Abstract

Oxidative stress (OS) is a phenomenon induced by excessive production and accumulation of reactive oxygen species (ROS) in living cells. These increased ROS productions connected, coupled with many neurological and physiological diseases. Several antioxidants were utilized recently to combat OS, and lactic acid bacteria have a potent radical-scavenging activity to minimize OS. The present work was designed to find out the protective effects of Lactobacillus brevis MG000874 (L. brevis MG000874) against oxidative injuries induced by D-galactose (D-gal) in vivo and to explore the gene expression of OS-related gene mice. Sixty male mice were randomly split into six groups. The first four groups were different control groups as no treatment (N), positive (G), probiotic (B), and ascorbic acid (A); the remaining two groups were treatment groups such as probiotic treatment (BG) and ascorbic acid treatment (AG). L. brevis MG000874 (0.2ml of 1010CFU/ml) and ascorbic acid (0.2ml of 25mg/ml) were administered orally daily for 5weeks. It was revealed that these significantly affect the weight of treated mice: 40.22 ± 1.5 and 33.0 ± 0.57g on days 0 and 36, respectively. D-gal induction in mice declined the levels of SOD and CAT determined by spectrophotometer. Administration of L. brevis MG000874 improved the antioxidant status of the stress mice and recovered the antioxidant activities of SOD and CAT enzymes. In addition, L. brevis MG000874-altered gene expression of OS marker at the messenger RNA (mRNA) levels was determined by RT-PCR in the mouse model. L. brevis MG000874 significantly improved the GST, GPX, SOD, CAT, and ß-actin levels in the kidney and the liver of the D-gal-induced mice (p < 0.05). Moreover, the histological investigation indicated that L. brevis MG000874 mitigated damage to the kidney and liver effectively in mice induced by D-gal. Therefore, it could be concluded from the current results that L. brevis MG000874 may act as a powerful antioxidant agent, and this study can provide the baseline data for drug development against OS-linked diseases.

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