首页> 中文期刊> 《中国免疫学杂志》 >替普瑞酮诱导肺纤维化大鼠肺HSP70表达及干预肺纤维化的研究

替普瑞酮诱导肺纤维化大鼠肺HSP70表达及干预肺纤维化的研究

         

摘要

目的:研究替普瑞酮(GGA)对博莱霉素(BLM)诱导的肺纤维化大鼠肺组织HSP70表达的影响及对大鼠肺纤维化的干预作用.方法:SD大鼠30只,随机分为假手术组(SO)、模型组(M)和替普瑞酮组(GGA).M组和GGA组大鼠气管内一次性注射BLM 5 mg/kg,SO组大鼠气管内注射等体积的生理盐水.造模后第1天开始隔天灌胃给予GGA,持续到处死动物的前1天,模型组灌服等体积的生理盐水.记录大鼠每日体重,造模后第28天时处死大鼠,测定肺纤维化大鼠的肺系数、肺组织内HSP70表达及羟脯氨酸(HYP)的含量,观察肺组织病理改变.结果:GGA能提高博莱霉素处理后大鼠肺组织HSP70的表达(P<0.01);与M组相比,大鼠体重下降得到明显恢复(P<0.01),而肺组织的肺系数和羟脯氨酸(HYP)含量则明显降低(P<0.05),病理结果显示肺泡内结构完整,未出现类似M组肺组织实变现象,肺纤维化程度较轻.结论:替普瑞酮能诱导BLM肺纤维化模型大鼠肺组织HSP70表达,减轻肺纤维化程度.%Objective: To study whether Geranylgeranylacetone ( GGA) could induce the expression of heat shock protein 70 and protect against bleomycin-induced pulmonary fibrosis in rats. Methods: Totally 30 health SD rats were randomly divided into sham operated group (SO) , model group (M) and GGA group, each groups were assigned to receive intratracheal instillation of bleomycin at 5 mg/kg (group M and group GGA) or saline (group CN) Respectively. The rats of GGA group were given GGA 800 mg/kg by gavage one time every other day, daily weight were recorded in each group. All rats were sacrificed on the 28th day, the pulmonary coefficient was calculated based on the lung weight and body weight of each rats. The expression of HSP70 and the hydroxyproline content of lung tissue were detected by Western blot and Hydroxyproline Assay Kit, respectively. Additionally, histological changes of lung tissue were evaluated by HE and Masson staining. Results;The expression of HSP70 in bleomycin-induced fibrotic rats was induced by GGA. As compared with M group, the weight loss has significantly restored, and pulmonary coefficient and HYP concentrations were decreased in GGA group. Pathology results showed that GGA group keep the structural integrity of the alveolar monolayer, without the lung tissue consolidation, and lessened the hyperplasia of BLM-induced pulmonary fibrosis in rats. Conclusion:GGA could induce the expression of HSP70 in BLM induced pulmonary fibrosis model rats and produce a protective effect on pulmonary fibrosis.

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