Pyrin重组蛋白对博来霉素诱导的大鼠肺纤维化的影响
发布时间：2018-11-01 15:39
【摘要】：目的:讨论Pyrin重组蛋白对博莱霉素诱导的大鼠肺纤维化是否有作用,Pyrin重组蛋白是否通过VEGF/VEGFR2/MMP-9信号通路来影响肺纤维化。实验方法:随机将60只SD大鼠分成4组,正常对照组、博来霉素模型组、Pyrin重组蛋白组、SU5416阳性对照组。所有组于第14天及第28天分两批进行取材,用HE染色和MASSON染色分别观察肺泡炎程度及肺纤维化程度,免疫组化及RT-PCR分别检钡VEGF、VEGFR-2、MMP-9蛋白和mmRNA表达情况。结果:1.各组大鼠肺组织病理变化:HE染色分级示:肺泡炎程度的比较中博来霉素模型组最为严重,而正常对照组无明显肺泡炎改变(P0.05)。Pyrin重组蛋白组在第14天及第28天时肺泡炎程度较正常对照组明显加重,而较博来霉素模型组减轻(P0.05)。Masson染色分级示:博来霉素模型组在纤维化程度最为严重,而正常对照组未见明显肺纤维化(P0.05)。而在第14天及第28天时Pyrin重组蛋白组的肺纤维化程度均较博来霉素模型组的肺纤维化程度减轻(P0.05)。2肺组织免疫组化染色(VEGF、VEGFR2、MMP-9):在第14天时,正常对照组肺组织中的VEGF、VEGFR2、MMP-9有少量表达,而博来霉素模型组大鼠肺组织的VEGF、VEGFR2、MMP-9表达明显增多(P0.05);SU5416阳性对照组和Pyrin重组蛋白组大鼠肺组织VEGF、VEGFR2、MMP-9表达较正常对照组明显增多,但较博来霉素模型组有所减弱(P0.05)。当第28天时,SU5416阳性对照组和Pyrin重组蛋白治疗组VEGF、VEGFR2、MMP-9表达水平仍较正常对照组明显增强(P0.05),但较博来霉素模型组VEGF、VEGFR2、MMP-9表达有所减弱(P0.05)。3.mRNA表达(VEGF、VEGFR2、MMP-9):博来霉素模型组、SU5416阳性对照组和Pyrin重组蛋白组的VEGF、VEGFR2、MMP-9表达水平均较正常对照组相比显著增高(P0.05)。其中第28天VEGF、VEGFR2、MMP-9表达水平与第14天相比有升高趋势,但未见显著性差异(P0.05)。而正常对照组肺组织的VEGF、VEGFR2、MMP-9 mRNA表达水平相对稳定,Pyrin重组蛋白组的VEGF、VEGFR2、MMP-9表达水平较博来霉素模型组相比在第14天及第28天均明显降低(P0.05)。结论:1.Pyrin重组蛋白可能通过下调VEGF/VEGFR2/MMP-9信号通路而抑制肺纤维化新生血管的生成。2.Pyrin重组蛋白可能通过下调VEGF/VEGFR2/MMP-9信号通路而抑制肺纤维化ECM的沉积。3.Pyrin重组蛋白可能通过下调VEGF/VEGFR2/MMP-9信号通路而发挥抗肺纤维化作用。
[Abstract]:Aim: to investigate the effects of Pyrin recombinant protein on bleomycin induced pulmonary fibrosis in rats and whether Pyrin recombinant protein affects pulmonary fibrosis through VEGF/VEGFR2/MMP-9 signaling pathway. Methods: sixty SD rats were randomly divided into 4 groups: normal control group, bleomycin model group, Pyrin recombinant protein group and SU5416 positive control group. The alveolitis degree and pulmonary fibrosis degree were observed by HE staining and MASSON staining. The expression of barium VEGF,VEGFR-2,MMP-9 protein and mmRNA were detected by immunohistochemistry and RT-PCR, respectively. The result is 1: 1. Pathological changes of lung tissue of rats in each group: HE staining grade showed that the degree of alveolitis was the most serious in bleomycin model group. But there was no obvious change of alveolitis in normal control group (P0.05) the degree of alveolitis in). Pyrin recombinant protein group was significantly worse than that in normal control group on the 14th and 28th day. But compared with bleomycin model group (P0.05). Masson staining grade: bleomycin model group in the fibrosis degree is the most serious, but the normal control group did not see significant pulmonary fibrosis (P0.05). On the 14th and 28th day, the degree of pulmonary fibrosis in the Pyrin recombinant protein group was lower than that in the bleomycin model group (P0.05). 2 the lung tissue immunohistochemical staining (VEGF,VEGFR2,MMP-9): on the 14th day, the pulmonary fibrosis degree of the Pyrin recombinant protein group was lower than that of the bleomycin model group (P0.05). There was a little expression of VEGF,VEGFR2,MMP-9 in lung tissue of normal control group, while the expression of VEGF,VEGFR2,MMP-9 in lung tissue of bleomycin model group was significantly increased (P0.05). The expression of VEGF,VEGFR2,MMP-9 in lung tissue of SU5416 positive control group and Pyrin recombinant protein group was significantly higher than that of normal control group, but decreased compared with bleomycin model group (P0.05). On the 28th day, the expression of VEGF,VEGFR2,MMP-9 in SU5416 positive control group and Pyrin recombinant protein treatment group was significantly higher than that in normal control group (P0.05), but it was higher than that in bleomycin model group (P0.05). MMP-9 expression decreased (P0.05). 3.mRNA expression (VEGF,VEGFR2,MMP-9): VEGF,VEGFR2, in bleomycin model group, SU5416 positive control group and Pyrin recombinant protein group The expression of MMP-9 was significantly higher than that of normal control group (P0.05). The expression of VEGF,VEGFR2,MMP-9 on the 28th day was higher than that on the 14th day, but there was no significant difference (P0.05). The expression of VEGF,VEGFR2,MMP-9 mRNA in lung tissue of normal control group was relatively stable, and the expression of VEGF,VEGFR2,MMP-9 in Pyrin recombinant protein group was significantly lower than that in bleomycin model group on the 14th and 28th day (P0.05). Conclusion: 1.Pyrin recombinant protein may inhibit angiogenesis of pulmonary fibrosis by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway, and 2.Pyrin recombinant protein may inhibit pulmonary fibrosis by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway. The deposition of fibrotic ECM. 3.Pyrin recombinant protein may play an anti-pulmonary fibrosis effect by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway.
【学位授予单位】：延边大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R563
，
本文编号：2304359
[Abstract]:Aim: to investigate the effects of Pyrin recombinant protein on bleomycin induced pulmonary fibrosis in rats and whether Pyrin recombinant protein affects pulmonary fibrosis through VEGF/VEGFR2/MMP-9 signaling pathway. Methods: sixty SD rats were randomly divided into 4 groups: normal control group, bleomycin model group, Pyrin recombinant protein group and SU5416 positive control group. The alveolitis degree and pulmonary fibrosis degree were observed by HE staining and MASSON staining. The expression of barium VEGF,VEGFR-2,MMP-9 protein and mmRNA were detected by immunohistochemistry and RT-PCR, respectively. The result is 1: 1. Pathological changes of lung tissue of rats in each group: HE staining grade showed that the degree of alveolitis was the most serious in bleomycin model group. But there was no obvious change of alveolitis in normal control group (P0.05) the degree of alveolitis in). Pyrin recombinant protein group was significantly worse than that in normal control group on the 14th and 28th day. But compared with bleomycin model group (P0.05). Masson staining grade: bleomycin model group in the fibrosis degree is the most serious, but the normal control group did not see significant pulmonary fibrosis (P0.05). On the 14th and 28th day, the degree of pulmonary fibrosis in the Pyrin recombinant protein group was lower than that in the bleomycin model group (P0.05). 2 the lung tissue immunohistochemical staining (VEGF,VEGFR2,MMP-9): on the 14th day, the pulmonary fibrosis degree of the Pyrin recombinant protein group was lower than that of the bleomycin model group (P0.05). There was a little expression of VEGF,VEGFR2,MMP-9 in lung tissue of normal control group, while the expression of VEGF,VEGFR2,MMP-9 in lung tissue of bleomycin model group was significantly increased (P0.05). The expression of VEGF,VEGFR2,MMP-9 in lung tissue of SU5416 positive control group and Pyrin recombinant protein group was significantly higher than that of normal control group, but decreased compared with bleomycin model group (P0.05). On the 28th day, the expression of VEGF,VEGFR2,MMP-9 in SU5416 positive control group and Pyrin recombinant protein treatment group was significantly higher than that in normal control group (P0.05), but it was higher than that in bleomycin model group (P0.05). MMP-9 expression decreased (P0.05). 3.mRNA expression (VEGF,VEGFR2,MMP-9): VEGF,VEGFR2, in bleomycin model group, SU5416 positive control group and Pyrin recombinant protein group The expression of MMP-9 was significantly higher than that of normal control group (P0.05). The expression of VEGF,VEGFR2,MMP-9 on the 28th day was higher than that on the 14th day, but there was no significant difference (P0.05). The expression of VEGF,VEGFR2,MMP-9 mRNA in lung tissue of normal control group was relatively stable, and the expression of VEGF,VEGFR2,MMP-9 in Pyrin recombinant protein group was significantly lower than that in bleomycin model group on the 14th and 28th day (P0.05). Conclusion: 1.Pyrin recombinant protein may inhibit angiogenesis of pulmonary fibrosis by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway, and 2.Pyrin recombinant protein may inhibit pulmonary fibrosis by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway. The deposition of fibrotic ECM. 3.Pyrin recombinant protein may play an anti-pulmonary fibrosis effect by down-regulating VEGF/VEGFR2/MMP-9 signaling pathway.
【学位授予单位】：延边大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R563
，
本文编号：2304359
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