Short Chain Fatty Acid Acetate Protects against Ethanol-Induced Acute Gastric Mucosal Lesion in Mice

Abstract

Short chain fatty acids acetate and propionate have been demonstrated protective function in the intestinal mucosa. However, their impact on gastric mucosa has not yet been elucidated. The current study aimed to investigate the potential protective effects of acetate and propionate against ethanol-induced gastric mucosal lesion and the underlying mechanism in mice. ICR mice were orally treated with acetate and propionate, respectively, 30 min prior to the establishment of gastric mucosal injury model by challenge with absolute ethanol. The gastric samples were collected for the detection of oxidative, inflammatory and apoptotic related parameters. Acetate, but not propionate, attenuated the severity of gastric mucosal damage as evidenced by the gross changes of gastric mucosa, pathological aberrations. Acetate alleviated oxidative stress as shown by the increase in glutathione (GSH) content and superoxide dismutase (SOD) activities, and the decrease of malondialdehyde (MDA) level. The elevated concentrations of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6, and the activation of nuclear factor-kappaB (NF-κB) p65 by ethanol stimulation was also reduced by acetate. Moreover, the anti-inflammatory factors, IL-4, LXA4 and IL-10, were up-regulated in acetate treated group. With respect to gastric mucosal apoptosis, acetate suppressed caspase-3 activity and BAX expression in favor of cell survival. These favorable actions were maybe associated with up-regulation of the gastric MUC5AC, the key defense factor of gastric mucosal system. These findings accentuate the gastroprotective actions of acetate in ethanol-induced gastric injury which were mediated via concerted multiprolonged actions, including suppression of gastric oxidation, inflammation and apoptosis and promotion of MUC5AC expression.

Proteobacteria Overgrowth and Butyrate-Producing Taxa Depletion in the Gut Microbiota of Glycogen Storage Disease Type 1 Patients

“…As well as acetate, propionate seems to exert protective and anti-inflammatory activities in IBD, ameliorating the intestinal mucosa lesion [45]. The higher propionate concentration is in agreement with the enrichment in Veillonellaceae family among GSD patients [46]; the genus Veillonella was found positively related to starch intake in patients, probably because of their peculiar diet.…”

Amelioration of Alcohol Induced Gastric Ulcers Through the Administration of Lactobacillus plantarum APSulloc 331261 Isolated From Green Tea

“…Overconsumption of alcohol is known to impair the gastric mucosal barrier causing extensive hemorrhagic injuries, accumulate oxidative stress and increase inflammation through the production of cytokines such as IL1β, IL6, and TNF-α (Liu et al, 2017). The excessive use of alcohol not only causes organ dysfunction and health problems, but also disrupts the stability of the intestinal microbiome, resulting in what is generally known as dysbiosis (Engen et al, 2015).…”

“…On the other hand, the treatment of probiotics induced a shift in the three phyla in the opposite direction (Bull-Otterson et al, 2013). Furthermore, beneficial effects through the direct consumption of SCFAs, known as microbial by-products, have previously been proved effective in alcohol induced murine models (Liu et al, 2016(Liu et al, , 2017. In pilot studies several attempts have been made for the direct delivery of SCFAs as postbiotic, either via enemas or orally through a pH-dependent slow release mechanism.…”

“…The short chain fatty acids, acetate, propionate and butyrate are produced by bacterial fermentation of indigestible carbohydrates within the gut (Morrison and Preston, 2016). Liu et al (2017) reported that although the administration of propionate did not show attenuation of gastric erosion in the alcohol induced model, it is widely known for its immunomodulatory effects in various gastrointestinal diseases, e.g. by inhibiting pro-inflammatory cytokines such as TNF-α, IL8 and IL6 in inflammatory bowel disease (Tedelind et al, 2007).…”

“…A recent publication also demonstrated the protective effect of acetate against ethanol-induced acute gastric ulcers through the regulation of inflammation in the gastric mucosa (Liu et al, 2017). Even when the efficacy of probiotics, butyrate-producing species and short chain fatty acids on gastric erosion has been reported (Wang et al, 2015;Liu et al, 2017), data obtained in studies on the relationship between these administrations and the modulation of the gut microbiota in alcohol erosion models need further critical assessment in support of a better understanding on protective processes.…”