ABSTRACT
Acute lung injury (ALI) is an adverse disease of the respiratory system, and one of its prevalent causes is sepsis induction. Cell pyroptosis facilitates the progression of ALI and lncRNAs play critical roles in ALI. Thus, this research seeks to investigate the specific mechanism of NEAT1 in sepsis-ALI.BEAS-2B cells were exposed to lipopolysaccharide (LPS) to construct a cell model of sepsis-induced ALI. The gene and protein expression were assessed using qRT-PCR and western blot. Cell viability was identified by CCK-8. Cell death was discovered using PI staining. The secretion of IL-1ß and IL-18 was examined using ELISA. The interconnections among NEAT1, miR-26a-5p, and ROCK1 were confirmed using starbase, luciferase assay, and RIP.LPS treatment augmented NEAT1 and ROCK1 levels while mitigating miR-26a-5p level in BEAS-2B cells. Additionally, LPS treatment facilitated cell death and cell pyroptosis, whereas NEAT1 silencing could reverse these effects in BEAS-2B cells. Mechanistically, NEAT1 positively mediated ROCK1 expression by targeting miR-26a-5p. Furthermore, miR-26a-5p inhibitor offset NEAT1 depletion-mediated suppressive effects on cell death and cell pyroptosis. ROCK1 upregulation decreased the inhibitory impacts produced by miR-26a-5p overexpression on cell death and cell pyroptosis. Our outcomes demonstrated NEAT1 could reinforce LPS-induced cell death and cell pyroptosis by repressing the miR-26a-5p/ROCK1 axis, thereby worsening ALI caused by sepsis. Our data indicated NEAT1, miR-26a-5p, and ROCK1 might be biomarkers and target genes for relieving sepsis-induced ALI.
Subject(s)
Acute Lung Injury , MicroRNAs , RNA, Long Noncoding , Sepsis , Humans , MicroRNAs/metabolism , Lipopolysaccharides/toxicity , RNA, Long Noncoding/physiology , Pyroptosis/genetics , Sepsis/genetics , Sepsis/complications , Apoptosis , rho-Associated Kinases/genetics , rho-Associated Kinases/metabolismABSTRACT
Simple procedures for extraction and chromatographic determination of dimethachlon residues in fresh tobacco leaves and cut-tobacco are described. The determination was carried out by capillary gas chromatography (GC) with electron capture detection (ECD) and confirmed by GC-MS. The mean recoveries and relative standard deviation (RSD) were 93.2%~112.9% and 3.5%~6.7%, respectively at levels ranging from 0.01 to 0.1 mg/kg. The limit of determination was 0.001 mg/kg. Tobacco samples in routine check were successfully analyzed using the proposed method.
