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Abstract

The pathogenesis and progression of liver disease are associated with free radical injury and oxidative stress, which can be partially attenuated by antioxidants and free radical scavengers. Lactic acid bacteria, which have been traditionally used in the production of various fermented foods, are important intestinal microflora and natural antioxidants. The hypothesis that lactic acid bacteria can prevent or decrease tert-butyl hydroperoxide (r-BHP)-induced oxidative damage in HepG2 cells was investigated. Intracellular extracts and heat-killed cells of Lactobacillus acidophilus La12, Lactobacillus delbrueckii ssp. bulgaricus Lb23, Bifidobacterium longum Bl36 and Streptococcus salivarius ssp. thermophilus St28 were used in this study. Lactate dehydrogenase (LDH), alanine aminotransferase (ALT), reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GRd), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were determined to explore the influence of lactic acid bacteria intervention on cell damage and antioxidative status. Toxic damage to hepatocytes by t-BHP was attenuated by lactic acid bacteria (which exerted protective effects by decreasing the risk of accumulated ROS and by reactivating antioxidant enzymes) in HepG2 cells treated with lactic acid bacteria before t-BHP exposure. The results of this study provide new insights into the mechanisms by which lactic acid bacteria with antioxidative properties can help to protect the liver.

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