脓毒症中胆汁淤积的分子发病机制。
The molecular pathogenesis of cholestasis in sepsis.
作者信息
Bhogal Harjit K, Sanyal Arun J
机构信息
Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University School of Medicine, Richmond, VA 23298-0341, USA.
出版信息
Front Biosci (Elite Ed). 2013 Jan 1;5(1):87-96. doi: 10.2741/e598.
Abstract
Sepsis-induced cholestasis is a complication of infection. Infections cause systemic and intrahepatic increase in proinflammatory cytokines which result in impaired bile flow ie. cholestasis. Several other mediators of impairment in bile flow have been identified under conditions of sepsis such as increased nitric oxide production and decreased aquaporin channels. The development of cholestasis may also further worsen inflammation. The molecular basis of normal bile flow and mechanisms of impairment in sepsis are discussed.
摘要
脓毒症诱导的胆汁淤积是一种感染并发症。感染导致全身和肝内促炎细胞因子增加，从而导致胆汁流动受损，即胆汁淤积。在脓毒症情况下，还发现了其他几种导致胆汁流动受损的介质，如一氧化氮生成增加和水通道蛋白通道减少。胆汁淤积的发展也可能进一步加重炎症。本文讨论了正常胆汁流动的分子基础以及脓毒症中胆汁流动受损的机制。
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