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目的:观察内质网应激相关蛋白葡萄糖调节蛋白78(GRP78)及核因子-κB(NF-κB)在盐酸博来霉素诱导的肺纤维化中的变化及中药丹芍化纤胶囊对其表达的影响。方法:选取SD大鼠30只,随机分为正常组、肺纤维化模型组和丹芍化纤胶囊治疗组,每组各10只。正常组气管内滴注生理盐水,模型组和丹芍组气管内一次性灌注盐酸博来霉素5mg/kg诱导肺纤维化,丹芍组于造模第2天给予丹芍化纤胶囊混悬液灌胃(0.8g.kg-1.d-1)治疗,正常组及模型组则给予等量生理盐水灌胃。实验第28天称大鼠体质量,处死各组大鼠,称肺湿重并收集肺组织,行HE和Masson染色观察肺组织病理变化;采用免疫组织化学的方法检测肺组织中GRP78及NF-κB蛋白的表达情况。结果:与正常组比较,模型组大鼠肺组织中GRP78及NF-κB表达明显升高(P<0.01);经丹芍化纤治疗后,大鼠肺组织中GRP78及NF-κB蛋白表达显著降低(P<0.01)。结论:GRP78及NF-κB可能参与了盐酸博来霉素诱导的肺纤维化过程。丹芍化纤胶囊对肺纤维化的干预机制可能与抑制肺组织中GRP78及NF-κB的表达,减轻内质网应激所引起的损伤有关。
Objective: To observe the changes of endoplasmic reticulum stress-related proteins glucose regulatory protein 78 (GRP78) and nuclear factor-κB (NF-κB) in bleomycin-induced pulmonary fibrosis and the expression of Danshenhuaxian capsule Impact. Methods: Thirty SD rats were randomly divided into normal group, pulmonary fibrosis model group and Dan Shao Huaxian Capsule treatment group, with 10 rats in each group. Normal group, intratracheal instillation of saline, model group and Dan Shao group tracheal infusion of bleomycin hydrochloride 5mg / kg induced pulmonary fibrosis, Dan Shao group in the second day of modeling given Dan Shaofu capsule suspension Gavage (0.8g.kg-1.d-1) treatment, the normal group and model group were given equal volume of saline gavage. The rats were sacrificed on the 28th day of the experiment, and the rats in each group were sacrificed. The lungs were weighed and wetted. The pathological changes of the lungs were observed by HE and Masson staining. The expressions of GRP78 and NF- κB protein expression. Results: Compared with the normal group, the expression of GRP78 and NF-κB in the lung tissue of the model group was significantly increased (P <0.01), while the expression of GRP78 and NF-κB in the lung tissue of the model group was significantly decreased (P <0.01). Conclusion: GRP78 and NF-κB may be involved in bleomycin hydrochloride-induced pulmonary fibrosis. The intervention mechanism of Danshaohuaxian Capsule on pulmonary fibrosis may be related to inhibiting the expression of GRP78 and NF-κB in lung tissue and reducing the damage caused by endoplasmic reticulum stress.