Locusta migratoria hydrolysates attenuate lipopolysaccharide (LPS)/D-Galactosamine (D-Gal)-induced cytotoxicity and inflammation in Hep G2 cells via NF-κB signaling suppression

The prolonged state of hepatic inflammation can lead to liver damage, a critical driving force in the progression of liver-related diseases. Locusta migratoria (LM), an edible insect, is recognized for its protein richness and potential to produce a range of bioactive polypeptides, presenting a novel solution for liver disease. This study investigated the hepatoprotective effects of LM hydrolysates in human hepatoma G2 (Hep G2) cells challenged with lipopolysaccharide (LPS)/D-Galactosamine (D-Gal), a model of liver injury. Remarkably, LM hydrolysates significantly ameliorated cell damage, as evidenced by the inhibition of the LPS/D-Gal-induced decrease in cell viability and reduction in lactate dehydrogenase (LDH) release. Furthermore, LM hydrolysates alleviated the release of aspartate aminotransferase (AST) from cells exposed to LPS/D-Gal and lowered the secretion of inflammatory cytokines while suppressing the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), a key pathway in inflammation. In particular, LM-N hydrolysate mitigated hepatotoxicity by attenuation of inflammatory responses to reduce interleukin 6 (IL-6) levels, and NF-κB nuclear translocation. These findings suggest that LM hydrolysates could potentially offer hepatoprotective effects by mitigating the inflammatory responses induced by LPS/D-Gal.