文章来源：中国知网

摘要信息：目的：探讨西维来司他钠对脂多糖(LPS)诱导的大鼠心肌细胞损伤的保护作用。方法：海南省人民医院于2021年7月—2022年2月采用LPS建立大鼠H9c2心肌细胞损伤模型，分为对照组、LPS组、西维来司他钠+LPS组。其中西维来司他钠+LPS组分为高浓度组(LPS+high，10 μg/mL)、中浓度组(LPS+medium，4.8 μg/mL)、低浓度组(LPS+low，1.6 μg/mL)。LPS诱导心肌细胞损伤6 h后，检测心肌细胞上清液中的白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、丙二醛(MDA)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的水平，对比各组上述因子水平的差异性。结果：与对照组比较，LPS组及低浓度组、中浓度组、高浓度组的IL-6、TNF-α、IL-1β、LDH水平均显著升高，SOD均下降，差异均有统计学意义(P<0.05)；与对照组比较，LPS组及低浓度组、中浓度组的MDA水平均显著升高(P<0.05)；与LPS组比较，低浓度组、中浓度组、高浓度组的IL-6、TNF-α、IL-1β、MDA、LDH均下降，SOD水平均升高，差异均有统计学意义(P<0.05)。结论：西维来司他钠可减少LPS诱导的心肌细胞炎症因子和氧化应激因子的产生，减轻心肌细胞损伤，从而起到保护心肌细胞的作用。

摘要信息：Background:Acute lung injury (ALI) is one of the most common critical illnesses in clinical practice, with sepsis being the most common cause of ALI. Sivelestat sodium (SV) hydrate is a highly effective inhibitor of neutrophil elastase, specifically targeting ALI related to systemic inflammatory response syndrome. The aim of this study is to examine the mechanisms by which SV can reduce the severity of ALI resulting from sepsis. Methods:Cecum ligation and puncture (CLP) was employed for creating an animal model of ALI caused by sepsis. Primary human pulmonary microvascular endothelial cells (HPMECs) were treated with lipopolysaccharide (LPS) to develop an in vitro model of infection-induced ALI. Lung tissue damage was assessed by employing hematoxylin-eosin (H&E) and Masson staining. Lung edema was determined by calculating the lung wet-to-dry weight ratio. Lung tissue and cell samples were analyzed using Enzyme-linked immunosorbent assay (ELISA) to detect levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. The 5-ethynyl-2'-deoxyuridine (EdU) and wound-healing assay were used to determine the cell proliferation and migration, while flow cytometry was used for detecting cell apoptosis. The association between microRNA (miR)-744 and transforming growth factor (TGF)-β1 was discovered and confirmed through the utilization of bioinformatics analyses and dual-luciferase gene reporter assay. The analysis of TGF-β1, p-Smad3, and Smad3 was carried out through western blotting and immunohistochemistry in both in vitro and in vivo scenarios. Results:In both in vivo and in vitro settings of ALI models of sepsis, there was a significant decrease in the level of miR-744-5p, a significant elevation in the expression of inflammatory factors, and a significant intensification of lung tissue damage. Administration of SV resulted in a significant increase in the level of miR-744-5p, suppressed the inflammatory response, and ultimately improved lung injury. Cell proliferation was significantly enhanced by SV and cell apoptosis was inhibited. The protection of SV was significantly reversed by inhibiting the effect of miR-744-5p. The double-luciferase reporter gene assay revealed substantial interactions occurring between miR-744-5p and TGF-β1. The TGF-β/Smad signaling pathway was significantly inhibited by SV, however, the inhibitory effect can be counteracted by utilizing the miR-744-5p inhibitor. Conclusions:The upregulation of miR-744-5p by SV inhibits the TGF-β/Smad signaling pathway, thereby reducing sepsis-induced ALI.

文章来源：免疫炎症事业部中央市场部

摘要信息：希为纳®️分科室拜访场景卡：综合、呼吸、急诊、心外、神外、胸外、肝外分科室拜访场景卡。

文章来源：免疫炎症事业部中央市场部

文章来源：免疫炎症事业部中央市场部

文章来源：免疫炎症事业部中央市场部

文章来源：免疫炎症事业部中央市场部

文章来源：免疫炎症事业部中央市场部

文章来源：免疫炎症事业部中央市场部