Abstract

Lactobacillus gasseri SBT2055 (LG2055) is one of the probiotic lactic acid bacteria. Recently, we demonstrated that feeding with LG2055 extended the lifespan of Caenorhabditis elegans and that the prolongevity effect was dependent upon the regulation of oxidative stress response. In this study, we assessed whether LG2055 regulated the oxidative stress response of mammalian cells. In NIH-3T3 cells and primary mouse embryonic fibroblast cells, low cell proliferation rates and high reactive oxygen species levels were observed following paraquat treatment. LG2055 treatment suppressed these responses in paraquat-treated cells, indicating that LG2055 protected against oxidative stress in mammalian cells. The mRNA expression of oxidative stress-related genes, total nuclear factor-erythroid-2-related factor 2 (Nrf2) protein levels, and the nuclear translocation of Nrf2 were increased by LG2055 treatment. These results suggested that the Nrf2-antioxidant response element (ARE) signaling pathway was activated by LG2055. Furthermore, c-Jun NH2-terminal kinase (JNK) was activated by LG2055 treatment and the inhibition of JNK suppressed the activation of the Nrf2-ARE signaling pathway in LG2055-treated cells. Together, these findings suggest that LG2055 activated the Nrf2-ARE signaling pathway by JNK activation, thus strengthening the defense system against oxidative stress in mammalian cells.

Highlights

  • The increase of oxidative stress is harmful for an organism and is related to various diseases such as Parkinson’s disease [1], Alzheimer’s disease [2], cancer [3], heart failure [4], and atherosclerosis [5, 6]

  • We exposed the cells to oxidative stress generated by paraquat, which is widely used as a generator of intracellular reactive oxygen species (ROS) [23]

  • This analysis showed that paraquat treatment increased the ROS accumulation in NIH-3T3 cells and that Lactobacillus gasseri SBT2055 (LG2055) treatment suppressed the accumulation induced by paraquat (Fig 1A)

Read more

Summary

Introduction

The increase of oxidative stress is harmful for an organism and is related to various diseases such as Parkinson’s disease [1], Alzheimer’s disease [2], cancer [3], heart failure [4], and atherosclerosis [5, 6]. During cellular response to oxidative stress, antioxidant enzymes or phase II metabolizing enzymes such as superoxide dismutase (SOD), catalase, heme oxygenase-1 (HO-1), and glutathione-S-transferases (GSTs) are induced to protect against the oxidative stress [7]. The genes for these enzymes contain antioxidant response elements (AREs) in their promoter regions. Nuclear factorerythroid-2-related factor 2 (Nrf2), a member of the NF-E2 family of basic leucine zipper

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call