| Summary: | Oxidative stress, an excess of endogenous or exogenous reactive oxygen species (ROS) in the human body, is closely aligned with inflammatory responses. ROS such as hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), superoxide, and radical hydroxyl ions serve essential functions in fighting infection; however, chronic elevation of these species irreversibly damages cellular components. Given the central role of inflammation in a variety of diseases, including Alzheimer’s disease and rheumatoid arthritis, a low-cost, extracellular, non-invasive assay of H<sub>2</sub>O<sub>2</sub> measurement is needed. This work reports the use of a platinum microelectrode array (Pt MEA)-based ceramic probe to detect time- and concentration-dependent variations in H<sub>2</sub>O<sub>2</sub> production by activated RAW 264.7 macrophages. First, these cells were activated by lipopolysaccharide (LPS) to induce oxidative stress. Chronoamperometry was then employed to detect the quantity of H<sub>2</sub>O<sub>2</sub> released by cells at various time intervals up to 48 h. The most stimulatory concentration of LPS was identified. Further experiments assessed the anti-inflammatory effect of dexamethasone (Dex), a commonly prescribed steroid medication. As expected, the probe detected significantly increased H<sub>2</sub>O<sub>2</sub> production by LPS-doped macrophages, subsequently diminishing the pro-inflammatory effect in LPS-doped cells treated with Dex. These results strongly support the use of this probe as a non-invasive, robust, point-of-care test of inflammation, with a high potential for multiplexing in further studies.
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