Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Int J Radiat Oncol Biol Phys. 2010 Mar 15;76(4):1225-34. doi: 10.1016/j.ijrobp.2009.09.063.

Inactivation of kupffer cells by gadolinium chloride protects murine liver from radiation-induced apoptosis.

Author information

  • 1Department of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Abstract

PURPOSE:

To determine whether the inhibition of Kupffer cells before radiotherapy (RT) would protect hepatocytes from radiation-induced apoptosis.

MATERIALS AND METHODS:

A single 30-Gy fraction was administered to the upper abdomen of Sprague-Dawley rats. The Kupffer cell inhibitor gadolinium chloride (GdCl3; 10 mg/kg body weight) was intravenously injected 24 h before RT. The rats were divided into four groups: group 1, sham RT plus saline (control group); group 2, sham RT plus GdCl3; group 3, RT plus saline; and group 4, RT plus GdCl3. Liver tissue was collected for measurement of apoptotic cytokine expression and evaluation of radiation-induced liver toxicity by analysis of liver enzyme activities, hepatocyte micronucleus formation, apoptosis, and histologic staining.

RESULTS:

The expression of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha was significantly attenuated in group 4 compared with group 3 at 2, 6, 24, and 48 h after injection (p <0.05). At early points after RT, the rats in group 4 exhibited significantly lower levels of liver enzyme activity, apoptotic response, and hepatocyte micronucleus formation compared with those in group 3.

CONCLUSION:

Selective inactivation of Kupffer cells with GdCl3 reduced radiation-induced cytokine production and protected the liver against acute radiation-induced damage.

Copyright 2010 Elsevier Inc. All rights reserved.

PMID:
20206021
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk