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Related Concept Videos

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
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...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...

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Related Experiment Video

Updated: Jul 18, 2026

Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays
11:31

Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays

Published on: July 4, 2018

Progesterone inhibits mast cell secretion.

M Vasiadi1, D Kempuraj, W Boucher

  • 1Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Tufts-New England Medical Center, Boston, MA, USA.

International Journal of Immunopathology and Pharmacology
|December 15, 2006
PubMed
Summary

Progesterone inhibits histamine secretion from mast cells, potentially explaining why inflammatory conditions improve during pregnancy. This finding offers new insights into mast cell regulation and reproductive health.

More Related Videos

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis
16:01

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis

Published on: January 26, 2015

Related Experiment Videos

Last Updated: Jul 18, 2026

Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays
11:31

Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays

Published on: July 4, 2018

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis
16:01

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis

Published on: January 26, 2015

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Mast cells mediate allergic reactions by releasing inflammatory mediators.
  • Mast cells are implicated in conditions like IBS and migraines, which fluctuate with hormonal changes.
  • Estrogen enhances mast cell secretion, while its role in pregnancy-related symptom reduction is unclear.

Purpose of the Study:

  • To investigate the effect of progesterone on mast cell secretion.
  • To explore the potential role of progesterone in regulating inflammatory conditions during pregnancy.

Main Methods:

  • Purified rat peritoneal mast cells were used.
  • Cells were stimulated immunologically or with Substance P (SP).
  • Histamine secretion was measured, and electron microscopy was employed.

Main Results:

  • Progesterone (100 nM) significantly inhibited histamine secretion.
  • Cholesterol did not affect histamine secretion.
  • Electron microscopy confirmed the inhibitory effect of progesterone on mast cell degranulation.

Conclusions:

  • Progesterone regulates mast cell secretion, specifically inhibiting histamine release.
  • This hormonal regulation may explain the reduced symptoms of certain inflammatory diseases during pregnancy.
  • Further research into progesterone's role in mast cell-mediated conditions is warranted.