Acute lung injury (ALI) is the most vulnerable organ in sepsis, however, its underlying mechanism remains unclear. Cell viability and apoptosis were detected by cell counting kit‐8 and flow cytometry. The expressions of miR‐574, Complement 3 (C3), glucose regulatory protein 78 (GRP78), C/EBP homologous protein (CHOP) and Caspase‐12 were determined using quantitative real time (qRT)‐PCR and Western blot. Histopathology of mice was stained by haematoxylin and eosin staining. The levels of tumour necrosis factor‐α (TNF‐α) and interleukin (IL)‐1β were determined using ELISA. The expression of miR‐574 was positively correlated with cell viability in lipopolysaccharide (LPS)‐treated cells. Cell viability was improved and apoptosis was inhibited by mimics. Meanwhile, the levels of GRP78, CHOP and Caspase‐12 were suppressed by mimics and agomir in LPS‐treated human bronchial epithelial (HBE) cells and cecal ligation and puncture (CLP)‐treated mice. In vivo, lung tissue damages were ameliorated by agomir, which also decreased the levels of neutrophils, macrophages and albumin. C3 was a target gene of miR‐574 and could be decreased by mimics. SiC3 enhanced cell viability and inhibited apoptosis, however, it suppressed the mRNA levels of GRP78, CHOP and Caspase‐12. Up‐regulation of miR‐574 attenuated sepsis‐induced lung injury may be by promoting C3 down‐regulation and reducing sepsis‐induced endoplasmic reticulum stress (ERS).

中文翻译：

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microRNA-574的上调减弱了与急性肺损伤相关的脂多糖或盲肠的结扎和穿刺引起的败血症。

急性肺损伤（ALI）是脓毒症中最脆弱的器官，但是其潜在机制仍不清楚。通过细胞计数试剂盒8和流式细胞仪检测细胞活力和凋亡。使用定量实时（qRT）-PCR和Western blot检测miR-574，补体3（C3），葡萄糖调节蛋白78（GRP78），C / EBP同源蛋白（CHOP）和Caspase-12的表达。用苏木精和曙红染色将小鼠的组织病理学染色。使用ELISA测定肿瘤坏死因子-α（TNF-α）和白介素（IL）-1β的水平。在脂多糖（LPS）处理的细胞中，miR-574的表达与细胞活力呈正相关。模拟提高了细胞活力，并抑制了细胞凋亡。同时，GRP78的水平 在LPS处理的人支气管上皮（HBE）细胞和盲肠结扎穿刺（CLP）处理的小鼠中，CHOP和Caspase-12被模拟物和agomir抑制。在体内，agomir改善了肺组织损伤，这也降低了中性粒细胞，巨噬细胞和白蛋白的水平。C3是miR-574的靶基因，可以被模拟物降低。SiC3增强了细胞活力并抑制了细胞凋亡，但是它抑制了GRP78，CHOP和Caspase-12的mRNA水平。可能通过促进C3下调并减少败血症引起的内质网应激（ERS）来上调miR‐574败血症诱导的肺损伤。巨噬细胞和白蛋白。C3是miR-574的靶基因，可以被模拟物降低。SiC3增强了细胞活力并抑制了细胞凋亡，但是它抑制了GRP78，CHOP和Caspase-12的mRNA水平。可能通过促进C3下调并减少败血症引起的内质网应激（ERS）来上调miR‐574败血症诱导的肺损伤。巨噬细胞和白蛋白。C3是miR-574的靶基因，可以被模拟物降低。SiC3增强了细胞活力并抑制了细胞凋亡，但是它抑制了GRP78，CHOP和Caspase-12的mRNA水平。可能通过促进C3下调并减少败血症引起的内质网应激（ERS）来上调miR‐574败血症诱导的肺损伤。