摘要
目的 研究牡荆素抑制Ras同源类似物C(RhoC)/Rho激酶(ROCK)信号对慢性阻塞性肺疾病大鼠肺组织炎症和气道重塑的影响.方法 SD大鼠分成对照组、模型组(慢性阻塞性肺疾病模型)、低剂量实验组(建模后给予1.5 mg·kg-1的牡荆素治疗)、中剂量实验组(建模后给予3.0 mg·kg-1的牡荆素治疗)、高剂量实验组(建模后给予6.0 mg·kg-1的牡荆素治疗)、高剂量+溶血磷脂酸(LPA)实验组(建模后给予6.0 mg·kg-1的牡荆素和LPA1 mg治疗).用蛋白质印迹法检测RhoC蛋白表达,检测大鼠肺功能指标,用苏木精-伊红染色观察肺组织病理学,评价大鼠气道炎症评分、气道平滑肌厚度,用酶联免疫吸附试验法检测肺泡灌洗液中白细胞介素-6(IL-6)含量,用免疫组化检测肺组织中碱性成纤维细胞生长因子(bFGF)表达.结果 对照组、模型组、高剂量实验组、高剂量+LPA实验组的RhoC蛋白表达水平分别为0.25±0.02、0.71±0.09、0.31±0.03和0.47±0.04,用力肺活量(FVC)分别为(8.25±0.62)、(4.12±0.24)、(7.21±0.54)和(6.44±0.52)mL,炎症评分分别为 0.52±0.04、2.54±0.15、1.23±0.11 和 1.79±0.32,平滑肌厚度分别为(19.28±1.52)、(28.43±1.74)、(19.45±1.18)和(25.85±1.57)μm,IL-6 含量分别为(2.40±0.08)、(5.67±0.44)、(2.85±0.23)和(4.01±0.29)ng·L-1,bFGF 蛋白表达水平分别为0.19±0.02、0.52±0.05、0.24±0.02 和 0.43±0.05.模型组的上述指标与对照组比较,高剂量实验组的上述指标与模型组比较,高剂量+LPA实验组的上述指标与高剂量实验组比较,在统计学上差异均有统计学意义(均P＜0.05).结论 牡荆素抑制RhoC/Rock信号改善慢性阻塞性肺疾病大鼠肺组织炎症和气道重塑.
Abstract
Objective To study the effect of vitexin inhibiting Ras homology C(RhoC)/Rho-associated kinase(ROCK)signaling on lung inflammation and airway remodeling in rats with chronic obstructive pulmonary disease.Methods SD rats were divided into control group,model group(chronic obstructive pulmonary disease model),experimental-L group(chronic obstructive pulmonary disease model,1.5 mg·kg-1 vitexin treatment),experimental-M group(chronic obstructive pulmonary disease model,3.0 mg·kg-1 vitexin treatment),experimental-H group(chronic obstructive pulmonary disease model,6.0 mg·kg-1 vitexin treatment),experimental-H+LPA group(chronic obstructive pulmonary disease mode,6.0 mg·kg-1 vitexin,lysophosphatidic acid 1 mg treatment),Western blot detection of RhoC protein expression,detection of pulmonary function indexes in rats,hematoxylin-eosin staining to observe lung histopathology,and evaluation of airway inflammation in rats score,airway smooth muscle thickness,enzyme-linked immunosorbent assay method to detect interleukin-6(IL-6)content in bronchoalveolar lavage fluid,immunohistochemistry to detect basic fibroblast growth factor(bFGF)in lung tissue.Results The expression levels of RhoC protein in the control group,model group,experimental-H group,and experimental-H+LPA group were 0.25±0.02,0.71±0.09,0.31±0.03,0.47±0.04;forced vital capacity(FVC)were(8.25±0.62),(4.12±0.24),(7.21±0.54),(6.44±0.52)mL;inflammation score were 0.52±0.04,2.54±0.15,1.23±0.11,1.79±0.32;smooth muscle thickness were(19.28±1.52),(28.43±1.74),(19.45±1.18),(25.85±1.57)μm;IL-6 content were(2.40±0.08),(5.67±0.44),(2.85±0.23),(4.01±0.29)ng·L-1;bFGF protein expression were 0.19±0.02,0.52±0.05,0.24±0.02,0.43±0.05.There were statistically significant differences in the above indicators between the model group and the control group,between the experimental-H group and the model group,and between the experimental-H+LPA group and the experimental-H group(all P＜0.05).Conclusion Vitexin inhibits RhoC/Rock signaling to improve lung inflammation and airway remodeling in chronic obstructive pulmonary disease rats.
国家科技期刊平台
NSTL
维普
万方数据