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急性肺损伤小鼠肺内TREM-1与内质网应激相关性研究 被引量:2

Relationship between intrapulmonary TREM-1 and endoplasmic reticulum stress in mice with acute lung injury
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摘要 目的观察急性肺损伤(ALI)小鼠肺内髓样细胞表达的触发受体-1(TREM-1)与内质网应激的相关性。方法以Balb/c小鼠为研究对象,气管注射脂多糖(LPS,5 mg/kg)复制小鼠ALI模型,采用real-time PCR法检测肺组织TREM-1与内质网应激相关蛋白CHOP和GRP78 mRNA的表达,并分析TREM-1与内质网相关蛋白基因表达的相关性。LPS(100 ng/mL)诱导小鼠原代腹腔巨噬细胞炎症反应,检测巨噬细胞TREM-1、CHOP和GRP78 mRNA表达并分析其相关性。采用TREM-1激活抗体处理小鼠巨噬细胞后,观察其对CHOP和GRP78表达的影响。结果 ALI小鼠肺内TREM-1 mRNA与内质网应激相关蛋白CHOP和GRP78 mRNA表达显著增加,TREM-1与CHOP和GRP78表达呈正相关。LPS可上调小鼠巨噬细胞TREM-1、CHOP和GRP78 mRNA的表达,且TREM-1与CHOP和GRP78呈正相关。激活TREM-1可增加CHOP和GRP78 mRNA表达。结论 ALI小鼠肺内TREM-1和内质网应激呈正相关,激活TREM-1可增强巨噬细胞内质网应激。 Objective To observe the correlation of intrapulmonary TREM- 1 with endoplasmic reticulum stress in mice with acute lung injury (ALI). Methods Balb/c mice were tracheally injected with lipopolysaccharide(LPS, 5 mg/kg) to induce ALI. Real-time PC R and Western blot were used to detect the expressions of TREM-1, CHOP and GRP78. The correlation of TREM- i with endoplasmic reticulum-related proteins was analyzed. LPS ( 100 ng/mL) was used to induce inflammation in mouse primary peritoneal macrophages, and expressions of TREM -1, CHOP and GRP78 mRNA were detected by real-time PCR. The effect of TREM-1 activation on the expressions of CHOP and GRP78 was observed in macrophages. Results The expressions of TREM- 1, CHOP and GRP78 mRNA were increased in ALI mice. TREM-1 mRNA expression was positively correlated with CHOP and GRP78 mRNA expression. In vitro, LPS up-regulated the expressions of TREM- 1, CHOP and GRP78, and TREM- 1 was positively correlated with CHOP and GRP78. Activation of TREM- 1 increased CHOP and GRP78 mRNA expressions. Conclusions TREM- 1 is positively related to the endoplasmic reticuium stress. The activation of TREM- 1 enhances endoplasmic reticuium in mouse macrophages.
出处 《实用医学杂志》 CAS 北大核心 2017年第22期3710-3713,共4页 The Journal of Practical Medicine
基金 国家自然科学基金(编号:81660021) 遵义医学院大学生创新创业训练计划项目(编号:20162312)
关键词 急性肺损伤 髓样细胞表达的触发受体1 内质网应激 巨噬细胞 acute lung injury triggering receptor expressed on myeloid ceils-l endopiasmic reticulure stress macrophage
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