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胃饥饿素在脓毒症中的抑制作用机制。

Mechanism of the inhibitory effect of ghrelin in sepsis.

作者信息

Jacob Asha, Wu Rongqian, Zhou Mian, Coppa Gene F, Wang Ping

机构信息

Department of Surgery, North Shore University Hospital and Long Island Jewish Medical Center, and The Feinstein Institute for Medical Research, Manhasset, NY, USA.

出版信息

Hepat Med. 2010 Feb 23;2:33-8. doi: 10.2147/hmer.s7187.

Abstract

Sepsis and septic shock are the leading causes of death in intensive care units. Approximately 40%-70% of the mortality is associated with severe sepsis and septic shock. Systemic antibiotic usage, surgical intervention, aggressive fluid resuscitation and careful monitoring are common measures currently used to treat sepsis. Despite the advances in the understanding of the pathophysiology of sepsis, very little progress has been made towards therapeutic interventions. Recently we have shown that ghrelin, a stomach-derived peptide which is an endogenous ligand for the growth hormone secretagogue receptor (GHSR-1a), is beneficial in attenuating the inflammatory response, organ injury and mortality in an experimental model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). In this review, we describe the mechanism of action of ghrelin in sepsis, highlight the role ghrelin plays in attenuating the hepatic dysfunction induced by sepsis and septic shock and suggest in developing ghrelin as a potential therapy for sepsis.

摘要

脓毒症和脓毒性休克是重症监护病房患者死亡的主要原因。约40%-70%的死亡率与严重脓毒症和脓毒性休克相关。全身使用抗生素、手术干预、积极的液体复苏以及密切监测是目前治疗脓毒症常用的措施。尽管在脓毒症病理生理学的理解方面取得了进展,但在治疗干预方面进展甚微。最近我们发现,胃源肽ghrelin是生长激素促分泌素受体(GHSR-1a)的内源性配体,在盲肠结扎穿孔(CLP)诱导的多微生物脓毒症实验模型中,对减轻炎症反应、器官损伤和死亡率有益。在这篇综述中,我们描述了ghrelin在脓毒症中的作用机制,强调了ghrelin在减轻脓毒症和脓毒性休克所致肝功能障碍中的作用,并建议将ghrelin开发为脓毒症的潜在治疗方法。

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