Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

812
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
812
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

946
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
946
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

1.1K
The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
1.1K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

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

781
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...
781
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

855
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...
855
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

2.9K
The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
2.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Separation and determination of furanocoumarins in shatian pomelo juice by HPLC-MS].

Se pu = Chinese journal of chromatography·2007
Same author

Effect of neuregulin-1 on histopathological and functional outcome after controlled cortical impact in mice.

Journal of neurotrauma·2007
Same author

Decreased expression of ING2 gene and its clinicopathological significance in hepatocellular carcinoma.

Cancer letters·2007
Same author

Compound Salvia droplet pill, a traditional Chinese medicine, for the treatment of unstable angina pectoris: a systematic review.

Medical science monitor : international medical journal of experimental and clinical research·2007
Same author

Ezrin silencing by small hairpin RNA reverses metastatic behaviors of human breast cancer cells.

Cancer letters·2007
Same author

The effect of nitric oxide on metal release from metallothionein-3: gradual unfolding of the protein.

Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry·2007

Related Experiment Video

Updated: Nov 11, 2025

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:09

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

208

PPARγ: The Central Mucus Barrier Coordinator in Ulcerative Colitis.

Jian Fang1,2, Hui Wang3, Zhe Xue1

  • 1Department of Preventive Medicine, Zhejiang Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, Zhejiang Province, People's Republic of China.

Inflammatory Bowel Diseases
|March 27, 2021
PubMed
Summary

Ulcerative colitis (UC) involves a compromised intestinal mucus barrier, a key factor in disease severity and relapse. Peroxisome proliferator-activated receptor gamma (PPARγ) shows promise as a therapeutic target for UC by regulating the mucus barrier and host-microbiota interactions.

Keywords:
PPARγcolonocyte metabolismmucin secretionmucus barrierulcerative colitis

More Related Videos

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
06:31

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

Published on: June 2, 2023

1.3K
An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
07:32

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance

Published on: December 3, 2020

6.2K

Related Experiment Videos

Last Updated: Nov 11, 2025

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:09

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

208
Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
06:31

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

Published on: June 2, 2023

1.3K
An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
07:32

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance

Published on: December 3, 2020

6.2K

Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory colon disorder with a relapsing-remitting course.
  • The intestinal mucus barrier protects against microbial invasion and its impairment correlates with UC severity.
  • Mucus barrier depletion is the sole independent predictor of UC relapse.

Purpose of the Study:

  • To investigate the role of Peroxisome proliferator-activated receptor gamma (PPARγ) in ulcerative colitis.
  • To explore PPARγ's potential as a therapeutic target for UC by examining its effects on the mucus barrier and host-microbiota interactions.

Main Methods:

  • Review of existing patient and animal study data.
  • Analysis of PPARγ's known functions in inflammation, mucus secretion, and host-microbiota interactions.
  • Exploration of PPARγ's influence on colonocyte metabolism and intestinal oxygen availability.

Main Results:

  • PPARγ regulates inflammatory cytokine expression and promotes mucus secretion.
  • PPARγ influences host-microbiota interactions by modulating colonocyte energy metabolism and gut oxygen levels.
  • Gut microbiota homeostasis, crucial for butyrate production, is linked to colonocyte energy.

Conclusions:

  • PPARγ plays a central role in coordinating the intestinal mucus barrier.
  • PPARγ modulation presents a potential therapeutic strategy for ulcerative colitis.