Related Experiment Video
Updated: Jul 17, 2026

Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation
Published on: July 27, 2022
Influence of Viburnum opulus proanthocyanidins on stress-induced gastrointestinal mucosal damage
O S Zayachkivska1, M R Gzhegotsky, O I Terletska
1Department of Physiology, Lviv National Medical University, Lviv, Ukraine. zay_oksana@yahoo.com
Abstract:
Recent studies demonstrated that the proanthocyanidins (PA), the polymers of flavan-3-ols, naturally occurring plant metabolites widely available in fruits, vegetables, nuts, seeds, flowers and bark, have anti-inflammatory, anticarcinogenic, anti-allergic, antioxidant and vasodilatory actions. We hypothesized that Viburnum opulus PA (VOPA, Caprifoliaceae), due to activation of multifactorial gastrointestinal mucosal defense mechanisms, exert gastroduodenoprotective effects. The aim of the study was: 1) to investigate VOPA effects on gastroduodenal mucosal integrity and pattern of carbohydrate binding proteins and nitric oxide (NO) content in intact mucosa and that exposed to non-topical ulcerogens (stress) in rats without and with capsaicin (125 mg/kg, sc) denervation; and 2), to assess the role of activity of antioxidizing enzymes superoxide dismutase (SOD), catalase (CAT), gluthatione peroxidase (GPx) in VOPA-induced gastroduodenoprotection against water immersion and restraint stress (WRS) in rats. VOPA was administered orally in dose of 25, 50 or 75 mg/kg body weight. Gastroduodenal mucosal damage detected by routine light microscopic investigation and lectin histochemistry set, purified from plant and animal sources of Carpatian region. NO content, pro-and antioxidant system were determined by routine laboratory methods. Pretreatment with VOPA afforded gastroduodenoprotection and was accompanied by an increase in NO expression, both changes being reversed by sensory denervation, as well as by the rise of SOD, CAT activity and fall in MDA content. Our study shows that VOPA exerts a potent gastroduodenoprotective activity via an increase in endogenous NO generation, suppression of lipid peroxidation and mobilization of antioxidant activity and changes in glycoconjugate content of the gastroduodenal mucosa of rat.
Related Concept Videos
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...

