| 曹国栋.去氢骆驼蓬碱对LPS+香烟烟雾复合诱导大鼠COPD模型肺功能及氧化应激的影响[J].安徽医药,待发表. |
| 去氢骆驼蓬碱对LPS+香烟烟雾复合诱导大鼠COPD模型肺功能及氧化应激的影响 |
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| 投稿时间：2025-10-06 录用日期：2025-11-11 |
| DOI： |
| 中文关键词: 去氢骆驼蓬碱 慢性阻塞性肺疾病 脂多糖 香烟烟雾 肺功能 |
| 英文关键词: |
| 基金项目:新疆维吾尔自治区自然科学基金（2025D01B40、202501A26）、新疆维吾尔自治区卫生健康科研项目（2025001QNKYXM654027021） |
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| 中文摘要: |
| 目的 探讨去氢骆驼蓬碱（harmine，HM）对脂多糖（lipopolysaccharide，LPS）联合香烟烟雾（cigarette smoke，CS）复合诱导大鼠慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）模型肺功能及肺组织氧化应激的干预作用。方法 将60只SPF级雄性SD大鼠随机分为5组（n=12）：正常对照组、COPD模型组、HM低剂量组（20 mg/kg）、HM中剂量组（40 mg/kg）、HM高剂量组（80 mg/kg）。采用“LPS气管滴注+CS暴露”法构建大鼠COPD模型：第1、14天气管滴注LPS（50 μg/只），其余时间每日暴露于CS（10支/次，2次/d，每次30 min，持续28 d）；HM各剂量组自建模第1天起每日灌胃给药1次，正常对照组与模型组给予等体积生理盐水。建模结束后，检测大鼠肺功能指标:第0.3秒用力呼气量（FEV）、用力肺活量（FVC）、FEV/FVC、呼气峰流速（PEF）；取肺组织制备匀浆，采用比色法检测超氧化物歧化酶（SOD）活性、谷胱甘肽过氧化物酶（GSH-Px）活性及丙二醛（MDA）含量；HE染色观察肺组织病理学改变并进行病理评分。结果 与正常对照组比较，模型组大鼠FEV、FVC、FEV/FVC、PEF降低，肺组织SOD、GSH-Px活性下降，MDA含量升高，肺组织病理显示气道黏膜损伤、炎性细胞浸润、肺泡壁断裂融合，病理评分升高（P<0.05）。与模型组比较，HM各剂量组可改善肺功能（FEV、FVC、FEV?.?/FVC、PEF升高，提升肺组织SOD、GSH-Px活性，降低MDA含量，肺组织病理损伤减轻，病理评分降低（P<0.05），且呈剂量依赖性。结论 去氢骆驼蓬碱可改善LPS+CS复合诱导的大鼠COPD模型肺功能，其机制可能与抑制肺组织氧化应激、恢复氧化-抗氧化平衡有关。 |
| 英文摘要: |
| Objective To investigate the intervention effect of harmine (HM) on pulmonary function and pulmonary oxidative stress in a rat model of chronic obstructive pulmonary disease (COPD) induced by lipopolysaccharide (LPS) combined with cigarette smoke (CS). Methods Sixty SPF-grade male Sprague-Dawley (SD) rats were randomly divided into 5 groups (n=12 each): normal control group, COPD model group, HM low-dose group (20 mg/kg), HM medium-dose group (40 mg/kg), and HM high-dose group (80 mg/kg). The rat COPD model was established by the "LPS intratracheal instillation + CS exposure" method: on days 1 and 14, LPS (50 μg per rat) was instilled intratracheally; during the remaining days, the rats were exposed to CS (10 cigarettes per session, twice a day, 30 minutes per session) for 28 consecutive days. Rats in each HM dose group were given HM by gavage once a day starting from day 1 of modeling, while those in the normal control group and model group were given an equal volume of normal saline. After modeling, pulmonary function indices [forced expiratory volume in 0.3 seconds (FEV), forced vital capacity (FVC), FEV?.?/FVC ratio, and peak expiratory flow (PEF)] were measured. Pulmonary tissue homogenate was prepared, and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the content of malondialdehyde (MDA) were detected by colorimetry. Hematoxylin-eosin (HE) staining was used to observe pathological changes of pulmonary tissue, and pathological scoring was performed. Results Compared with the normal control group, the model group showed significantly decreased FEV?.?, FVC, FEV/FVC ratio, and PEF; reduced SOD and GSH-Px activities in pulmonary tissue; increased MDA content; obvious pathological changes (airway mucosal injury, inflammatory cell infiltration, alveolar wall rupture and fusion); and elevated pathological score (all P<0.05). Compared with the model group, each HM dose group exhibited improved pulmonary function (increased FEV, FVC, FEV/FVC ratio, and PEF), enhanced SOD and GSH-Px activities in pulmonary tissue, decreased MDA content, alleviated pathological damage of pulmonary tissue, and reduced pathological score (all P<0.05), with a dose-dependent manner. Conclusion Harmine can improve pulmonary function in LPS + CS-induced COPD rat models, and its mechanism may be related to inhibiting pulmonary oxidative stress and restoring the oxidation-antioxidation balance. |
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