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苍术素调节JNK/p38MAPK信号通路对AECOPD大鼠肺损伤和气道炎症的影响
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| 篇名： | 苍术素调节JNK/p38MAPK信号通路对AECOPD大鼠肺损伤和气道炎症的影响 |
| TITLE： | Effects of atractylodin on lung injury and airway inflammation in rats with AECOPD by regulating JNK/p38 MAPK signaling pathway |
| 摘要： | 目的 探讨苍术素（ATR）对慢性阻塞性肺疾病急性加重期（AECOPD）大鼠肺损伤和气道炎症的影响机制。方法采用烟熏法联合气管内注射脂多糖的方法建立AECOPD模型，将造模成功的大鼠随机分为模型组和ATR低、中、高剂量组（25、50、100mg/kg）以及高剂量ATR+茴香霉素[ANS，c-Jun氨基端激酶（JNK）激活剂]组（100mg/kg的ATR+5mg/kg的ANS），另设不造模的对照组，每组12只。各组大鼠腹腔注射相应药液/生理盐水，每天1次，连续14d。末次给药后，检测大鼠肺功能[呼气峰值流速（PEF）、用力呼气量（FEV）/用力肺活量（FVC）比值、动脉血氧分压（PaO2）]以及支气管肺泡灌洗液（BALF）中炎症细胞数量和炎症因子[白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、IL-1β]水平；观察大鼠肺组织病理学形态；检测大鼠肺上皮细胞凋亡情况；检测大鼠肺组织中JNK/p38丝裂原活化蛋白激酶（p38MAPK）信号通路相关蛋白表达水平。结果与对照组比较，模型组大鼠PEF、FEV/FVC、PaO2均显著减慢或降低（P＜0.05）；BALF中白细胞、中性粒细胞、淋巴细胞、巨噬细胞数量和IL-1β、TNF-α、IL-6水平，病理学评分，肺上皮细胞凋亡率和肺组织中JNK、p38MAPK蛋白磷酸化水平均显著增多或升高（P＜0.05）；肺损伤严重，细胞排列无序，出现明显的炎症细胞浸润。与模型组比较，ATR各剂量组大鼠上述定量指标水平均显著改善，且具有剂量依赖性（P＜0.05）；肺损伤减轻，细胞排列规则有序。与ATR高剂量组比较，高剂量ATR+ANS组大鼠上述定量指标水平均显著逆转（P＜0.05），肺损伤加重。结论ATR可通过抑制JNK/p38MAPK信号通路活性，抑制气道炎症，从而改善AECOPD大鼠肺损伤。 |
| ABSTRACT： | OBJECTIVE To discuss the effect mechanism of atractylodin （ATR） on lung injury and airway inflammation in rats with acute exacerbation of chronic obstructive pulmonary disease （AECOPD）. METHODS AECOPD model was established using smoke exposure and intratracheal injection of lipopolysaccharide. Rats were randomly grouped into model group， ATR low-， medium- and high-dose groups （25， 50 and 100 mg/kg）， as well as high-dose ATR+anisomycin [ANS， c-Jun N-terminal kinase （JNK） activator] group （100 mg/kg ATR+5 mg/kg ANS）. Additionally， a non-modeled control group was set up， with 12 rats in each group. Rats in each group were intraperitoneally injected with the corresponding drug solution/normal saline once daily for 14 consecutive days. After the last medication， lung function [peak expiratory flow （PEF）， the ratio of forced expiratory volume （FEV） to forced vital capacity （FVC）， arterial partial pressure of oxygen （PaO2）]， as well as the number of inflammatory cells and the levels of inflammatory cytokines [interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and IL-1β] in bronchoalveolar lavage fluid （BALF）， were measured. The pathological morphology of lung tissue in rats was observed. 163.com The apoptosis of lung epithelial cells was detected， and the expression levels of proteins related to the JNK/p38 mitogen-activated protein kinase （p38 MAPK） signaling pathway in rat lung tissues were detected. RESULTS Compared with control group， PEF， FEV/FVC and PaO2 of model group were slowed or decreased significantly （P＜0.05）. The number of white blood cells， neutrophils， lymphocytes and macrophages， as well as the levels of IL-1β， TNF-α and IL-6 in BALF， along with the pathological score， the apoptosis rate of lung epithelial cells， and the phosphorylation levels of JNK and p38 MAPK proteins in lung tissues， were all increased or raised significantly （P＜0.05）； lung tissue exhibited severe damage， with disordered cell arrangement and marked infiltration of inflammatory cells. Compared with model group， the levels of above quantitative indicators in rats from all ATR dosage groups showed significant improvement in a dose-dependent manner （P＜0.05）； moreover， the pathological damage in lung tissue was alleviated， with cells arranged in a regular and orderly fashion. Compared with ATR high-dose group， the levels of the above quantitative indicators in rats from the high-dose ATR+ANS group were significantly reversed （P＜0.05）， and the pathological damage in lung tissue was exacerbated. CONCLUSIONS ATR inhibits airway inflammation by suppressing the activity of the JNK/p38 MAPK signaling pathway， thereby improving lung tissue damage in AECOPD rats. |
| 期刊： | 2025年第36卷第23期 |
| 作者： | 孙智颖；王英哲；刘源；赵亚鹏；周亭亭 |
| AUTHORS： | SUN Zhiying，WANG Yingzhe，LIU Yuan，ZHAO Yapeng，ZHOU Tingting |
| 关键字： | 苍术素；慢性阻塞性肺疾病急性加重期；肺损伤；气道炎症；JNK/p38 MAPK信号通路 |
| KEYWORDS： | atractylodin； acute exacerbation of chronic obstructive pulmonary disease； lung injury； airway inflammation； JNK/ |
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