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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.
Keywords: Sepsis-associated liver injury, liver injury, oxidative stress, reactive oxygen species
