The gastroprotective effects of hydroalcoholic extract of Monolluma quadrangula against ethanol-induced gastric mucosal injuries in Sprague Dawley rats

Abstract

Monolluma quadrangula (Forssk.) Plowes is used in Saudi traditional medicines to treat gastric ulcers. The hydroalcoholic extract of M. quadrangula (MHAE) was used in an in vivo model to investigate its gastroprotective effects against ethanol-induced acute gastric lesions in rats. Five groups of Sprague Dawley rats were used. The first group was treated with 10% Tween 20 as a control. The other four groups included rats treated with absolute ethanol (5 mL/kg) to induce an ulcer, rats treated with 20 mg/kg omeprazole as a reference drug, and rats treated with 150 or 300 mg/kg MHAE. One hour later, the rats were administered absolute ethanol (5 mL/kg) orally. Animals fed with MHAE exhibited a significantly increased pH, gastric wall mucus, and flattening of the gastric mucosa, as well as a decreased area of gastric mucosal damage. Histology confirmed the results; extensive destruction of the gastric mucosa was observed in the ulcer control group, and the lesions penetrated deep into the gastric mucosa with leukocyte infiltration of the submucosal layer and edema. However, gastric protection was observed in the rats pre-fed with plant extracts. Periodic acid–Schiff staining of the gastric wall revealed a remarkably intensive uptake of magenta color in the experimental rats pretreated with MHAE compared to the ulcer control group. Immunohistochemistry staining revealed an upregulation of the Hsp70 protein and a downregulation of the Bax protein in rats pretreated with MHAE compared with the control rats. Gastric homogenate showed significantly increased catalase and superoxide dismutase, and the level of malondialdehyde (MDA) was reduced in the rats pretreated with MHAE compared to the control group. In conclusion, MHAE exhibited a gastroprotective effect against ethanol-induced gastric mucosal injury in rats. The mechanism of this gastroprotection included an increase in pH and gastric wall mucus, an increase in endogenous enzymes, and a decrease in the level of MDA. Furthermore, protection was given through the upregulation of Hsp70 and the downregulation of Bax proteins.

Anti-ulcerogenic effect of KFP-H008 against ethanol-induced gastric ulcerviap38 MAPK/NF-κB pathway

“…There are growing evidences that oxidative stress is an essential factor in the pathogenesis of gastrointestinal mucosal diseases, 20 and excessive generation of reactive oxygen species (ROS) poses a serious problem to bodily homeostasis and causes oxidative tissue damage. 21,22 The imbalance of ROS generation and the endogenous antioxidant defense system lead to oxidative stress.…”

The Gastroprotective Effect of Small Molecule Oligopeptides Isolated from Walnut (Juglans regia L.) against Ethanol-Induced Gastric Mucosal Injury in Rats

“…Gastric mucosal injury is a multifactorial pathological process that involved endogenous and exogenous factors, its basic pathophysiology mechanism includes imbalance between some pro-inflammation factors (including hydrochloric acid, pepsin, and reactive oxygen species) and defensive factors (such as mucus-bicarbonate barrier, mucosal blood flow, and some cytokines) [35][36][37][38]. Although the complex pathological mechanism of ethanol-induced gastric mucosal damage, the interaction of gastric acid and pepsin is still considered to be the major cause of gastric mucosal injury [39].…”

“…Therefore, increased activity of scavenging enzymes is an effective way to alleviate oxidative damage, which plays a major defensive role in the genesis of ethanol-induced gastric ulcers induced by ethanol [4,48,51]. Meanwhile, malondialdehyde (MDA) is the final production of lipid peroxidation and is a key marker to estimate indirectly the level of lipid peroxidation [5,35]. Our project outcomes indicated that administration with of 5 mL/kg absolute ethanol reduced the levels of SOD, CAT, and GSH, while it elevated the MDA levels in ethanol-administered rats.…”

Antioxidant and gastroprotective actions of butanol fraction ofZingiber officinaleagainst diclofenac sodium-induced gastric damage in rats

“…Many authors have reported that gastric ulcer induced by NSAID is accompanied by over production of ROS, which may lead to lipid peroxidation (Heeba, Hassan, & Amin, ). Lipid peroxidation is considered as a major cause of membrane damage and cell dysfunction (Cemek, Yilmaz, & Büyükokuroğlu, ; Rahim, Hassandarvish, Colbabapour, Tayyab, & Abdulla, ). Diclofenac sodium administration resulted in a significant increase in MDA level, whereas CAT activity and GSH content were markedly reduced in stomach tissue in comparison with the negative control rats.…”