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Published on: March 16, 2018
Protective Effect of Agmatine Against Cisplatin- Induced Cellular Apoptosis in an Auditory Cell Line
Euyhyun Park1, Se Hee Lee1, Hak Hyun Jung1
1Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, Republic of Korea.
Background:
The aims of this study were to evaluate the protective effects of agmatine against cisplatin-induced cellular apoptosis in an audi- tory cell line and to prove the protective mechanism of agmatine.
Methods:
The House Ear Institute-Organ of Corti 1 cells were co-treated with agmatine at different concentrations and 15 μM of cisplatin for 48 hours. Cell viability and proliferation were measured. Annexin V-fluorescein isothiocyanate /propidium iodide staining was performed to analyze apoptosis. The levels of intracellular reactive oxygen species were measured using flow cytometry. The expression of BCL2-associated X protein and the enzymatic activity of caspase-3 was measured to examine the pathway of apoptosis induction.
Results:
In normal conditions, the maximal protective effect occurred with 10 mM of agmatine. However, in the presence of cisplatin, the maximal protective effect was observed from 8 mM of agmatine. Thus, 8 mM was chosen as the ideal agmatine concentration for the analysis of protective effects against cisplatin-induced cytotoxicity. Agmatine exerted a significant protective effect against 15 μM of cisplatin when applied for 48 hours and reduced the proportion of necrotic and late apoptotic cells. Agmatine did not significantly reduce the cisplatin-induced increase in reactive oxygen species but decreased the expression of BCL2-associated X protein and the activity of caspase-3.
Conclusion:
Agmatine protected against cisplatin-induced cellular apoptosis in an auditory cell line. These effects were mediated by the pro- tection of mitochondrial function and inhibition of apoptosis.
Insights
Agmatine protects auditory cells from cisplatin-induced apoptosis by preserving mitochondrial function and inhibiting cell death pathways. This study demonstrates agmatine
Area of Science:
- Ototoxicity research
- Cellular biology
- Pharmacology
Background:
- Cisplatin is a chemotherapy drug known to cause ototoxicity.
- Auditory cell lines are susceptible to cisplatin-induced damage and apoptosis.
- Agmatine's protective potential against cellular damage requires investigation.
Purpose of the Study:
- To assess agmatine's protective effects on auditory cells against cisplatin.
- To elucidate the mechanism underlying agmatine's protective action.
Main Methods:
- Auditory cells (HEI-OC1) were co-treated with varying concentrations of agmatine and cisplatin.
- Cell viability, proliferation, and apoptosis were analyzed using Annexin V/propidium iodide staining.
- Reactive oxygen species (ROS) levels, BCL2-associated X protein expression, and caspase-3 activity were measured.
Main Results:
- Agmatine (8 mM) significantly protected auditory cells from cisplatin-induced cytotoxicity.
- Agmatine reduced necrotic and late apoptotic cell populations.
- While not significantly reducing ROS, agmatine decreased BCL2-associated X protein expression and caspase-3 activity.
Conclusions:
- Agmatine demonstrates significant protective effects against cisplatin-induced apoptosis in auditory cells.
- These protective mechanisms involve preserving mitochondrial function and inhibiting apoptotic pathways.
