Piceid protects SH-SY5Y cells against hypoxia–reoxygenation Injury
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Abstract
Piceid (PIC) is a bioactive compound that has been reported to possess antioxidant and anti-inflammatory properties and to exert neuroprotective effects in several pathological conditions. However, its protective mechanism in SH-SY5Y cells under hypoxia–reoxygenation injury has not yet been fully elucidated. Objective: This study aimed to evaluate the protective effects of PIC on SH-SY5Y neuronal cells subjected to HR injury. Methods: An in vitro hypoxia–reoxygenation model was established using a hypoxic incubator. SH-SY5Y cells were cultured under normal conditions (control) or HR conditions. Cell viability, intracellular reactive oxygen species levels, cardiolipin content, and mitochondrial membrane potential were assessed using appropriate commercial assay kits. Results: The results showed that treatment with piceid (12.5–100 µM) significantly improved the viability of SH-SY5Y cells under HR conditions, with the most pronounced protective effect observed at 25 µM. HR markedly reduced cardiolipin content and mitochondrial membrane potential while increasing intracellular ROS levels. Piceid treatment effectively restored cardiolipin levels, stabilized mitochondrial membrane potential, and significantly suppressed excessive ROS production (p < 0.05). Conclusion: These findings provide preliminary evidence that piceid exerts a protective effect against hypoxia–reoxygenation–induced neuronal injury by targeting mitochondrial dysfunction, suggesting its potential as a neuroprotective agent in ischemic–reperfusion–related disorders.
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Keywords
Piceid; mitochondria; neuronal cells.
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