单克隆抗体在百草枯中毒模型中的作用
Experimental study in the role of monoclonal antibody in pulmonary fibrosis induced by paraquat in the mice model
目的 探讨白细胞介素17单克隆抗体(IL-17 monoclonal antibody,IL-17 MAb)在百草枯致小鼠肺纤维化模型中的作用.方法 将雄性C57BL/6小鼠60只,随机(随机数字法)分为三组:对照组(n=12)腹腔注射生理盐水0.1 mL,染毒组(n=24)腹腔注射百草枯(25 mg/kg)溶液0.1 mL和治疗组(n=24)腹腔注射百草枯(25 mg/kg)同时予尾静脉注射IL-17MAb(5μg/mice);在注射处理后第1、7、14天采血,并用酶联免疫吸附法检测各组小鼠的白介素-17A (IL-17A)、转化生长因子-β1 (TGF-β1)、干扰素-γ(IFN-γ)的表达水平;肺组织切片进行HE染色,并观察其病理变化;记录各组病死数量,并计算生存率.运用SPSS 21.0软件进行统计分析,其中各细胞因子分泌水平的动态变化以及在各实验组间的差异都采用单因素方差分析(One-Way-ANOVA),各实验组的生存率差异采用费希尔精确检验(Fisher's exact test).结果 百草枯注射处理后,细胞因子IL-17A和TGF-β1的分泌水平都升高(P<0.01),IL-17MAb的干预可抑制该升高程度;相反地,细胞因子IFN-γ的分泌水平在百草枯处理后呈下降的表达模式(P<0.01),IL-17MAb的干预可抑制其下降程度;肺组织切片的病理组织学显示,百草枯注射能导致肺组织损伤,呈肺纤维化表现,而IL-17MAb的干预能减轻这种损伤;IL-17MAb的干预能提高百草枯致病的生存率(P<0.05).结论 IL-17MAb能降低细胞因子IL-17A、TGF-β1的表达水平,增强IFN-γ分泌,从而改善百草枯致肺纤维化的进程.
更多Objective To explore the positive role of IL-17 MAb (IL-17 Monoclonal Antibody) in pulmonary fibrosis model induced by paraquat (PQ) in mice.Methods A total of 60 C57BL/6 male mice were randomly (random number) assigned into three groups:the control group (n =12),PQ poisoning group (n =24) induced by an intra-peritoneal injection of PQ (25 mg/kg) and treatment group (n =24)induced by an intra-peritoneal injection of PQ (25 mg/kg) treated with an caudal vein injection of IL-17MAb (5 μg/mice).In control group,saline was injected intra-peritoneally instead of PQ.Blood samples from 3 groups were collected on day 1,day 7 and day 14,respectively for determining the levels of IL-17 A,TGF-β1 and IFN-γ by using ELISA (enzyme linked immunosorbent assay).HE (Hematoxylin-eosin)staining was used to observe the pathological changes in lung tissues.Data were analyzed with SPSS 21.0software to achieve statistical results.The changes of levels of cytokines and the differences among experimental groups were analyzed with One-Way ANOVA,while the difference in survival rate among groups were analyzed with Fisher's exact test.Results After the injection of PQ,both IL-17 A and TGF-β1 were increased (P < 0.01),and the IL-17 MAb attenuated these effects.On the contrary,the level of IFN-γwas lowered after the injection of PQ (P < 0.01),and the IL-t7 MAb also lessened this effect.PQ contributed to lung tissue damage,resulting in pulmonary fibrosis.However,IL-17 MAb ameliorated this damage.The IL-17 MAb improved the survival rate in the mouse models of pulmonary fibrosis induced by PQ (P < 0.05).Conclusions IL-I7 MAb can lower the levels of both IL-17 A and TGF-β1,and enhance the release of IFN-γ,making a high survival rate in the paraquat-induced pulmonary fibrosis mice.
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