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Graphene Oxide-Silver Nanocomposite Induced Apoptosis in Human Hepatoma (HepG2) Cells Through Oxidative Stress and Caspase Dependent Signalling Pathway

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Title Graphene Oxide-Silver Nanocomposite Induced Apoptosis in Human Hepatoma (HepG2) Cells Through Oxidative Stress and Caspase Dependent Signalling Pathway
 
Creator Sharma, Neelima
Mondal, Surajit
Yadav, Hari Om
Sharma, Rishi
 
Subject Apoptosis
Caspase
Graphene oxide
Nanocomposite
Oxidative stress
 
Description 298-304
At present, the nanotechnology-based therapeutic agents have been emerged as the most reliable tool for various
dangerous disorders including cancer. Liver cancer is one of the top five deadliest cancers. Hepatocellular Carcinoma (HCC)
is the third most leading cause of death after lung and stomach cancer. Graphene Oxide, due to its unique chemical,
mechanical, and optical properties, has offered a wide range of applications in biomedical fields. Silver nanoparticles can
easily enter into mammalian cells, accumulate in the macrophages, and interact with biological molecules. In the present
investigation, the effects of Graphene Oxide-Ag nanocomposites on human Hepatoma Cells (HepG2) have been
investigated. Graphene oxide has been synthesised by modified Hummer’s method and further, Graphene Oxide-Ag
nanocomposites have been prepared. The effect of nanoparticles on cell viability has been observed. For understanding the
molecular pathway, the effects on oxidative stress (ROS and GSH levels), Caspase-3 Activity and Apoptotic Cell Population
have been examined. Further, to confirm the role of oxidative stress and caspase-3 activity, the cell viability has been
measured in the presence or absence of specific inhibitors. The results demonstrate that GO-Ag nanocomposites induce
cytotoxicity, oxidative stress and apoptosis in HepG2 cells through caspase dependent pathway. The oxidative stress plays a
crucial role in GO-Ag nanocomposites induced caspase dependent apoptosis. Thus, it can be concluded that GO-Ag
nanocomposites show therapeutic efficacy in cancer cells.
 
Date 2023-06-22T09:53:59Z
2023-06-22T09:53:59Z
2023-06
 
Type Article
 
Identifier 0971-4588 (Print); 0975-1017 (Online)
http://nopr.niscpr.res.in/handle/123456789/62052
https://doi.org/10.56042/ijems.v30i2.1633
 
Language en
 
Publisher NIScPR-CSIR, India
 
Source IJEMS Vol.30(2) [April 2023]