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Remifentanil attenuated LPS-induced hepatic injury, and this effect was found to be associated with modulation of oxidative stress responses, inflammatory alterations, and necroptosis-related gene expression.
It is suggested that DEX attenuates HFCS-induced liver injury through a multi-target mechanism involving suppression of oxidative damage, apoptosis, and inflammasome-associated pyroptotic signaling in young adult rats.
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