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

Abstract

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.

Rutaecarpine Ameliorates Ethanol-Induced Gastric Mucosal Injury in Mice by Modulating Genes Related to Inflammation, Oxidative Stress and Apoptosis

“…Mucosal damage may occur when the toxic factors such as gastric acid, pepsin, bile acid, ethanol, Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) invade and exceed the defense function load of gastric mucosa (Guth et al, 1979;Lee et al, 2017;Khan et al, 2018). Some other factors, such as inadequate dietary habits, excessive ethanol consumption, cigarette smoking, stress and hereditary predisposition, also may lead to the development of GU (Søreide et al, 2015;Jeon et al, 2020). Yet, the clinical treatment for the disease focuses on the use of antisecretory drugs such as H2 receptor antagonist (cimetidine) or proton pump inhibitors (omeprazole), antibiotics (clarithromycin), antacids (aluminum hydroxide), prostaglandin analogues and mucosal protective agents (bismuth) currently (Wallace, 2008).…”

Heat-Killed Enterococcus faecalis EF-2001 Attenuate Lipid Accumulation in Diet-Induced Obese (DIO) Mice by Activating AMPK Signaling in Liver

“…Therefore, each mouse is best given 307.5 mg/kg/day probiotics. With reference to previous animal experiments [ 16 , 17 , 18 ], we reduced the dose to 200 mg/kg/day. In the same way, the dose of orlistat in mice was calculated to be 60 mg/kg/day.…”

“…A probiotic strain of E. faecalis EF-2001 was isolated from healthy human feces and characterized. It has been reported that EF-2001 possesses radioprotective, antitumor, anti-chronic enteritis, and anti-atopic dermatitis properties [ 15 , 16 , 17 , 18 ]. In this way, EF-2001 can be used without the risk of infection or antibiotic resistance.…”

Characteristics of Lactococcus petauri GB97 lysate isolated from porcine feces and its in vitro and in vivo effects on inflammation, intestinal barrier function, and gut microbiota composition in mice

“…Heat-killed probiotics, such as Enterococcus faecalis , and fractionated cell components, such as cell wall preparations from Lactobacillus spp. and lysate from L. plantarum or L. casei , enhance host resistance and stimulate innate immune responses ( 15 – 18 ).…”