摘要
目的探讨腹腔注射阿米福汀对博来霉素致肺纤维化大鼠的保护作用及机制。方法选择24只成年雄性SD大鼠,随机分为对照组、模型组和干预组。对照组气管内注入生理盐水;模型组注射博莱霉素;干预组注射博莱霉素和阿米福汀。第28 d采集静脉血后处死大鼠,检测层粘连蛋白(LN)、Ⅲ型前胶原(PCⅢ)和Ⅳ型胶原(CⅣ)、转化生长因子-β1(TGF-β1);取肺组织石蜡切片观察其病理变化;并测定羟脯氨酸(Hyp)含量。结果与对照组相比,模型组及干预组可见间质炎症细胞浸润及胶原纤维沉积,且干预组程度较模型组减轻(P<0.05)。模型组及干预组血清LN、PCⅢ、CⅣ、TGF-β1含量高于对照组,且干预组上述指标低于模型组(P<0.05)。模型组及干预组Hyp高于对照组,且干预组Hyp低于模型组(P<0.05)。结论腹腔注射阿米福汀能减轻博来霉素所致大鼠肺纤维化,其机制可能与抑制转化TGF-β1表达、降低血清LN、PCⅢ和CⅣ型胶原含量有关。
Objective To investigate protective effect and mechanism of Amifostine by intraperitoneal injection on Bleomycin-induced pulmonary fibrosis in rats.Methods A total of 24 adult male Sprague-Dawley rats were randomly divided into control group,model group and intervention group.Control group was intratracheally injected with physiological saline,and model group was injected with Bleomycin,while intervention group was injected with Bleomycin and Amifostine.Among three groups,rats were sacrificed after collecting venous blood samples on the 28th d after intratracheal drug injection,and levels of laminin(LN),procollagen type III(PCIII),collagen type IV(PCIV)and transforming growth factor-β1(TGF-β1)were detected;paraffin sections of lung tissues were collected,and pathological changes of lung tissue were observed;content of hydroxyproline(Hyp)was determined by alkaline hydrolysis method.Results Compared with those in control group,infiltration of interstitial inflammatory cells and deposition of collagen fibers in model and intervention groups were found,and the degrees in intervention group were less than those in model group.Levels of serum LN,PC III,PC IV and TGF-β1 in model and intervention groups were higher than those in control group,and levels of the above indexes in intervention group were lower than those in model group(P<0.05).Hyp contents in model and intervention groups were higher than that in control group,and the content in intervention group was lower than that in model group(P<0.05).Conclusion Amifostine by intraperitoneal injection may alleviate pulmonary fibrosis induced by Bleomycin in rats,and its mechanism may be related to inhibition of TGF-β1 expression and decrease of LN,PC III and PC IV levels.
作者
王源
代文静
李万成
WANG Yuan;DAI Wen-jing;LI Wan-cheng(Department of Respiratory Medicine,the First Affiliated Hospital of Chengdu Medical College,Chengdu 610000,China)
出处
《解放军医药杂志》
CAS
2019年第11期1-4,10,共5页
Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
基金
四川省教育厅科研计划项目(16ZB0292)
成都医学院科研计划项目(CYZ17-32)
