Novel insights for systemic inflammation in sepsis and hemorrhage.
Novel insights for systemic inflammation in sepsis and hemorrhage.
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DOI：
10.1155/2010/642462
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发表时间：
2010
影响因子：
4.6
通讯作者：
Ulloa L
中科院分区：
文献类型：
--
作者：
Cai B;Deitch EA;Ulloa L
脓毒症和出血中的炎症反应仍然是死亡的主要原因。临床上普遍认为，脓毒症和出血性休克的发生机制不同。然而，炎症细胞因子作为一种常见的致死途径的认识已成为共识。促炎细胞因子如肿瘤坏死因子（TNF）或高迁移率族蛋白1（HMGB1）被狂热地释放，并导致致命的多器官功能障碍。抑制这些细胞因子可以防止炎症反应和器官损伤。在寻求潜在的抗炎策略中，我们报道了丙酮酸乙酯和α 7烟碱乙酰胆碱受体（α 7 nAChR）激动剂有效抑制细胞因子的产生，从而在实验性脓毒症和出血中提供治疗益处。在这里，我们回顾了脓毒症和出血实验模型中的炎症反应和抗炎策略，因为尽管它们的病理生理过程不同，但它们可能具有一致的炎症途径。
The inflammatory responses in sepsis and hemorrhage remain a major cause of death. Clinically, it is generally accepted that shock in sepsis or hemorrhage differs in its mechanisms. However, the recognition of inflammatory cytokines as a common lethal pathway has become consent. Proinflammatory cytokines such as tumor necrosis factor (TNF) or high-mobility group box1 (HMGB1) are fanatically released and cause lethal multiorgan dysfunction. Inhibition of these cytokines can prevent the inflammatory responses and organ damage. In seeking potential anti-inflammatory strategies, we reported that ethyl pyruvate and alpha7 nicotinic acetylcholine receptor (alpha7nAChR) agonists effectively restrained cytokine production to provide therapeutic benefits in both experimental sepsis and hemorrhage. Here, we review the inflammatory responses and the anti-inflammatory strategies in experimental models of sepsis and hemorrhage, as they may have a consistent inflammatory pathway in spite of their different pathophysiological processes.
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影响因子：
5.3
作者：
Cai B;Chen F;Ji Y;Kiss L;de Jonge WJ;Conejero-Goldberg C;Szabo C;Deitch EA;Ulloa L
通讯作者：
Ulloa L
影响因子：
8.8
作者：
Abraham, E;Matthay, MA;Repine, JE
通讯作者：
Repine, JE
影响因子：
8.8
作者：
Claridge, JA;Schulman, AM;Young, JS
通讯作者：
Young, JS
影响因子：
20.1
作者：
Bowden, RA;Ding, ZM;Burns, AR
通讯作者：
Burns, AR
影响因子：
4.4
作者：
Huber-Lang, M;Sarma, VJ;Ward, PA
通讯作者：
Ward, PA