| 陈丽展,吴 朔,张 艳,张 瑶,方 圆.盐酸氨溴索对烟所致慢性阻塞性肺疾病大鼠肺组织细胞凋亡和血管重塑的作用机制研究[J].,2020,(15):2817-2823 |
| 盐酸氨溴索对烟所致慢性阻塞性肺疾病大鼠肺组织细胞凋亡和血管重塑的作用机制研究 |
| Mechanism of Ambroxol Hydrochloride on Cell Apoptosis and Vascular Remodeling of Lung Tissue in Rats with Chronic Obstructive Pulmonary Disease Caused by Tobacco |
| 投稿时间：2020-02-28 修订日期：2020-03-26 |
| DOI：10.13241/j.cnki.pmb.2020.15.004 |
| 中文关键词: 盐酸氨溴索 慢性阻塞性肺疾病 细胞凋亡 血管重塑 |
| 英文关键词: Ambroxol hydrochloride Chronic obstructive pulmonary disease Apoptosis Vascular remodeling |
| 基金项目:国家重大科学研究计划项目(2012CB933300)；国家自然科学基金面上项目(81272586) |
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| 中文摘要: |
| 摘要 目的：盐酸氨溴索对烟所致慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)大鼠肺组织细胞凋亡和血管重塑的作用机制研究。方法：将SD大鼠随机分为4组，每组20只，依次为正常组、模型组、实验组、对照组。模型组、实验组、对照组大鼠采延安香烟烟熏64天构建慢性阻塞性肺大鼠模型，正常组大鼠室温下正常饲养。烟熏结束后，实验组、对照组大鼠每日分别皮下注射5ml盐酸氨溴索（20 mg/kg）和5 mL的盐酸班布特罗（20 mg/kg），正常组、模型组分别腹腔注射等剂量的生理盐水。在药物干预28天后，苏木精-伊红染色(hematoxylin-eosinstaining，HE)、弹力纤维(elastic van gieson，EVG)染色、TUNNEL染色、免疫组化染色、Western blot检测各组大鼠肺组织病理、血管重塑、肺组织的细胞凋亡、α-平滑肌肌动蛋白(α-smoothmus-cleactin，α-SMA)和血管内皮生长因子（Vascular endothelial growth factor，VEGF）的表达、以及Caspase-3、Bax和Bcl-2的表达水平。结果：与正常组相比，模型组肺组织损伤明显，肺小动脉中膜厚度明显增加，血管肌化程度、细胞的凋亡率、α-SMA和VEGF、Caspase-3、Bax的表达明显升高，Bcl-2的表达明显降低，差异均具有统计学意义（P<0.05）；与模型组相比，实验组和对照组大鼠肺组织损伤明显改善，肺小动脉中膜厚度明显减小，血管肌化程度、细胞的凋亡率、α-SMA和VEGF、Caspase-3、Bax的表达明显降低，Bcl-2的表达明显升高，差异均具有统计学意义（P<0.05）。结论：盐酸氨溴索能抑制肺组织的细胞凋亡以及改善其血管重塑，保护COPD大鼠的肺组织。 |
| 英文摘要: |
| ABSTRACT Objective: To explore mechanism of Ambroxol Hydrochloride on cell apoptosis and vascular remodeling of lung tissue in Rats with chronic obstructive pulmonary disease caused by tobacco. Methods: SD rats were randomly divided into 4 groups, 20 in each group, followed by normal group, model group, experimental group, and control group. Rats in the model group, experimental group and control group were smoked for 64 days with Yan'an cigarettes to construct a chronic obstructive pulmonary rat model, and the normal group rats were kept at room temperature. After smoking, rats in the experimental group and the control group were injected subcutaneously with 5 mL ambroxol hydrochloride (20 mg / kg) and 5 mL banbutrolol hydrochloride (20 mg / kg) daily. The normal group and the model group were injected intraperitoneally with the same dose of normal saline. After 28 days of drug intervention, hematoxylin-eosinstaining (HE), elastic van gieson (EVG) staining, TUNNEL staining, immunohistochemical staining, and Western blot were used to detect the lung tissue pathology of each group of rats, Vascular remodeling, cell apoptosis of lung tissue, the expression of α-smoothmus-cleactin (α-SMA) and Vascular endothelial growth factor (VEGF), the expression levels of Caspase-3, Bax And Bcl-2. Results: Compared with the normal group, the lung tissue of the model group was significantly damaged, the thickness of the pulmonary arterioles was significantly increased, the degree of vascular myogenesis, the apoptosis rate of cells, and the expressions of α-SMA and VEGF, Caspase-3, and Bax were significantly increased. The expression of Bcl-2 was significantly reduced, and the differences were statistically significant (P<0.05). Compared with the model group, the lung damage of the experimental group and the control group was significantly improved, the thickness of the pulmonary arterioles was significantly reduced, the degree of vascular myogenesis, the apoptosis rate of cells. The expressions of α-SMA and VEGF, Bax were significantly reduced, and the expression of Bcl-2 was significantly increased, and the differences were statistically significant (P <0.05). Conclusion: Ambroxol hydrochloride can inhibit the apoptosis of lung tissue, improve its vascular remodeling, and protect the lung tissue of COPD rats. |
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