SOCS1 蛋白在内毒素耐受小鼠模型中的表达及其受 mir-150 调控的机制。
Expression of SOCS1 Protein in Endotoxin-Tolerant Mouse Model and Its Regulation Mechanism by mir-150.
机构信息
Department of Burns Plastic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, China.
Department of Ophthalmology, Affiliated Hospital of Zunyi Medical University, Guizhou Branch of National Clinical Research Center for Ophthalmopathy, Special Key Laboratory of Ocular Diseases of Guizhou Province, Zunyi 563003, China.
出版信息
Contrast Media Mol Imaging. 2022 Sep 2;2022:3241812. doi: 10.1155/2022/3241812. eCollection 2022.
In order to investigate the expression of Suppressor of Cytokine Signaling 1 (SOCS1) and its regulatory mechanism by mir-150 in a lipopolysaccharide (LPS) tolerant mouse model of endotoxin, a total of 60 male BALB/C mice were randomly divided into 2 groups. The LPS is used to construct the endotoxin resistant mouse model and the mice are included in the model group ( = 30), 0.9% sodium chloride injection is used to construct the normal control group ( = 30). And tumor necrosis factor- (TNF-) is determined by Elisa to determine whether the model was successfully constructed. The correlation between SOCS1 protein and mir-150 is analyzed by the Pearson correlation coefficient. In the experiments, the results show that the expression of TNF- in the macrophage fluid of the model group is significantly decreased ( < 0.05), indicating that the endotoxin tolerance mouse model is successfully constructed, so the secretion of TNF- is reduced.
为了研究抑制细胞因子信号转导 1（SOCS1）及其在脂多糖（LPS）耐受的内毒素小鼠模型中通过 mir-150 调节的机制，将 60 只雄性 BALB/C 小鼠随机分为 2 组。用 LPS 构建内毒素耐药小鼠模型，将小鼠纳入模型组（n=30），用 0.9%氯化钠注射液构建正常对照组（n=30）。通过 Elisa 法测定肿瘤坏死因子-（TNF-），以确定模型是否构建成功。采用 Pearson 相关系数分析 SOCS1 蛋白与 mir-150 的相关性。在实验中，结果表明模型组巨噬细胞液中 TNF-的表达明显降低（<0.05），表明内毒素耐受小鼠模型构建成功，因此 TNF-的分泌减少。
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