Lactobacillus fermentum HFY06 attenuates D-galactose-induced oxidative stress and inflammation in male Kunming mice

• Published in: Food & function 2021-12, Vol.12 (24), p.12479-12489
• Main Authors: Li, Fang, Huang, Hui, Wu, Yangkun, Lu, Zhe, Zhou, Xianrong, Tan, Fang, Zhao, Xin
• Format: Article
• Language: English
• Subjects: Aging; Aging (artificial); Animals; Animals, Outbred Strains; Antioxidants; Antioxidants - metabolism; Antioxidants - pharmacology; Atrophy; Brain; D-Galactose; Degenerative diseases; Disease Models, Animal; Galactose; Galactose - metabolism; IL-1β; Inflammation; Inflammation - metabolism; Inflammation - prevention & control; Interleukin 6; Kidneys; Lactobacillus fermentum; Lactobacillus fermentum - metabolism; Liver; Male; Mice; Nitric-oxide synthase; Oxidative stress; Oxidative Stress - drug effects; Signal transduction; Spleen; Superoxide dismutase; Tumor necrosis factor-α; γ-Interferon
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/d1fo00982f

There has been considerable research on oxidative stress and inflammation, and their relationship with degenerative diseases. This study investigated the effect of HFY06 on aging mice induced by D-galactose. The results showed that HFY06 inhibited the atrophy of the brain, kidneys, liver, and spleen, increased serum SOD, GSH, CAT, and MDA, and decreased IL-6, IL-1β, TNF-α, and IFN-γ. Quantitative PCR showed that HFY06 upregulated the expression of Nrf2, γ-GCS, NOS1, NOS3, SOD1, SOD2, and CAT in the liver and brain tissues, but decreased the expression of NOS2. Western blot analysis showed that HFY06 effectively upregulated the protein expression of SOD1, SOD2, and CAT in the livers and brains of mice. These results suggest that HFY06 can effectively alleviate D-galactose-induced aging in mice, and may activate the Nrf2 signaling pathway and increase the levels of downstream regulatory inflammatory factors and antioxidant enzymes. In conclusion, consumption of HFY06 may prevent aging or reduce oxidative stress.