
School of Podiatric Medicine - Medical Student Research
Document Type
Poster
Publication Date
2024
Abstract
Introduction and Hypothesis: Zoledronate (Zol) is an antiosteoclastic drug widely utilized for osteoporosis and bone metastases, and it may be used off-label for managing diabetic Charcot neuroarthropathy1. Since macrophages share common precursors with osteoclasts, their function may also be affected by Zol. Herein, we hypothesize that Zol impairs macrophage responses, potentially hindering their viability and host defense in diabetic conditions.
Methodology: Raw 264.7 macrophages were seeded at 2.5 x 103 in 96-well plates for viability assays. Cells were tested under normal glucose (25 mM), high glucose (ranging from 45 to 70 mM), and high oxidative stress (ranging from 0.2 mM to 0.4 mM H2O2) conditions. Cells were exposed to varying concentrations of Zol (0.1 to 100 µM). Viability was assessed using tetrazolium compound assay with absorbance measured at 490 nm. Quantitative data was analyzed using One Way ANOVA followed by Tukey, with a significance level set at 0.05%.
Results: High glucose significantly increased macrophage proliferation to 109.98% at 45 mM and 111.55% at 70 mM. High oxidative stress decreased macrophage viability to 68.55% at 0.2 mM and 71.67% at 0.4 mM H2O2. Additionally, Zol treatment significantly reduced macrophage proliferation from 89% at 1 µM to 62.83% at 100 µM (p< 0.05).
Discussion and Conclusion: Both oxidative stress and Zol significantly decreased macrophage viability, while high glucose levels enhance their proliferation. For future studies we will selected 0.2 mM H2O2, 45 mM glucose, and 10 µM Zol to explore their combined effects on metabolism and polarization of macrophages.
Recommended Citation
Liu, Bryan; Cantu, Denae; Seixas, Deborah; and Biguetti, Cláudia Cristina, "Comparative Effect of Zoledronic Acid, High Glucose Levels, and Oxidative Stress on Macrophage Viability" (2024). School of Podiatric Medicine - Medical Student Research. 6.
https://scholarworks.utrgv.edu/sopm_mspub/6