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Related Concept Videos

Cholecystitis01:20

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...
Gallbladder01:17

Gallbladder

The gallbladder is a small, pear-shaped organ that plays a crucial role in our digestive system. Measuring about 10 cm in length, it is comparable in size to a kiwi fruit and is located in a hollow area on the lower surface of the liver. The gallbladder's primary function is to store and concentrate bile, a fluid produced by the liver that aids in digestion.
The gallbladder's anatomy consists of three regions: the fundus, body, and neck. Extending from the neck, the cystic duct joins the common...

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Murine Model of Metastatic Liver Tumors in the Setting of Ischemia Reperfusion Injury
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Murine Model of Metastatic Liver Tumors in the Setting of Ischemia Reperfusion Injury

Published on: August 30, 2019

Tempol protects the gallbladder against ischemia/reperfusion.

Pedro J Gomez-Pinilla1, Pedro J Camello, Jesus A F Tresguerres

  • 1Department of Physiology, Nursing School, University of Extremadura, 10071 Caceres, Spain.

Journal of Physiology and Biochemistry
|June 24, 2010
PubMed
Summary

Antioxidant tempol treatment improved gallbladder function and reduced inflammation following ischemia/reperfusion (I/R) injury. This suggests tempol

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05:59

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Published on: April 2, 2017

Area of Science:

  • Gastroenterology
  • Physiology
  • Pharmacology

Background:

  • Acute acalculous cholecystitis involves impaired gallbladder emptying and contractility, linked to ischemia/reperfusion (I/R) injury.
  • Understanding the mechanisms of I/R-induced gallbladder dysfunction is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the protective effects of the antioxidant tempol on I/R-induced gallbladder dysfunction.
  • To elucidate the mechanisms underlying tempol's effects on gallbladder contractility and inflammation.

Main Methods:

  • Experimental gallbladder I/R was induced in guinea pigs via bile duct ligation.
  • Isometric tension recordings assessed contractile capacity; F-actin content and Ca(2+) influx were measured.
  • Mitochondrial membrane potential and inflammatory mediator expression (NF-kappaB, COX-2, iNOS) were analyzed.

Main Results:

  • I/R impaired gallbladder contractility, reduced F-actin, and disrupted Ca(2+) influx.
  • I/R led to mitochondrial depolarization and increased expression of NF-kappaB, COX-2, and iNOS.
  • Tempol treatment restored contractility, improved Ca(2+) handling and F-actin content, and normalized mitochondrial function and inflammatory markers.

Conclusions:

  • Antioxidant therapy with tempol protects the gallbladder against I/R injury.
  • Tempol normalizes Ca(2+) handling, F-actin content, and inflammatory pathways in I/R-affected gallbladders.
  • Tempol demonstrates potential therapeutic benefits for ischemia/reperfusion injury in the gallbladder.