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IL-6-mediated activation of STAT3a prevents trauma/hemorrhagic shock-induced liver inflammation

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We used microarrays to detail the global gene expression in response to T/HS and the effect of IL-6 on this model with and without pharmacologic blockade of Stat3-mediated IL-6 and identified distinct members of the inflammasome de-regulated during T/HS that normalized with IL-6 administration during resuscitation.

我们利用基因微阵列(microarrays)技术,详细表征了T/HS应答过程中的全基因表达谱,以及白细胞介素6(IL-6)在存在或不存在信号转导与转录激活因子3(Stat3)介导的IL-6药理学阻断的该模型中的调控作用;同时鉴定出T/HS期间发生失调的炎性体(inflammasome)不同成员,上述失调的炎性体成员在复苏阶段给予IL-6干预后可恢复至正常水平。

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