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Deacetyl epoxyazadiradione protects aminoglycoside antibiotic-induced renal cell apoptosis, in vitro
Raghul Murugan1, Ravi Rajesh2, Manikandan Velayutham1
1Department of Biotechnology, College of Science and Humanities, SRM Institute of Science and Technology, Kattankulathur, Chennai, Tamil Nadu, India.
Abstract:
Aminoglycoside antibiotics such as gentamicin are used frequently to treat bacterial infections in humans. Excessive consumption of these antibiotics lead to renal dysfunction. One of the factors contributing to renal dysfunction is oxidative damage, which causes apoptosis. Hence, this study investigates the effect of the antioxidant compound deacetyl epoxyazadiradione (DEA) in reducing cell death induced by gentamicin treatment in kidney cells (Madin-Darby canine kidney cells). The antioxidant experiments showed that reactive oxygen species level is decreased up to 27.06 ± 0.18% in 150 µM of DEA treatment. At this concentration, the activity of antioxidant enzymes such as superoxide dismutase increased from 0.4 ± 0.04 to 1.46 ± 0.05 µmol/min/L and catalase increased from 7.48 ± 0.39 to 17.6 ± 0.74 U/mg. The relative folds of gene expression of mitochondrial enzymes such as GST, GPx and GR restored from 0.596 ± 0.019, 0.521 ± 0.013 and 0.775 ± 0.014 to 0.866 ± 0.013, 0.669 ± 0.015 and 0.8615 ± 0.028, respectively. Consequently, the percentage of cell viability increases upto 91.8 ± 2.01 from 61.93 ± 1.63 with much less fragmentation in genomic DNA. Additionally, molecular docking results showed that DEA could bind to Bax, Bcl- 2, Caspase- 3 and Caspase- 9 proteins. These results indicate that DEA could reduce cell apoptosis by reducing oxidative stress due to antibiotics and interrupting the apoptotic signal pathway in kidney cells.
Insights
The antioxidant deacetyl epoxyazadiradione (DEA) reduces gentamicin-induced kidney cell death by decreasing oxidative stress and apoptosis. DEA treatment significantly improved cell viability and antioxidant enzyme activity, protecting kidney cells from antibiotic damage.
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Gentamicin, an aminoglycoside antibiotic, is crucial for treating bacterial infections but can cause renal dysfunction.
- Oxidative damage and apoptosis are key mechanisms contributing to gentamicin-induced nephrotoxicity.
Purpose of the Study:
- To investigate the protective effects of deacetyl epoxyazadiradione (DEA), an antioxidant compound, against gentamicin-induced apoptosis in kidney cells.
- To elucidate the underlying mechanisms of DEA's protective action.
Main Methods:
- Madin-Darby canine kidney cells were treated with gentamicin and varying concentrations of DEA.
- Assays were performed to measure reactive oxygen species (ROS) levels, antioxidant enzyme activities (superoxide dismutase, catalase), and gene expression of key enzymes (GST, GPx, GR).
- Cell viability and genomic DNA fragmentation were assessed, and molecular docking was used to predict interactions with apoptotic proteins.
Main Results:
- DEA treatment (150 µM) significantly reduced ROS levels by 27.06%.
- Activities of superoxide dismutase and catalase increased, and the gene expression of GST, GPx, and GR was restored.
- Cell viability increased to 91.8% with reduced DNA fragmentation, and molecular docking indicated DEA binds to apoptotic proteins (Bax, Bcl-2, Caspase-3, Caspase-9).
Conclusions:
- Deacetyl epoxyazadiradione (DEA) exhibits significant protective effects against gentamicin-induced nephrotoxicity.
- DEA mitigates kidney cell apoptosis by reducing oxidative stress and modulating apoptotic signaling pathways.
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