The research aims to explore the roles and underlying mechanisms of microRNA-21 (miR-21) in lipopolysaccharide (LPS)-induced inflammation in MH7A cells. Cells were treated with LPS and/or transfected with miR-21 mimic/inhibitor or pc-sucrose nonfermentable 5 (SNF5). Cell viability was detected by CCK-8. ELISA and western blot were respectively conducted to measure the protein levels of pro-inflammatory factors, NF-κB or PTEN/PI3K/AKT key proteins and SNF5. miR-21/U6 was measured by qRT-PCR. The association between miR-21 and SNF5 was determined by luciferase reporter assay. Cell viability and the protein expression levels of interleukin-1β (IL-1β), IL-6, and p/t-p65, p/t-IκBα, p/t-PI3K, and p/t-AKT were significantly elevated by LPS, but with an inhibition of p-PTEN. Besides, LPS upregulated miR-21, whose overproduction or silence enhanced or alleviated the LPS stimulation on those elements above, respectively. miR-21 mimic notably inhibited SNF5, which was accelerated by miR-21 inhibitor, and abundant SNF5 abolished the effect of miR-21 mimic on cell viability, pro-inflammatory mediators, and sensitivity of signaling pathways, representing a negative relationship between them. miR-21 augmented LPS-induced inflammation response through activating NF-κB and PTEN/PI3K/AKT pathways by silencing SNF5 in MH7A cell line.

中文翻译：

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microRNA-21通过靶向SNF5加剧MH7A细胞中脂多糖诱导的炎症。

该研究旨在探讨microRNA-21（miR-21）在脂多糖（LPS）诱导的MH7A细胞炎症中的作用和潜在机制。用LPS处理细胞和/或用miR-21模拟物/抑制剂或pc-蔗糖不可发酵的5（SNF5）转染细胞。通过CCK-8检测细胞活力。分别进行ELISA和Western blot检测促炎因子，NF-κB或PTEN / PI3K / AKT关键蛋白和SNF5的蛋白水平。通过qRT-PCR测量miR-21 / U6。miR-21和SNF5之间的关联是通过萤光素酶报告基因测定来确定的。白细胞介素-1β（IL-1β），IL-6和p / t-p65，p /t-IκBα，p / t-PI3K和p / t-AKT的细胞活力和蛋白质表达水平显着提高LPS，但具有对p-PTEN的抑制作用。此外，LPS上调了miR-21，其过度生产或沉默分别增强或减轻了上述元素对LPS的刺激。miR-21模拟物显着抑制了SNF5，后者被miR-21抑制剂加速了，大量的SNF5消除了miR-21模拟物对细胞生存力，促炎介质和信号传导途径敏感性的影响，代表它们之间的负相关关系。miR-21通过使MH7A细胞系中的SNF5沉默来激活NF-κB和PTEN / PI3K / AKT途径，从而增强LPS诱导的炎症反应。代表他们之间的消极关系。miR-21通过使MH7A细胞系中的SNF5沉默来激活NF-κB和PTEN / PI3K / AKT途径，从而增强LPS诱导的炎症反应。代表他们之间的消极关系。miR-21通过使MH7A细胞系中的SNF5沉默来激活NF-κB和PTEN / PI3K / AKT途径，从而增强LPS诱导的炎症反应。