mTOR及S6K1在免疫介导再生障碍性贫血模型小鼠骨髓中的表达

发布时间：2018-05-25 09:09

本文选题：贫血 + 再生障碍性　；参考：《中华临床医师杂志(电子版)》2017年02期

【摘要】：目的通过检测再生障碍性贫血模型小鼠骨髓中脂肪调控因子哺乳动物雷帕霉素靶蛋白(m TOR)及通路下游核糖体蛋白激酶S6K1的表达,研究再生障碍性贫血小鼠骨髓脂肪化的机制。方法 (1)制备免疫介导再生障碍性贫血小鼠模型。(2)造模开始后观察记录小鼠状态并定期测小鼠血常规以验证造模是否成功。(3)免疫组织化学方法检测骨髓细胞m TOR及S6K1的表达情况。所有数据采用SPSS 22.0软件进行统计学分析,数据经正态性检验,两组均数的比较采用单样本t检验,相关分析采用Pearson相关性检验。结果 (1)再生障碍性贫血小鼠造模成功:与对照组相比,再生障碍性贫血组小鼠第5天开始出现精神状态不佳、皮毛光泽度降低、体质量下降,造模14 d后死亡5只。外周血细胞计数明显下降,表现为白细胞(WBC)、血红蛋白(Hb)、血小板(PLT)三系均减少,造模14 d时血常规分别为:对照组(10.52±0.73)×109/L,(132±6.3)g/L,(469±114)×109/L,再生障碍性贫血组(0.97±0.57)×109/L,(74±9.3)g/L,(57±32)×109/L(P均0.001)。(2)免疫组化显示再生障碍性贫血小鼠骨髓m TOR及S6K1的表达明显高于对照组,分别表现为对照组74.84±6.33、63.45±5.38,再生障碍性贫血组113.27±16.23、108.56±12.77(P均0.001)。(3)相关分析显示再生障碍性贫血小鼠m TOR及S6K1与WBC、Hb、PLT呈负相关,m TOR与S6K1呈正相关。结论 m TOR及S6K1在再生障碍性贫血模型小鼠骨髓细胞的表达明显增加,与血细胞变化呈负相关,m TOR及S6K1可能在骨髓脂肪细胞的形成中起一定作用即参与了再生障碍性贫血小鼠骨髓的脂肪化,继而可能抑制了骨髓造血。
[Abstract]:Objective to investigate the mechanism of bone marrow adipogenesis in aplastic anemia mice by detecting the expression of rapamycin target protein (ORM) and ribosomal protein kinase (S6K1) downstream in bone marrow of mice with aplastic anemia. Methods 1) the mouse model of immune-mediated aplastic anemia was established. (2) after the establishment of the model, the status of the mice was recorded and the blood routine was measured regularly to verify the success of the model. 3) Immunohistochemical method was used to detect the m TOR of bone marrow cells. And the expression of S6K1. All the data were statistically analyzed by SPSS 22.0 software. The data were tested by normality test, the two groups of mean were compared by single sample t test, and the correlation analysis was carried out by Pearson correlation test. Results 1) the model of aplastic anemia mice was successful: compared with the control group, the mice in the aplastic anemia group began to appear the mental state on the 5th day, the fur gloss decreased, the body mass decreased, and 5 mice died after 14 days of modeling. The number of peripheral blood cells decreased obviously, which showed that WBC, HB, PLT were all decreased. On the 14th day, the blood routine were as follows: the expression of bone marrow m TOR and S6K1 in the control group (10.52 卤0.73) 脳 10 9 / L (132 卤6.3g / L) 469 卤114 脳 10 9 / L, and in the aplastic anemia group (0.97 卤0.57) 脳 10 9 / L (74 卤9.3 g / L 57 卤32) 脳 109/L(P respectively) the expression of bone marrow m TOR and S6K1 in the aplastic anemia mice was significantly higher than that in the control group. The correlation analysis showed that m TOR and S6K1 were negatively correlated with S6K1 and m TOR in control group (74.84 卤6.33) and aplastic anemia (113.27 卤16.23108.56 卤12.77) (P < 0.05). Conclusion the expression of m TOR and S6K1 in bone marrow cells of aplastic anemia model mice was significantly increased. TOR and S6K1 may play a certain role in the formation of adipocytes in bone marrow, that is, they may play a role in adipogenesis of bone marrow in aplastic anemia mice, and then inhibit bone marrow hematopoiesis.
【作者单位】：山西医科大学第一医院血液科;
【基金】：山西省科技攻关项目(20150313006-7)
【分类号】：R556.5;R-332

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