Abstract
Gastric ulcers are among the most broadly perceived illnesses affecting individuals. Alcohol consumption is the main cause of gastric ulceration. This study assessed the protective effects of Salvadora persica (SP) extract against ethanol-induced gastric ulcer and elucidated the conceivable underlying mechanisms involved. For this purpose, 40 rats were allotted into 4 equal groups (control, ethanol- (EtOH-) treated, and SP-treated “SP200 and SP400” groups). The control and EtOH-treated groups were given phosphate buffer saline (PBS), and both the SP200 and SP400 groups were given SP extract dissolved in PBS at doses of 200 and 400 mg/kg b.w., respectively. All treatments were given orally for 7 constitutive days. On the 8th day, all rats were fasted for 24 h followed by oral gavage of PBS in the control group and chilled absolute ethanol solution (5 ml/kg b.w.) in the EtOH- and SP-treated groups to induce gastric lesions. One hour later, the rats were sacrificed and the stomachs were harvested. Gross and microscopic examinations of the EtOH-treated group showed severe gastric hemorrhagic necrosis, submucosal edema, destruction of epithelial cells, and reduced glycoprotein content at the mucus surface. These pathological lesions were defeated by SP extract treatment. Administration of SP extract modulated the oxidative stress and augmented the antioxidant defenses. The elevated ethanol-expressed tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) genes, as well as bcl-2-like protein 4 (Bax) and inducible nitric oxide synthase (iNOS), were diminished in the SP-treated group. Curiously, SP extract upregulated endothelial nitric oxide synthase (eNOS) and transforming growth factor-β1 (TGF-β1) gene expression comparable to that of the EtOH-treated rats. Aggregately, SP exerted antiulcer activities in ethanol-induced gastric ulcer rat models via modulation of oxidant/antioxidant status, mitigation of proinflammatory cytokines, and apoptosis, as well as remodeling of both NOS isoforms.
Highlights
Gastric ulceration mainly occurs as a result of disharmony between 5 inverse factors at the gastric mucosa [1]
The oxidative stress that leads to the production of reactive oxygen species (ROS) along with the decline in antioxidative enzymes at the gastric mucosa induced by ethanol ingestion is implicated in the pathogenesis of ethanol-induced gastric ulceration [5]
One of them is the endothelial nitric oxide synthase that produces NO to assist gastric ulcer healing mainly through stimulation of blood vessels’ formation, increasing blood flow, and anti-inflammatory action [11], while NO generated from inducible nitric oxide synthase functions in gastric ulcer induction via the formation of ROS and toxic effects on cells [12]
Summary
Gastric ulceration mainly occurs as a result of disharmony between 5 inverse factors at the gastric mucosa [1]. Nonsteroidal anti-inflammatory drugs, smoking, stress, and Helicobacter pylori [2]. This is in contrast to the gastroprotective factors that are attributed to adequate secretion of mucus and prostaglandins, maintenance of anti-inflammatory and antioxidative agents, and normal mucosal blood flow [3]. Alcohol-induced gastric damage has been mediated through hypersecretion of gastric acid [8], proinflammatory cytokines and ROS generation [9], apoptosis induction, and depletion of nitric oxide (NO) and prostaglandin E2 [10]. One of them is the endothelial nitric oxide synthase (eNOS) that produces NO to assist gastric ulcer healing mainly through stimulation of blood vessels’ formation, increasing blood flow, and anti-inflammatory action [11], while NO generated from inducible nitric oxide synthase (iNOS) functions in gastric ulcer induction via the formation of ROS and toxic effects on cells [12]
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