Abstract

Sepsis is a systemic inflammatory response that caused by infection or trauma, often resulting in multiple organ dysfunction. Its mortality rate is relatively high, ranging between 54% and 68%, and ineffective treatment and poor prognosis pose significant challenges to healthcare in recent years. One of the main pathogeneses of sepsis-induced liver injury is oxidative stress (OS), which refers to a state where the antioxidant system cannot balance oxidative products, leading to the accumulation of excessive oxidative products in the body. When sepsis occurs, the amount of reactive oxygen species produced by the body increases far beyond the levels that can be scavenged by the antioxidant system, thus damaging liver cells and aggravating liver damage. This article introduces the oxidative/antioxidant system, oxidative stress-related pathways, and the molecular mechanism of OS in various types of hepatocytes, with emphasis on the antioxidant treatment on different hepatocytes, in order to understand the mechanism of OS involved in the development and progression of sepsis-associated liver injury. As the research deepens, improving liver function through the treatment of different cells and facilitating related clinical research are expected to provide a new target pathway for the treatment of sepsis-associated liver injury.

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