...
首页> 外文期刊>Chemico-biological interactions >delta-Amyrone inhibits lipopolysaccharide-induced inflammatory cytokines and protects against endotoxic shock in mice
【24h】

delta-Amyrone inhibits lipopolysaccharide-induced inflammatory cytokines and protects against endotoxic shock in mice

机译:δ-淀粉糊精抑制脂多糖诱导的炎症细胞因子并保护小鼠免受内毒素性休克

获取原文
获取原文并翻译 | 示例
           

摘要

delta-Amyrone (13(18)-Oleanen-3-one), which is an active constituent extracted and separated from Sedum lineare Thunb., has been found to possess a potent anti-inflammatory effect in different inflammation model animals. But its effects on lipopolysaccharide (LPS)-induced endotoxic shock have not been previous explored. The aim of this study is to evaluate the effect of delta-Amyrone on LPS-induced inflammatory cytokines and the protective effect on endotoxic shock mice. Experimental animals received delta-amyrone (4 and 8 mg/kg, i.p.) and dexamethasone (DEX) (5 mg/kg, i.p.) at 24 and 1 h before LPS injection. delta-Amyrone treatment significantly decreased mortality rate, tissues myeloperoxodase (MPO) activity, p65 NF-kappa B protein expression when compared with the LPS groups. The levels of tumor nectosis factor-alphagene (TNF-alpha) and interleukin-6 (IL-6) both in serum and lung, liver, kidney tissues, as well as the accumulation of nitric oxide (NO) in serum were decreased by delta-amyrone in response to p65 nuclear factors-kappa B (NF-kappa B). These results suggest that the protective activity of delta-amyrone on LPS-induced endotoxic shock is attributed to reducing NO production and mediating the pro-inflammatory cytokines, inhibited NF-kappa B expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
机译:从线性景天属中提取并分离出的活性成分δ-淀粉糊精(13(18)-Oleanen-3-one)已发现在不同的炎症模型动物中具有有效的抗炎作用。但是其对脂多糖(LPS)诱导的内毒素休克的影响尚未进行过探索。这项研究的目的是评估δ-淀粉糊精对LPS诱导的炎症细胞因子的影响以及对内毒素休克小鼠的保护作用。实验动物在注射LPS之前的24和1小时接受了δ-蒽醌(4和8 mg / kg,腹腔注射)和地塞米松(DEX)(5 mg / kg,腹膜内注射)。与LPS组相比,δ-淀粉糊精治疗可显着降低死亡率,组织髓过氧化物酶(MPO)活性,p65NF-κB蛋白表达。血清和肺,肝,肾组织中的肿瘤Nectα-α基因(TNF-α)和白介素-6(IL-6)的水平以及血清中一氧化氮(NO)的积累均降低了δ -对p65核因子-κB(NF-kappa B)有反应的戊二酮。这些结果表明,δ-蒽环酮对LPS诱导的内毒素休克的保护活性归因于减少NO的产生和介导促炎性细胞因子,抑制NF-κB的表达。 (C)2015 Elsevier Ireland Ltd.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号