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Related Experiment Video

Updated: May 13, 2026

Kupffer Cell Isolation for Nanoparticle Toxicity Testing

Kupffer Cell Isolation for Nanoparticle Toxicity Testing

Published on: August 18, 2015

Effects of carbendazim on Kupffer cell functioning.

A V Viktorov¹, V A Yurkiv

¹Laboratory for Molecular Mechanisms of Infections, Central Research Institute of Epidemiology, Moscow, Russia. viktorov_av@yahoo.com

Bulletin of Experimental Biology and Medicine

|March 15, 2013

Summary

Carbendazim suppressed tumor necrosis factor-alpha (TNF-α) and nitric oxide (NO) release in rat Kupffer cells. It also impaired the cells' ability to engulf particles, indicating reduced phagocytosis.

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Area of Science:

Immunology
Toxicology
Cell Biology

Background:

Kupffer cells are key immune cells in the liver.
Lipopolysaccharide (LPS) is a potent activator of Kupffer cells.
TNF-α and NO are critical inflammatory mediators.

Purpose of the Study:

To investigate the effects of carbendazim on Kupffer cell function.
To assess carbendazim's impact on LPS-induced inflammatory responses.
To evaluate carbendazim's influence on Kupffer cell phagocytosis.

Main Methods:

Primary culture of rat Kupffer cells.
Stimulation with LPS.
Measurement of TNF-α and NO secretion.
Assessment of phagocytosis using latex particle engulfment.

Main Results:

Carbendazim significantly inhibited LPS-induced TNF-α secretion.
Carbendazim significantly inhibited LPS-induced NO secretion.
Carbendazim preincubation led to a significant decrease in Kupffer cell phagocytosis.

Conclusions:

Carbendazim exhibits immunomodulatory effects on Kupffer cells.
Carbendazim suppresses key inflammatory pathways in Kupffer cells.
Carbendazim impairs Kupffer cell phagocytic activity, potentially affecting liver immune surveillance.