Polygonum hydropiper extract attenuates ethanol-induced gastric damage through antioxidant and anti-inflammatory pathways

Abstract

The present study was conducted to investigate the underlying mechanisms and effective components of Polygonum hydropiper in ethanol-induced acute gastric mucosal lesions. The ethanol extract was purified on an AB-8 macroporous resin column and eluted with 60% ethanol and was then injected into the HPLC system for quantitative analysis. Sprague-Dawley rats were orally pretreated with P. hydropiper extract (PHLE; 50, 100, and 200 mg/kg) for 5 days and then absolute ethanol was administered to induce gastric mucosal damage. One hour after ethanol ingestion, the rats were euthanized and stomach samples were collected for biochemical analysis. Antioxidant enzymes and anti-inflammatory cytokines were quantified. Western blotting was used to detect the expression levels of proteins. Cell proliferation was assayed by CCK-8 assays. The proportion of total flavonoids in the final extract of P. hydropiper was 50.05%, which contained three major bioactive flavonoid constituents, including rutin, quercitrin, and quercetin. PHLE significantly increased cell viability and effectively protected human gastric epithelial cells-1 against alcohol-induced damage in vitro. PHLE pretreatment attenuated gastric mucosal injuries in a dose-dependent manner in rats, and increased the activity of superoxide dismutase, glutathione peroxidase, and glutathione, and decreased the levels of malondialdehyde in gastric tissue. Pretreatment with PHLE also reduced the generation of the proinflammatory cytokines tumor necrosis factor-a and interleukin-1b in gastric tissue by downregulating the expression of nuclear factor-kappa B. PHLE exerted protective effects against gastric injury through antioxidant and anti-inflammatory pathways. Flavonoids might be the main effective components of P. hydropiper against gastric mucosal injury.

Mechanisms of Dendrobium officinale polysaccharides in repairing gastric mucosal injuries based on mitogen-activated protein kinases (MAPK) signaling pathway

“…Anhydrous ethanol (5 mL/kg) (Biyuntian, China) was given 1 h after the last administration to construct a gastric mucosal injury (gastric ulcer) model [ 13 ]. Another one hour later, all of the Sprague Dawley (SD) rats were sacrificed under anesthesia with excessive pentobarbital sodium (100 mg/kg) to collected the gastric tissue and serum [ 14 , 15 ].…”

“…The gastric tissue was initially fixed, cut open along the great curvature of the stomach, and spread for the determination of the gastric ulcer area and its inhibition rate. The calculation formula was as following: Inhibition rate of gastric ulcer = (Gastric ulcer area in the model rat group – Gastric ulcer area in the administration group)/Gastric ulcer area in the model rat group × 100% [ 15 , 16 ].…”

Profiling of secondary metabolites and DNA typing of three different Annona cultivars grown in Egypt

“…Gastro-duodenal ulcers are associated with marked alterations in multiple biochemical parameters (Esmaeilnejad et al, 2012 ).A substantial increase in MDA, SOD, CAT, NO, and GSH was observed in the current study. Gastric mucosal MDA levels in patients with peptic ulcer and gastritis are likely to indicate free radical-mediated gastric mucosal damage (Ren et al, 2021 ). Hydroxyl radicals oxidize essential cellular structural and functional proteins, as well as membrane lipids.…”

Gastric Mucosal Protective Effects of Cinnamomum cassia in a Rat Model of Ethanol-Induced Gastric Injury

“…Among these, ethanol is known to contribute to the severity of gastric mucosal injury by disrupting the mucosal integrity, gastric mucosal bleeding, and mucosal cell death [ 2 ]. Gastric mucosal damage induced by neutrophil infiltration into gastric tissues is closely associated with elevated levels of pro-inflammatory cytokines [ 3 ]. Oxidative stress plays a significant role in the pathogenesis of alcohol-induced gastritis [ 4 ].…”