Effect of heat-killed Enterococcus faecalis EF-2001 on ethanol-induced acute gastric injury in mice: Protective effect of EF-2001 on acute gastric ulcer.
D-B JeonH-G ShinB-W LeeS-H JeongJ-H KimJ-H HaJ-Y ParkH-J KwonW-J KimY-B RyuIn-Chul LeePublished in: Human & experimental toxicology (2020)
Enterococcus faecalis is a facultative anaerobic gram-positive commensal bacterium common in the gastrointestinal tract of animals and humans. This study aimed to investigate the protective effects of heat-killed E. faecalis EF-2001 (EF-2001) on acute gastric ulcer using a murine model of ethanol (EtOH)-induced acute gastric injury. EF-2001 (20, 40, and 80 mg/kg/day) was administered by oral gavage for 5 days before EtOH treatment (10 mL/kg body weight). EF-2001 effectively attenuated EtOH-induced gastric mucosal injury with reduced gastric mucosal ulcer and histological damage score. Pretreatment of EF-2001 markedly suppressed the phosphorylation of mitogen-activated protein kinases (MAPKs; ERK1/2, JNK, and p38MAPK). In addition, EF-2001 significantly inhibited phosphorylation of nuclear factor kappa B (NF-κB) and subsequently suppressed the upregulation of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 in gastric tissues. Taken together, these results suggest that EF-2001 exerts a gastroprotective effect against acute gastric injury, and the underlying mechanism might be associated with the suppression of MAPKs and NF-κB signaling and consequent reduction of pro-inflammatory mediators or cytokines.
Keyphrases
- nuclear factor
- signaling pathway
- liver failure
- nitric oxide synthase
- body weight
- cell proliferation
- oxidative stress
- drug induced
- microbial community
- rheumatoid arthritis
- hepatitis b virus
- lps induced
- type diabetes
- metabolic syndrome
- adipose tissue
- acute respiratory distress syndrome
- endothelial cells
- insulin resistance
- inflammatory response
- aortic dissection
- high glucose
- stress induced