This study aimed to research the effect of miR-149 on endoplasmic reticulum stress (ERS)-induced inflammation and apoptosis in non-alcoholic fatty liver disease (NAFLD). The mouse model with NAFLD was established by feeding with a high-fat diet, and the model establishment was subsequently confirmed by H&E staining and oil red O staining. MiR-149 agomir was injected into NAFLD mice to observe changes in liver tissues. After cell transfection, qRT-PCR and Western blot were performed to measure the expressions of lipid metabolism-related proteins (SCD-1, PPARα, and ABCA1), miR-149 and ATF6. Luciferase reporter gene assay was applied to verify the relationship between miR-149 and ATF6. Inflammatory factors (TNF-α, IL-1β, IL-6 and NF-κB) and apoptotic-related factors (caspase-12 and CHOP) were measured by ELISA and flow cytometry. qRT-PCR and Western blot were applied to detect expressions of ATF6 signaling pathway-related proteins (GRP94 and Akt). NAFLD progression was attenuated in mice injected with miR-149 agomir. The expression of miR-149 was reduced in liver tissues of NAFLD mice, while the expression of ATF6 was increased. Transfection of miR-149 can result in a decrease of ATF6 expression. ATF6 was a target gene of miR-149. MiR-149 could down-regulate the expressions of inflammatory factors and apoptotic-related factors. MiR-149 could down-regulate expressions of ATF6 signaling pathway-related proteins. MiR-149 alleviates ERS-induced inflammation and apoptosis by down-regulating the ATF6 signaling pathway, thus inhibiting the progression of NAFLD.

中文翻译：

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MiR-149通过负向靶向ATF6途径减轻非酒精性脂肪肝疾病中内质网应激诱导的炎症和细胞凋亡。

本研究旨在研究miR-149对内质网应激（ERS）诱导的非酒精性脂肪肝疾病（NAFLD）炎症和细胞凋亡的影响。通过饲喂高脂饮食建立具有NAFLD的小鼠模型，随后通过H＆E染色和油红O染色确认模型建立。将MiR-149 agomir注射到NAFLD小鼠中以观察肝组织的变化。细胞转染后，进行qRT-PCR和Western blot检测脂质代谢相关蛋白（SCD-1，PPARα和ABCA1），miR-149和ATF6的表达。应用萤光素酶报告基因检测miR-149和ATF6之间的关系。ELISA和流式细胞仪检测炎症因子（TNF-α，IL-1β，IL-6和NF-κB）和凋亡相关因子（caspase-12和CHOP）。采用qRT-PCR和Western blot检测ATF6信号通路相关蛋白（GRP94和Akt）的表达。在注射miR-149 agomir的小鼠中，NAFLD的进展减弱。在NAFLD小鼠的肝组织中，miR-149的表达减少，而ATF6的表达增加。miR-149的转染可导致ATF6表达减少。ATF6是miR-149的靶基因。MiR-149可能下调炎症因子和凋亡相关因子的表达。MiR-149可能下调ATF6信号通路相关蛋白的表达。MiR-149通过下调ATF6信号通路来减轻ERS诱导的炎症和细胞凋亡，从而抑制NAFLD的进程。在注射miR-149 agomir的小鼠中，NAFLD的进展减弱。在NAFLD小鼠的肝组织中，miR-149的表达减少，而ATF6的表达增加。miR-149的转染可导致ATF6表达减少。ATF6是miR-149的靶基因。MiR-149可能下调炎症因子和凋亡相关因子的表达。MiR-149可能下调ATF6信号通路相关蛋白的表达。MiR-149通过下调ATF6信号通路来减轻ERS诱导的炎症和细胞凋亡，从而抑制NAFLD的进程。在注射miR-149 agomir的小鼠中，NAFLD的进展减弱。在NAFLD小鼠的肝组织中，miR-149的表达减少，而ATF6的表达增加。miR-149的转染可导致ATF6表达减少。ATF6是miR-149的靶基因。MiR-149可能下调炎症因子和凋亡相关因子的表达。MiR-149可能下调ATF6信号通路相关蛋白的表达。MiR-149通过下调ATF6信号通路来减轻ERS诱导的炎症和细胞凋亡，从而抑制NAFLD的进程。ATF6是miR-149的靶基因。MiR-149可能下调炎症因子和凋亡相关因子的表达。MiR-149可能下调ATF6信号通路相关蛋白的表达。MiR-149通过下调ATF6信号通路来减轻ERS诱导的炎症和细胞凋亡，从而抑制NAFLD的进程。ATF6是miR-149的靶基因。MiR-149可能下调炎症因子和凋亡相关因子的表达。MiR-149可能下调ATF6信号通路相关蛋白的表达。MiR-149通过下调ATF6信号通路来减轻ERS诱导的炎症和细胞凋亡，从而抑制NAFLD的进程。