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Nootkatone debilitate bleomycin-induced pulmonary toxicity in lung cancer A549 cells: In silico and genomic evolution

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Title Nootkatone debilitate bleomycin-induced pulmonary toxicity in lung cancer A549 cells: In silico and genomic evolution
 
Creator Ansari, Mushtaq Ahmad
Shahid, Mudassar
Ahmad, Sheikh Fayaz
Kumar, Ashok
Ali, Nemat
 
Subject Gene expression
Molecular docking
Oxidative stress
Phytocompound
 
Description 779-787
The biggest issue with bleomycin (BLM) chemotherapy is pulmonary damage. BLM manifests oxidative stress via an
uncontrolled progression of reactive oxygen species in pneumocystis, a relative deficit of the deactivation enzyme BLM
hydrolase and the formation of inflammatory cytokines leading to apoptosis. There have been several attempts to treat
patients for this adverse effect by giving them antioxidant rich supplements to minimise free radicals. Compounds that are
extracted from plants or that are based on plants emphasise more on curing such patient issues in order to support treatment,
rejuvenate, or manage normal metabolism. Hence, in this study we concentrated on pretreatment of lung cancer derived
A549 cells with phytocompound nootkatone (NKT) to prevent BLM-mediated oxidative stress. We find in our study, the
BLM-exposed cells have displayed morphological anomalies such as shrinkage, blabbing, and chromatin condensation,
among others. Yet, even after exposure to BLM, no such abnormalities were seen in NKT pretreated cells. In NKT
pretreatment cells, there was a significant surge in endogenous antioxidants and a decrease in lipid peroxidation, in contrast,
cells exposed to BLM had lower levels of antioxidants and greater levels of lipid peroxidation. In gene expression analysis,
the pro-apoptotic gene Bcl-2/Bax and the apoptotic executor caspase 3 were significantly suppressed in the NKT pretreated
cells, which attenuated BLM-mediated apoptosis. The current investigation, showed that the NKT pretreatment has
displayed merit for pulmonary protective activity against BLM-induced oxidative stress by boosting the intracellular
antioxidant defence.
 
Date 2024-11-05T12:06:50Z
2024-11-05T12:06:50Z
2024-10
 
Type Article
 
Identifier 0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscpr.res.in/handle/123456789/64831
https://doi.org/10.56042/ijeb.v62i10.10032
 
Language en
 
Publisher NIScPR-CSIR,India
 
Source IJEB Vol.62(10) [October 2024]