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MiR155 Relieves Acute Heart Transplantation in Mice by Modulating Th1/Th17 Immune Response

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单位: [1]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Cardiovasc Surg, Wuhan 430000, Peoples R China
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关键词: Heart Transplantation Immune Response Th1 Th17 MiR155

摘要:
Heart transplantation is an effective method for the treatment of end-stage heart disease. Therefore, this article aimed to establish a stable and effective mouse abdominal heart transplantation model. MiR155 alleviates the acute heart transplantation response by regulating Th1 / Th17 immune cytokines. This paper used the control method of randomly selecting samples to classify 30 healthy mice that met the conditions. First, C57BL / 6 mice were used as recipients, and Balb / c mouse hearts were used as donors to establish mouse hearts as a transplantation acute reaction model. A chronic rejection model of mouse heart transplantation was established by C57BL / 6 mice as recipients and Bm12 mouse hearts as donors. The survival time of the two groups of transplanted hearts was carefully recorded. The results of the study showed that in the heart transplantation acute/chronic rejection model, the average survival time of the donor's heart in the allograft group was (7.5 +/- 0.37) / (63.4 +/- 4.37) days, which was the same compared with the two groups. Therefore, in-depth analysis of the experimental control results and conclusions from the experimental results of the mice, this study can better respond to the pathological changes of acute/chronic rejection and reach the standard of model establishment. MiR155 relieves heart transplantation by regulating Th1 / Th17 immune response acute reaction.

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出版当年[2021]版:
大类 | 4 区 生物学
小类 | 4 区 生化与分子生物学 4 区 细胞生物学
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出版当年[2020]版:
Q4 CELL BIOLOGY Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
最新[2023]版:
Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Q4 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

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第一作者单位: [1]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Cardiovasc Surg, Wuhan 430000, Peoples R China
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