Aim <p>Neuroinflammation plays a crucial role in various central nervous system (CNS) disorders. This study aims to investigate the potential neuroprotective effects of radiofrequency electromagnetic fields (RF-EMF) and pulsed magnetic fields (PMF) on oxidative stress, apoptosis, and neuroinflammation in lipopolysaccharide (LPS)-induced acute neuroinflammation model in rats.</p> Methods <p>Forty female Wistar Albino rats were randomly assigned to five groups (Control, LPS, LPS + PMF, LPS + RF-EMF, and LPS + RF-EMF + PMF). Acute neuroinflammation was induced by intraperitoneal LPS administration. Rats were subsequently exposed to radiofrequency electromagnetic fields and/or pulsed magnetic fields under controlled conditions. Neuroinflammatory damage was evaluated by histopathological and immunohistochemical analyses targeting apoptosis, inflammation, and myelin integrity. Oxidative stress status was assessed spectrophotometrically, and key genes related to cell survival and neurovascular regulation were analyzed using RT-qPCR.</p> Results <p>LPS administration induced pronounced neuroinflammation, characterized by histopathological damage, increased apoptotic and inflammatory marker expression, myelin loss, oxidative stress, and suppression of survival- and angiogenesis-related genes. RF-EMF and PMF treatments significantly alleviated these alterations by reducing tissue injury, apoptosis, inflammation, and oxidative stress while restoring myelin integrity. Moreover, RF-EMF and PMF markedly upregulated phosphoinositide 3-kinase/ protein kinase B alpha/ hypoxia-inducible factor 1 alpha signaling and enhanced endothelial nitric oxide synthase and vascular endothelial growth factor expression, indicating improved neurovascular regulation. The combined RF-EMF + PMF therapy produced the most robust protective effects across all evaluated parameters.</p> Conclusion <p>RF-EMF and/or PMF treatment has features approved by the World Health Organization exerts significant neuroprotective effects by reducing oxidative stress, apoptosis, and neuroinflammation while enhancing cell survival and neurovascular function. The combination of RF-EMF and PMF yielded the most pronounced effects, suggesting that electromagnetic field-based therapies may offer a promising approach for treating neuroinflammation-associated disorders.</p>

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Radiofrequency and pulsed magnetic fields attenuate LPS-induced neuroinflammation and demyelination via PI3K/AKT/HIF-1α–mediated neurovascular protection

  • Ahmet Bindal,
  • Halil Asci,
  • Sanem Asci,
  • Muhammet Yusuf Tepebasi,
  • Ilter Ilhan,
  • Ozlem Ozmen,
  • Selcuk Comlekci

摘要

Aim

Neuroinflammation plays a crucial role in various central nervous system (CNS) disorders. This study aims to investigate the potential neuroprotective effects of radiofrequency electromagnetic fields (RF-EMF) and pulsed magnetic fields (PMF) on oxidative stress, apoptosis, and neuroinflammation in lipopolysaccharide (LPS)-induced acute neuroinflammation model in rats.

Methods

Forty female Wistar Albino rats were randomly assigned to five groups (Control, LPS, LPS + PMF, LPS + RF-EMF, and LPS + RF-EMF + PMF). Acute neuroinflammation was induced by intraperitoneal LPS administration. Rats were subsequently exposed to radiofrequency electromagnetic fields and/or pulsed magnetic fields under controlled conditions. Neuroinflammatory damage was evaluated by histopathological and immunohistochemical analyses targeting apoptosis, inflammation, and myelin integrity. Oxidative stress status was assessed spectrophotometrically, and key genes related to cell survival and neurovascular regulation were analyzed using RT-qPCR.

Results

LPS administration induced pronounced neuroinflammation, characterized by histopathological damage, increased apoptotic and inflammatory marker expression, myelin loss, oxidative stress, and suppression of survival- and angiogenesis-related genes. RF-EMF and PMF treatments significantly alleviated these alterations by reducing tissue injury, apoptosis, inflammation, and oxidative stress while restoring myelin integrity. Moreover, RF-EMF and PMF markedly upregulated phosphoinositide 3-kinase/ protein kinase B alpha/ hypoxia-inducible factor 1 alpha signaling and enhanced endothelial nitric oxide synthase and vascular endothelial growth factor expression, indicating improved neurovascular regulation. The combined RF-EMF + PMF therapy produced the most robust protective effects across all evaluated parameters.

Conclusion

RF-EMF and/or PMF treatment has features approved by the World Health Organization exerts significant neuroprotective effects by reducing oxidative stress, apoptosis, and neuroinflammation while enhancing cell survival and neurovascular function. The combination of RF-EMF and PMF yielded the most pronounced effects, suggesting that electromagnetic field-based therapies may offer a promising approach for treating neuroinflammation-associated disorders.