Record Details

Effect of selenium against doxorubicin-induced oxidative stress, inflammation, and apoptosis in the brain of rats: Role of TRPM2 channel

NOPR - NISCAIR Online Periodicals Repository

View Archive Info
 
 
Field Value
 
Title Effect of selenium against doxorubicin-induced oxidative stress, inflammation, and apoptosis in the brain of rats: Role of TRPM2 channel
 
Creator Yıldızhan, Kenan
Huyut, Zübeyir
Altındağ, Fikret
Ahlatcı, Adem
 
Subject Apoptosis
Doxorubicin
Oxidative stress
Selenium
TRPM2 channel
 
Description 177-185
Doxorubicin (DOX) is widely used as an anticancer drug in humans' various solid and haematological tumours. Although
many studies on the toxic effect of DOX are used in different organs, its impact on brain tissue has yet to be adequately
studied. This study investigated the protective effect of selenium (Se) and the role of transient receptor potential melastatin‐2
(TRPM2) channel activation against brain damage caused by DOX administration. Sixty rats were randomly divided into the
sham, dimethyl sulfoxide (DMSO), DOX, DOX + Se, DOX + N-(p-amylcinnamoyl) anthranilic acid (ACA), and
DOX + Se + ACA groups. The reactive oxygen species (ROS), poly [ADP-ribose] polymerase 1 (PARP1), and TRPM2
channel levels in brain tissues were measured by ELISA. In addition, a histopathological examination was performed in the
cerebral cortex and hippocampal areas, and the TRPM2 channel, NF-κB, and caspase-3 expression were determined
immunohistochemically. The levels of ROS, PARP1 and TRPM2 channel in the DOX group were higher than in the sham
and DMSO groups (P < 0.05). However, these parameters were decreased in the in DOX+Se and DOX+ACA groups by the
treatments of Se and ACA (P < 0.05). Also, we determined that Se and ACA treatment decreased the NF-κB, caspase-3, and
TRPM2 channel expression in the cerebral cortex and hippocampal areas in the DOX-induced rats. The data showed that Se
and/or ACA administration together with DOX administration could be used as a protective agent against DOX-induced
brain damage.
 
Date 2023-03-02T07:08:49Z
2023-03-02T07:08:49Z
2023-03
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://nopr.niscpr.res.in/handle/123456789/61472
https://doi.org/10.56042/ijbb.v60i3.67941
 
Language en
 
Publisher NIScPR-CSIR, India
 
Source IJBB Vol.60(03) [March 2023]