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在低反应性脂多糖(LPS)的C3H/HeJ小鼠品系中,SPG/IND诱导的脓毒症休克。

SPG/IND-induced septic shock in a LPS-low responder strain, C3H/HeJ mice.

作者信息

Saito Maki, Nameda Sachiko, Miura Noriko N, Adachi Yoshiyuki, Ohno Naohito

机构信息

Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.

出版信息

Microb Pathog. 2008 May;44(5):402-9. doi: 10.1016/j.micpath.2007.11.003. Epub 2007 Nov 22.

Abstract

The administration of beta-glucan (sonifilan; SPG) in combination with a non-steroidal anti-inflammatory drug, indomethacin (IND), induced lethal septic shock in mice. To demonstrate the influence of bacterial lipopolysaccharide (LPS) in this lethal toxicity, LPS non-responder C3H/HeJ mice were used to compare features of sepsis and physicochemical parameters in the present study. The administration of SPG and IND induced the death of C3H/HeJ mice, lowering rectal temperature, reducing body weight, increasing serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, shortening the gastrointestinal tract, and increasing the GOT/GPT level. Microbial translocation to various organs was also significantly increased. These results strongly suggested that LPS-non-responding strain also induced septic shock in this experimental model, and other pathogen-associated molecular patterns (PAMPs) may significantly contribute to the septic shock.

摘要

将β-葡聚糖(小丝菌素;SPG)与非甾体抗炎药吲哚美辛(IND)联合使用会在小鼠中诱发致死性脓毒症休克。为了证明细菌脂多糖(LPS)对这种致死毒性的影响,在本研究中使用了LPS无反应性的C3H/HeJ小鼠来比较脓毒症的特征和理化参数。给予SPG和IND会导致C3H/HeJ小鼠死亡,降低直肠温度,减轻体重,增加血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平,缩短胃肠道,并增加谷草转氨酶/谷丙转氨酶水平。微生物向各个器官的易位也显著增加。这些结果强烈表明,LPS无反应性菌株在该实验模型中也会诱发脓毒症休克,并且其他病原体相关分子模式(PAMPs)可能对脓毒症休克有显著影响。

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