| 杨晓敏,张 蓓,张鹏飞,谭柳萍,廖丽君,张华玲,潘运迎,王贝贝,卢岳虹.基于p38MAPK通路探讨银杏叶提取物对慢性阻塞性肺疾病大鼠气道黏液高分泌及血管重塑的影响[J].,2023,(9):1624-1630 |
| 基于p38MAPK通路探讨银杏叶提取物对慢性阻塞性肺疾病大鼠气道黏液高分泌及血管重塑的影响 |
| Based on P38MAPK Signaling Pathway to Explore the Effects of Ginkgo Biloba Extract in Intervention of Airway Mucus High Secretion and Vascular Remodeling in COPD Rats |
| 投稿时间：2022-11-23 修订日期：2022-12-18 |
| DOI：10.13241/j.cnki.pmb.2023.09.005 |
| 中文关键词: 银杏叶提取物 慢性阻塞性肺疾病 p38MAPK通路 气道黏液分泌 血管重塑 |
| 英文关键词: Ginkgo biloba extract Chronic obstructive pulmonary disease P38MAPK pathway Airway mucus secretion Vascular remodeling |
| 基金项目:广西自然科学基金项目（2020GXNSFBA297022）；国家自然科学基金项目（81904111） |
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| 中文摘要: |
| 摘要 目的：探讨银杏叶提取物（Ginkgo biloba extract, GBE）通过调控p38MAPK通路对慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）大鼠气道黏液高分泌及肺血管重塑的影响。方法：将90只大鼠随机分为空白对照组、COPD模型组、GBE高剂量组、GBE中剂量组、GBE低剂量组、SB203580组。采用香烟烟雾熏吸联合气道内注入脂多糖（LPS）的方法建立COPD大鼠模型，造模结束后分组给药；通过维多利亚蓝+VG染色观察大鼠肺小动脉病理改变，测量血管壁厚度占血管外径百分比（WT%）、管壁面积占血管面积百分比（WA%）的变化；酶联免疫吸附法（ELISA）检测大鼠肺泡灌洗液（BALF）与血清中TNF-α、TGF-β的表达；实时荧光定量法（RT-PCR）检测肺组织表皮生长因子受体（EGFR）、黏蛋白5AC（MUC5AC）mRNA表达；蛋白质印迹法（Western Blot）检测肺组织EGFR、MUC5AC、p-p38MAPK蛋白的表达。结果：与空白对照组比较，COPD模型组WT%、WA%明显升高（P＜0.05）；与COPD模型组比较，各药物干预组WT%、WA%明显降低（P＜0.05）；COPD模型组大鼠BALF及血清中TNF-α、TGF-β水平较空白对照组明显升高（P＜0.05），各药物干预组TNF-α、TGF-β水平较COPD模型组明显下降（P＜0.05）；COPD模型组大鼠肺组织EGFR、MUC5AC mRNA与空白对照组相比明显升高（P＜0.05），各药物干预组大鼠肺组织EGFR、MUC5AC mRNA与COPD模型组相比显著降低（P＜0.05）；COPD模型组大鼠肺组织中EGFR、MUC5AC、p-p38MAPK蛋白的表达与空白对照组相比明显升高（P＜0.05），各药物干预组大鼠肺组织中EGFR、MUC5AC、p-p38MAPK蛋白的表达与COPD模型组相比明显降低（P＜0.05），不同GBE剂量干预组中EGFR、MUC5AC、p-p38MAPK蛋白的表达量随着给药剂量增加而减少。结论：GBE能够抑制COPD大鼠气道黏液分泌、改善肺血管重塑，其机制可能与抑制p38MAPK通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To explore Ginkgo biloba extract, Effects of GBE on airway mucus hypersecretion and pulmonary vascular remodeling in chronic obstructive pulmonary disease (COPD) rats by regulating p38MAPK pathway. Methods: 90 rats were randomly divided into blank control group, COPD model group, GBE high-dose group, GBE medium-dose group, GBE low-dose group and SB203580 group. The rat model of COPD was established by injecting lipopolysaccharide (LPS) into the airway of cigarette smoke, and the rats were administered in groups after the model was established. The pathological changes of pulmonary arterioles in rats were observed by Victoria Blue +VG staining, and the changes of vessel wall thickness as a percentage of vessel outer diameter (WT%) and vessel wall area as a percentage of vessel area (WA%) were measured. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of TNF-α and TGF-β in alveolar lavage fluid (BALF) and serum of rats. The mrna expression of epidermal growth factor receptor (EGFR) and mucin 5ac (muc5ac) in lung tissue was detected by real-time quantitative RT-PCR. The expression of EGFR, MUC5AC and p-p38MAPK protein in lung tissue was detected by Western Blot. Results: Compared with the blank control group, the WT% and WA% of COPD model group were significantly higher (P<0.05). Compared with COPD model group, the WT% and WA% of each drug intervention group were significantly decreased (P<0.05). Compared with the blank control group, the levels of TNF-α and TGF-β in BALF and serum in COPD model group were significantly higher (P<0.05), and the levels of TNF-α and TGF-β in drug intervention groups were significantly lower compared with COPD model group (P<0.05). Compared with the blank control group, EGFR and MUC5AC mRNA in lung tissue of COPD model group increased significantly (P<0.05), Compared with COPD model group, the EGFR and MUC5AC mRNA in lung tissue of drug intervention group decreased significantly (P<0.05). The expression of EGFR, MUC5AC, p-p38MAPK protein in the lung tissue of COPD model group was significantly higher than that of the blank control group (P<0.05), and the expression of EGFR, MUC5AC, p-p38MAPK protein in the lung tissue of each drug intervention group was significantly lower than that of COPD model group (P<0.05). The expression levels of EGFR, MUC5AC and p-p38MAPK protein in different GBE dosage intervention groups decreased with the increase of dosage. Conclusion: GBE can inhibit airway mucus secretion and improve pulmonary vascular remodeling in COPD rats, and the mechanism may be related to the inhibition of p38MAPK pathway. |
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