萸碱低、高剂量组和地塞米松组大鼠肺组织病理改变均有不同程度缓解，上述各指标均显著逆转，而EGF组上述指标的变化趋势则相反（P＜0.05）；EGF能显著减弱高剂量吴茱萸碱对哮喘大鼠炎症反应的改善作用（P＜0.05）。结论吴茱萸碱可减轻哮喘大鼠炎症反应并减少气道上皮细胞凋亡，其作用机制可能与抑制p38MAPK/STAT1信号通路有关。 |
| 英文摘要： | OBJECTIVE To explore the effects and potential mechanism of evodiamine on inflammatory response and apoptosis of epithelial cells in asthma model rats. METHODS SD rats were separated into control group， model group， evodiamine low-dose group （10 mg/kg）， evodiamine high-dose group （20 mg/kg）， dexamethasone group （positive control， 0.5 mg/kg）， epidermal growth factor （EGF） group [mitogen-activated protein kinase （MAPK） activator， 10 μg]， evodiamine high-dose+EGF group （20 mg/kg evodiamine+10 μg EGF）， with 10 rats in each group. Except for the control group， the other groups were sensitized by 3-point injection of 10% ovalbumin（OVA）-aluminium hydroxide mixture and stimulated by inhalation of 2%OVA nebulized liquid to establish an asthma model. The count of inflammatory cells （macrophages and lymphocytes） in bronchoalveolar lavage fluid （BALF） was detected in each group； pathological changes of lung tissue in rats were observed； the apoptosis of airway epithelial cells， the levels of serum inflammatory factors [tumor necrosis factor-α， interleukin-6 （IL-6） and IL-4]， the expressions of pathway-related proteins p38 MAPK， phosphorylated p38 MAPK （p-p38 MAPK）， signal transduction and transcription activating factor 1 （STAT1）] and apoptosis-related proteins [B cell lymphoma-2 （Bcl-2） and Bcl-2 associated X protein （Bax）] were all detected in lung tissue. RESULTS Compared with the control group， bronchial mucosal edema， thickening of alveolar septa and extensive infiltration of inflammatory cells were observed in the lung tissue of rats in the model group； the number of inflammatory cells， apoptosis rate of airway epithelial cells， the levels of inflammatory factors， p-38 MAPK/p-38 MAPK， and the protein expressions of Bax and STAT1 were increased significantly； the expressions of Bcl-2 protein and Bcl-2/Bax were reduced significantly （P＜0.05）. Compared with the model group， the pathological changes in lung tissues were alleviated to varying degrees in evodiamine low-dose and high-dose groups， and dexamethasone groups， and the above indicators were significantly reversed. However， the change trends of corresponding indicators in the EGF group were opposite to the above （P＜0.05）. EGF could significantly attenuate the effect of high-dose evodiamine on inflammatory response in asthmatic rats （P＜0.05）. CONCLUSIONS Evodiamine can relieve inflammatory reactions and inhibit the apoptosis of airway epithelial cells in asthmatic rats， the mechanism of which may be associated with inhibiting p38 MAPK/STAT1 signaling pathway. |
| 期刊： | 2024年第35卷第11期 |
| 作者： | 雷俊；卢丽君；罗玲艳；乔松；童亚男；郑洋；姚蕾 |
| 英文作者： | LEI Jun，LU Lijun，LUO Lingyan，QIAO Song，TONG Yanan，ZHENG Yang，YAO Lei |
| 关键字： | 吴茱萸碱；哮喘；炎症反应；气道上皮细胞；凋亡；p38 MAPK/STAT1信号通路 |
| KEYWORDS： | evodiamine； asthma； inflammation； airway epithelial cells； apoptosis； p38 MAPK/STAT1 signaling pathway |
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