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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Two indole-2-carboxamide derivatives attenuate lipopolysaccharide-induced acute lung injury by inhibiting inflammatory response
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Two indole-2-carboxamide derivatives attenuate lipopolysaccharide-induced acute lung injury by inhibiting inflammatory response

机译:两种吲哚-2-甲酰胺衍生物通过抑制炎症反应来减弱脂多糖诱导的急性肺损伤

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摘要

Acute lung injury (ALI) is the leading cause of mortality in the intensive care unit. Currently, there is no effective pharmacological treatment for ALI. In our previous study, we reported that Lg25 and Lg26, two indole-2-carboxamide derivatives, inhibited the lipopolysaccharide (LPS)-induced inflammatory cytokines in vitro and attenuated LPS-induced sepsis in vivo. In the present study, we confirmed data from previous studies that LPS significantly induced pulmonary edema and pathological changes in lung tissue, increased protein concentration and number of inflammatory cells in bronchoalveolar lavage fluids (BALF), and increased inflammatory cytokine TNF-alpha expression in serum and BALF, pro-inflammatory genes expression, and macrophages infiltration in lung tissue. However, pretreatment with Lg25 and Lg26 significantly attenuated the LPS-induced changes in mice. Taken together, these data indicate that the newly discovered indole-2-carboxamide derivatives could be particularly useful in the treatment of inflammatory diseases such as ALI.
机译:急性肺损伤(ALI)是重症监护病房中死亡率的主要原因。目前,Ali没有有效的药理学治疗。在我们以前的研究中,我们报道了LG25和LG26,两个吲哚-2-甲酰胺衍生物,抑制脂多糖(LPS)诱导的炎症细胞因子在体外和减毒的LPS诱导的败血症。在本研究中,我们确认了先前研究的数据,即LPS显着诱导肺组织中的病理变化,血清血管灌洗液(BALF)中增加蛋白质浓度和炎性细胞数量,以及血清中的炎症细胞因子TNF-α表达增加和Balf,促炎基因表达,肺组织中的巨噬细胞浸润。然而,用LG25和LG26预处理显着减弱了小鼠的LPS诱导的变化。总之,这些数据表明新发现的吲哚-2-甲酰胺衍生物可特别有用于治疗炎性疾病,例如Ali。

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