Effect of Pulsed Electromagnetic Field (PEMF) on Infarct Size and Inflammation After Cerebral Ischemia in Mice

Abstract

Pulsed electromagnetic fields (PEMF) have been demonstrated to have anti-inflammatory and pro-regenerative effects in animals and humans. We used the FDA-approved Sofpulse (Ivivi Health Sciences, LLC) to study effect of PEMF on infarct size and poststroke inflammation following distal middle cerebral artery occlusion (dMCAO) in mice. Electromagnetic field was applied within 30-45 min after ischemic brain damage and utilized twice a day for 21 consecutive days. Ischemic infarct size was assessed using MRI and histological analysis. At 21 days after dMCAO, the infarct size was significantly (by 26%) smaller in PEMF-treated animals as compared to controls. Neuroinflammation in these animals was evaluated using specialized cytokine/chemokine PCR array. We demonstrate that PEMF significantly influenced expression profile of pro- and anti-inflammatory factors in the hemisphere ipsilateral to ischemic damage. Importantly, expression of gene encoding major pro-inflammatory cytokine IL-1α was significantly reduced, while expression of major anti-inflammatory IL-10 was significantly increased. PEMF application significantly downregulated genes encoding members of the major pro-apoptotic tumor necrosis factor (TNF) superfamily indicating that the treatment could have both anti-inflammatory and anti-apoptotic effects. Both reduction of infarct size and influence on neuroinflammation could have a potentially important positive impact on the poststroke recovery process, implicating PEMF as a possible adjunctive therapy for stroke patients.

In Vivo Inhibition of miR-155 Promotes Recovery after Experimental Mouse Stroke

“…dMCAO was used as an experimental model of cortical ischemia (Kuraoka et al, 2009;Pena-Philippides et al, 2014). This model produces an infarct in the frontal and parietal cortex, which over time progresses into adjacent temporal, frontal, and cingulate cortex.…”

Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents

“…They include, IL-1β, IL-6, plasma high sensitivity CRP (hs-CRP) and TNF-α, as well as other potential cytotoxic molecules including NO, ROS, and prostanoids [102-105]. Microglial suppression can reduce post-ischemic injuries, so this illustrates an attractive therapeutic strategy for ischemic stroke [106,107]. In addition to cytokines that are expressed in the resident brain cells, there are a peripherally derived cytokines that produce and secrete from T-lymphocytes, mononuclear phagocytes, NK cells and polymorpho-nuclear leukocytes which are involved in ischemic inflammation [108].…”

MicroRNA let-7c-5p protects against cerebral ischemia injury via mechanisms involving the inhibition of microglia activation

“…Cerebral ischemia was induced by reversible middle cerebral artery occlusion (MCAO) via an intraluminal suture technique, as previously described (Pena-Philippides et al, 2014). Briefly, in this technique, isoflurane was used to anesthetize the mice, and their body temperatures were sustained at 37.0 ± 0.5 with warming pads.…”