Canolol Alleviates Ethanol-Induced Gastric Ulcer by Inhibiting p38 MAPK/NF-κB/NLRP3 Pathway

Congcong Ma1,2, Li Zhang3,4, Qingde Huang1,2

  • 1Department of Nutriology, Oil Crops Research Institute, Chinese Academy of Agricultural Sciences, Wuhan 430062, China.

Insights

Canolol, a compound from rapeseed oil, protects against stomach ulcers in rats. It reduces inflammation, boosts antioxidants, and prevents cell death by inhibiting key signaling pathways.

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Natural Product Chemistry

Background:

  • Gastric ulcers (GU) are a widespread global health issue.
  • Ethanol consumption is a significant risk factor for developing gastric ulcers.
  • Natural compounds offer potential therapeutic avenues for digestive disorders.

Purpose of the Study:

  • To investigate the gastroprotective effects of canolol against ethanol-induced gastric ulcers in a rat model.
  • To elucidate the underlying molecular mechanisms of canolol's protective action.

Main Methods:

  • Ethanol-induced gastric ulcer model in rats.
  • Assessment of gastric mucosal damage (ulcer index, histopathology).
  • Measurement of gastric wall mucus, NP-SH, heat shock protein 70, and mucosal blood flow.
  • Quantification of pro-inflammatory (TNF-α, IL-1β, IL-6) and anti-inflammatory (IL-10) cytokines.
  • Evaluation of antioxidant enzyme activities (SOD, CAT, GPx) and glutathione (GSH) levels.
  • Assessment of apoptosis markers (TUNEL, BAX, caspase-3).
  • Analysis of signaling pathway activation (p38 MAPK, NF-κB, NLRP3).

Main Results:

  • Canolol pretreatment significantly reduced gastric ulcer index and improved histopathological scores.
  • Canolol counteracted ethanol-induced disruption of mucosal defense mechanisms.
  • Canolol alleviated gastric inflammation by modulating cytokine profiles and myeloperoxidase activity.
  • Canolol enhanced antioxidant capacity and mitigated oxidative stress.
  • Canolol suppressed ethanol-induced apoptosis in gastric mucosa.
  • Canolol inhibited the p38 MAPK/NF-κB/NLRP3 signaling pathway.

Conclusions:

  • Canolol exhibits significant gastroprotective effects against ethanol-induced gastric ulcers in rats.
  • Canolol exerts its protective effects by reducing inflammation, oxidative stress, and apoptosis.
  • The mechanism involves the inhibition of the p38 MAPK/NF-κB/NLRP3 pathway, highlighting its therapeutic potential.

Related Concept Videos

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
316
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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...
188
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
373
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
106
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
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...
494
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
54