| 张鹏飞,廖丽君,何智群,郭栋伟,张洪平,张华玲,吴仰聪.银杏叶提取物对COPD大鼠p38MAPK/NF-κB信号通路的影响[J].,2022,(24):4632-4638 |
| 银杏叶提取物对COPD大鼠p38MAPK/NF-κB信号通路的影响 |
| Effects of Ginkgo Biloba Extract on p38MAPK/NF-κB Signaling Pathway in Chronic Obstructive Pulmonary Disease Rats |
| 投稿时间：2022-07-01 修订日期：2022-07-24 |
| DOI：10.13241/j.cnki.pmb.2022.24.006 |
| 中文关键词: 银杏叶提取物 慢性阻塞性肺疾病 p38MAPK/NF-κB信号通路 炎症 |
| 英文关键词: Ginkgo biloba extract Chronic obstructive pulmonary disease p38MAPK/NF-κB signaling pathway Inflammation |
| 基金项目:国家自然科学基金项目（81904111）；广西自然科学基金项目（2020GXNSFBA297022） |
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| 中文摘要: |
| 摘要 目的：观察银杏叶提取物（Ginkgo biloba extract, GBE）对慢性阻塞性肺疾病( COPD) 大鼠肺p38丝裂原活化蛋白激酶（MAPK）/ 核转录因子-κB（NF-κB）信号通路的影响，探讨GBE对COPD抗炎作用的分子机制。方法：将90只雄性Wistar 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(p38MAPK抑制剂)组，共计6组，每组15只。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，空白对照组与COPD 模型组给予生理盐水腹腔注射，GBE高、中、低剂量组 (14, 7, 3.5 mg?kg-1?d-1)分别给予不同浓度的GBE腹腔注射，SB203580组予5 mg?kg-1?d-1腹腔注射，每天给药1次，连续给药14 d。通过HE染色法观察大鼠肺泡和气道的病理变化，酶联免疫吸附法（ELISA）测定大鼠肺泡灌洗液（BALF）和血清中IL-6、IL-8与IL-10水平，蛋白免疫印迹法(Western blot) 检测大鼠肺组织p38MAPK、NF-κB p65、NF-κB抑制蛋白α（IκBα）蛋白含量，采取实时荧光定量聚合酶链式反应(Real-time qPCR) 法检测大鼠肺组织中p38MAPK、NF-κB p65、IκBα mRNA表达。结果：与COPD模型组相比，各用药组均能抑制肺泡破坏与气道重塑，减轻肺泡与支气管周围炎症浸润；与空白对照组相比，COPD 模型组BALF与血清中IL-6、IL-8含量明显升高（P<0.05），IL-10含量明显降低（P<0.05），肺组织中p38MAPK、NF-κB p65蛋白与p38MAPK、NF-κB p65 mRNA表达量明显升高（P<0.05），IκBα蛋白与IκBα mRNA表达量明显下降（P<0.05）；与COPD模型组相比，各药物组均能明显降低大鼠BALF与血清中IL-8含量、提高IL-10含量（P<0.05），而GBE高剂量组与SB203580组效果更明显；GBE高剂量组与SB203580组BALF中IL-6含量较GBE低剂量组与COPD模型组明显降低（P<0.05）；与COPD模型组相比，各药物组均能明显降低大鼠肺组织中p38MAPK、NF-κB p65蛋白与p38MAPK、NF-κB p65 mRNA表达量（P<0.05），GBE高、中剂量组与SB203580组能明显提高IκBα蛋白与IκBα mRNA表达量（P<0.05）。结论：GBE能抑制COPD大鼠炎症反应与气道重塑，其机制可能与调控p38MAPK/NF-κB信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the effects of Ginkgo biloba extract (GBE) on p38 mitogen activated protein kinase (MAPK) / nuclear transcription factor-κB（NF-κB) in the lung of rats with chronic obstructive pulmonary disease (COPD). To explore the molecular mechanism of anti-inflammatory effect of GBE on COPD. Methods: 90 male Wistar rats were randomly divided into 6 groups: blank control group, COPD model group, GBE high dose group, GBE medium dose group, GBE low dose group and SB203580 (p38MAPK inhibitor) group, with 15 rats in each group. The COPD rat model was established by smoking cigarette smoke and injecting lipopolysaccharide (LPS) into the airway. After modeling, the drugs were administered in groups. The blank control group and COPD model group were given intraperitoneal injection of normal saline, the high, medium and low dose GBE groups (14, 7, 3.5 mg?kg-1?d-1) were given intraperitoneal injection of GBE of different concentrations, and the SB203580 group was given intraperitoneal injection of 5 mg?kg-1?d -1 once a day for 14 days. The pathological changes of rat alveoli and airways were observed by HE staining, the levels of IL-6, IL-8 and IL-10 in rat alveolar lavage fluid (BALF) and serum were measured by enzyme-linked immunosorbent assay (ELISA), The protein and mRNA expression of p38MAPK, NF-κB p65, IκBα in rat lung tissue were detected by Western blot and Real-time qPCR. Results: Compared with the COPD model group, each drug group could inhibit the destruction of alveoli and airway remodeling, and reduce the inflammatory infiltration around alveoli and bronchi; Compared with the blank control group, the contents of IL-6 and IL-8 in BALF and serum of COPD model group increased significantly (P<0.05), the contents of IL-10 decreased significantly (P<0.05), The expression of p38MAPK, NF-κB p65protein and p38MAPK, NF-κB mRNA in lung tissue increased significantly (P<0.05), IκBα Protein and IκBα mRNA expression decreased significantly (P<0.05); Compared with COPD model group, each drug group could significantly reduce the content of IL-8 in BALF and serum and increase the content of IL-10 (P<0.05), while the effect of GBE high dose group and SB203580 group was more obvious; The content of IL-6 in BALF in GBE high dose group and SB203580 group was significantly lower than that in GBE low dose group and COPD model group (P<0.05); Compared with COPD model group, each drug group could significantly reduce the expression of p38MAPK, NF-κB p65 protein, p38MAPK and NF-κB p65mRNA in rat lung tissue (P<0.05), and GBE high and medium dose groups and SB203580 groups could significantly increase IκBα protein and IκBα mRNA expression (P<0.05). Conclusion: GBE can inhibit inflammatory response and airway remodeling in COPD rats,the mechanism may be related to the regulation of p38MAPK/NF-κB signaling pathway. |
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