Krill oil prevents lipopolysaccharide-evoked acute liver injury in mice through inhibition of oxidative stress and inflammation.

Acute liver injury is a life-threatening syndrome that often results from the actions of viruses, drugs and toxins. Herein, the protective effect and potential mechanism of krill oil (KO), a novel natural product rich in long-chain n-3 polyunsaturated fatty acids bound to phospholipids and astaxanthin, on lipopolysaccharide (LPS)-evoked acute liver injury in mice were investigated. Male C57BL/6J mice were administered intragastrically with 400 mg kg KO or fish oil (FO) once per day for 28 consecutive days prior to LPS exposure (10 mg kg, intraperitoneally injected). The results revealed that KO pretreatment significantly ameliorated LPS-evoked hepatic dysfunction indicated by reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and attenuated hepatic histopathological damage. KO pretreatment also mitigated LPS-induced hepatic oxidative stress, as evidenced by decreased malondialdehyde (MDA) contents, elevated glutathione (GSH) levels, and elevated catalase (CAT) and superoxide dismutase (SOD) activities. Additionally, LPS-evoked overproduction of pro-inflammatory mediators in serum and the liver was inhibited by KO pretreatment. Furthermore, KO pretreatment suppressed LPS-induced activation of the hepatic toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/NOD-like receptor family pyrin domain containing 3 (NLRP3) signaling pathway. Interestingly, the hepatoprotective effect of KO was superior to that of FO. Collectively, the current findings suggest that KO protects against LPS-evoked acute liver injury inhibition of oxidative stress and inflammation.