肿瘤坏死因子-α诱导的蛋白-8样分子2促进热损伤小鼠CD4阳性T细胞凋亡

发布时间：2018-03-20 03:26

本文选题：肿瘤坏死因子α　切入点：蛋白-样分子　出处：《南方医科大学学报》2016年10期 　论文类型：期刊论文

【摘要】：目的探讨肿瘤坏死因子-α诱导的蛋白-8样分子2(TIPE2)对重度烫伤小鼠模型脾脏CD4~+T淋巴细胞的凋亡的影响。方法140只成年雄性BALB/C小鼠分为6组,应用小RNA干扰技术制作si TIPE2/过表达慢病毒,复制小鼠重度烫伤模型。分离BALB/c小鼠脾脏CD4~+T细胞,检测各组CD4~+T淋巴细胞凋亡,Smad2/Smad3、磷酸(P)-Smad2/P-Smad3以及B淋巴细胞瘤-2(Bcl-2)家族蛋白Bcl-2/Bim的表达。检测各组小鼠CD4~+T内线粒体膜电位改变情况及细胞色素C的变化和各组小鼠CD4~+T内含半胱氨酸的天冬氨酸蛋白水解酶(caspase-3)、(caspase-8)、(caspase-9)的活化情况。结果 si TIPE2-burn组CD4~+T淋巴细胞凋亡率为12.33%,较sham组外其余组减少,P-smad2/P-Smad3蛋白表达(灰度值)显著降低(P0.01)。si TIPE2-burn组Bcl-2的蛋白表达较其余组升高(P0.05),Bim的表达则降低(P0.05)。si TIPE2-burn组线粒体膜电位细胞色素C水平均较sham组外其余组降低(P0.05),caspase-3活性较TIPE2-burn组降低(P0.01),caspase-8、caspase-9活性较其余组降低(P0.05)。TIPE2-burn组凋亡率最高,TIPE2-burn组Smad2/Smad3蛋白表达较sham组明显升高(P0.05),P-smad2/P-Smad3蛋白表达较其余组显著升高(P0.05);CD4~+T内线粒体膜电位较其余组降低(P0.01),细胞色素C水平升高,caspase-3、caspase-8、caspase-9活性较其他组均升高(P0.05)。结论 TIPE2作为一种重要的负向调控分子,可通过促进转化生长因子β即TGF-β/Smads信号传导通路、线粒体相关凋亡途径加速T淋巴细胞凋亡。
[Abstract]:Objective to investigate the effect of tumor necrosis factor- 伪 (TNF- 伪) -induced protein 8 like molecule (TIPE2) on the apoptosis of CD4 ~ T lymphocytes in spleen of severe scalded mice. Methods 140 adult male BALB/C mice were divided into 6 groups. Si TIPE2/ overexpression lentivirus was made by using small RNA interference technique, and the model of severe scald was established in mice. CD4T cells were isolated from spleen of BALB/c mice. The expression of CD4 ~ T apoptotic Smad2 / Smad3, P-Smad3 and B-lymphocytoma Bcl-2) family proteins were detected in each group. The changes of mitochondrial membrane potential and cytochrome C in CD4T and CD4T in each group were detected. Results the apoptotic rate of CD4 ~ T lymphocytes in si TIPE2-burn group was 12.33, which decreased the expression of P-smad2 / P-Smad3 protein (grayscale value) significantly lower than that in sham group (P 0.01.si TIPE2-burn group). The activation of caspase-8 / caspase-9 by aspartate protein hydrolase (caspase-3) containing cysteine was observed. Results the apoptotic rate of CD4 ~ T lymphocytes in si TIPE2-burn group was 12.33%, which was significantly lower than that in other groups other than sham group. The level of cytochrome C of mitochondrial membrane potential in P0.05 TIPE2-burn group was lower than that in the rest of sham group. Compared with TIPE2-burn group, the activity of Caspase-3 was lower than that of TIPE2-burn group. The activity of P0.05. TIPE2-burn group was lower than that of other group. The apoptosis rate of TIPE2-burn group was higher than that of TIPE2-burn group. The apoptosis rate of TIPE2-burn group was higher than that of other group and the highest apoptotic rate of TIPE2-burn group was lower than that of TIPE2-burn group, and the highest apoptosis rate of TIPE2-burn group was lower than that of P0.05. TIPE2-burn group. Compared with the other groups, the expression of P-smad2 / P-Smad3 protein was significantly increased in the sham group. The mitochondrial membrane potential in P0.05 ~ T was significantly lower than that in the other groups, and the activity of caspase-3, caspase-8, caspase-9 was higher than that in the other groups. Conclusion TIPE2 is an important negative regulatory molecule. By promoting TGF- 尾 / Smads signaling pathway, mitochondrial related apoptosis pathway can accelerate apoptosis of T lymphocytes.
【作者单位】：解放军总医院急诊科;济南军区总医院急诊重症中心;解放军总医院第一附属医院全军烧伤研究所基础部;
【基金】：国家自然科学基金(81372054)~~
【分类号】：R644;R459.7

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