Bifidobacterium animalis A12 and Lactobacillus salivarius M18-6 Alleviate Alcohol Injury by keap1-Nrf2 Pathway and Thioredoxin System.

Excessive drinking can significantly damage people's health and well-being. Although some lactic acid bacterial strains have been previously shown to alleviate the symptoms of alcohol injury, the mechanism underlying these effects remains unclear. The aim of this study was to establish an alcohol injury model and examine the protective effect and mechanism of B. animalis A12 and L. salivarius M18-6. The results showed that A12 freeze-dried powder could maintain the survival rate of mice with alcohol injury at 100%. Compared with Alco group, L. salivarius M18-6 dead cell improved the survival rate of mice, attenuated liver steatosis, and significantly down-regulated serum Alanine transaminase (ALT) level; at the same time, it activated keap1-Nrf2 signaling pathway and up-regulated Superoxide dismutase (SOD), it protects mouse liver cells from oxidative stress induced by alcohol injury. In addition, B. animalis A12 can reduce the stress response to short-term alcohol intake and improve the ability of anti-oxidative stress by upregulating the level of isobutyric acid, reducing the level of keap1 protein in the liver of mice and upregulating the expression of thioredoxin genes (Txnrd1, Txnrd3, Txn1). Taken together, the results showed that B. animalis A12 and L. salivarius M18-6 alleviate alcohol injury in mice through keap1-Nrf2 signaling pathway and thioredoxin system.

Both live and heat-killed Bifidobacterium animalis J-12 alleviated oral ulcers in LVG golden Syrian hamsters by gavage by directly intervening in the intestinal flora structure.

Live and heat-killed Bifidobacterium has been proven to have anti-inflammatory and antioxidant effects. In this study, we evaluated the effects of live and heat-killed Bifidobacterium animalis J-12 (J-12) on the oral ulceration of LVG golden Syrian hamsters after buccal membrane injection with methyl viologen dichloride. Results showed that interleukin-1ß, glutathione, and malondialdehyde in serum were downregulated by the gavage of live and heat-killed J-12 bacteria. The J-12 live and heat-killed bacteria can reduce the expression of matrix metalloproteinase-9 by reducing the expression of nuclear factor kappa-B, thus reducing the expression of anti-inflammatory factors lipoxin A4 and prostaglandin E2. Reducing the expression of caspase-3 and adenosine diphosphate ribose polymerase resulted in a reduction of ulcer tissue DNA damage. In addition, regulating the structure of the intestinal flora prevented the process of oral ulcer formation. This study shows that J-12 can reduce the risk of oral ulcer formation while also having a positive effect on inhibiting existing oral ulcer growth.

Bifidobacterium animalis A12, a Probiotic Strain That Promotes Glucose and Lipid Metabolism, Improved the Texture and Aroma of the Fermented Sausage.

Bifidobacterium animalis A12 was used for the development of fermented sausage. The growth activity, tolerance, and enzyme activity of B. animalis A12 and its contribution to the texture and flavour of fermented sausages were evaluated. Additionally, the sensory texture, flavour components, and amino acid nutrients during the fermentation process were assessed. B. animalis had high tolerance to NaCl and nitrite, and B. animalis A12 had protease and lipase activities. The pH value of sausage fermented with B. animalis A12 was lower than that of sausage fermented without any fermentation strain. Hexanal, heptanal, decanal, cis-2-decanal, and 4-methoxy-benzaldehyde are the unique aldehydes flavour components of fermented sausages in the A12 group. The highest content of volatile flavour substances and amino acids, and the color and texture characteristics of fermented sausage in the experimental group at 18 h were better than those at other times. These results suggest that B. animalis A12 has the potential to be used as a starter culture for im-proving flavour and texture in fermented sausage.