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Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
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...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
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...

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Related Experiment Video

Updated: Jun 25, 2026

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
07:23

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures

Published on: July 25, 2022

Proton pump inhibitors exert anti-inflammatory effects and decrease human microglial and monocytic THP-1 cell

Sadayuki Hashioka1, Andis Klegeris, Patrick L McGeer

  • 1Department of Psychiatry, Kinsmen Laboratory of Neurological Research, The University of British Columbia, Vancouver, BC, Canada.

Experimental Neurology
|February 24, 2009
PubMed
Summary

Proton pump inhibitors (PPIs) demonstrate anti-inflammatory effects, reducing neurotoxicity from activated microglia. Combining PPIs with NSAIDs may offer new treatments for neurodegenerative diseases.

Related Experiment Videos

Last Updated: Jun 25, 2026

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
07:23

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures

Published on: July 25, 2022

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Microglia activation contributes to neuroinflammation and neurotoxicity in neurodegenerative diseases.
  • Proton pump inhibitors (PPIs) are commonly used for acid-related disorders.
  • The potential anti-inflammatory effects of PPIs on microglia remain largely unexplored.

Purpose of the Study:

  • To investigate the anti-inflammatory properties of lansoprazole (LPZ) and omeprazole (OPZ) on microglia.
  • To assess the impact of PPIs on microglial-induced neurotoxicity.
  • To evaluate the combined effects of PPIs and NSAIDs on neuroinflammation.

Main Methods:

  • Assessing the neurotoxic effects of stimulated microglia and THP-1 cell supernatants on SH-SY5Y neuroblastoma cells.
  • Measuring pro-inflammatory cytokine (TNF-alpha and IL-6) production using enzyme-linked immunosorbent assays (ELISAs).
  • Investigating the synergistic effects of PPIs with S-ibuprofen (IBP), a non-steroidal anti-inflammatory drug (NSAID).

Main Results:

  • Both LPZ and OPZ exhibited protective effects against microglial supernatant-induced neurotoxicity.
  • A synergistic neuroprotective effect was observed when PPIs were combined with S-ibuprofen.
  • PPIs significantly reduced TNF-alpha secretion from stimulated THP-1 cells in a dose-dependent manner, with a trend towards reduced IL-6.

Conclusions:

  • Proton pump inhibitors possess significant anti-inflammatory effects on microglia and monocytes.
  • PPIs can mitigate microglial and monocytic neurotoxicity.
  • Combination therapy with PPIs and NSAIDs shows promise for treating neurodegenerative diseases linked to microglial activation.