Objectives

Acute cerebral ischemia is characterized by several pathological processes evolving during time, which contribute to the final tissue damage. Secondary processes, such as prolonged inflammatory response, impaired mitochondrial function, and oxidative stress, are responsible for the progression of brain injury to the peri-infarct area, called “penumbra.” Adenosine has been shown to play a crucial role in regulating the inflammatory cascade following brain ischemia. Pulsed electromagnetic fields (PEMFs) act as modulators of adenosine receptors, increasing the functionality of the endogenous adenosine. In particular, PEMF exposure induces a significant upregulation of A_2A and A₃ adenosine receptors in different neuronal cell types. Several lines of evidence suggest that PEMF exposure might play a neuroprotective role after ischemic damage.

Materials and Methods

This review summarizes the current knowledge on the mechanism of action of PEMFs and their biological effects on neuronal damage both in preclinical and clinical studies.

Results

PEMFs counteract hypoxia-induced apoptosis and ROS production in neuronal-like cells and exert a strong anti-inflammatory effect on microglial cells. Data from stroke animal models showed that PEMFs exposure is able to reduce the size of the infarct area and decrease the levels of pro-inflammatory mediators. In clinical studies, PEMFs stimulation proved to be safe and well tolerated. Preliminary results on acute ischemic stroke patients showed a dose-dependent reduction in the lesion size.

Conclusions

Altogether, these data demonstrate the efficacy of PEMFs against several mechanisms underlying ischemic damage and suggest that PEMFs might represent a novel noninvasive adjunctive treatment for acute ischemic stroke, providing neuroprotection and reducing functional deficits following ischemia.

中文翻译：

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脉冲电磁场​​：急性脑缺血后神经保护的一种新的有吸引力的治疗机会

目标

急性脑缺血的特征在于随着时间的推移而演变的几种病理过程，这有助于最终的组织损伤。继发性过程，如炎症反应延长、线粒体功能受损和氧化应激，是导致脑损伤进展到梗死周围区域（称为“半影”）的原因。腺苷已被证明在调节脑缺血后的炎症级联反应中起关键作用。脉冲电磁场​​ (PEMF) 充当腺苷受体的调节剂，增加内源性腺苷的功能。特别是，PEMF 暴露诱导 A _2A和 A _{3的显着上调}不同神经元细胞类型中的腺苷受体。几条证据表明，PEMF 暴露可能在缺血性损伤后发挥神经保护作用。

材料和方法

本综述总结了目前在临床前和临床研究中关于脉冲电磁场​​的作用机制及其对神经元损伤的生物学影响的知识。

结果

PEMFs 在神经元样细胞中抵消缺氧诱导的细胞凋亡和 ROS 产生，并对小胶质细胞发挥强大的抗炎作用。来自中风动物模型的数据显示，PEMFs 暴露能够减小梗塞区域的大小并降低促炎介质的水平。在临床研究中，PEMFs 刺激被证明是安全且耐受性良好的。对急性缺血性卒中患者的初步结果显示，病灶大小呈剂量依赖性减小。

结论

总之，这些数据证明了 PEMFs 对缺血性损伤的几种机制的功效，并表明 PEMFs 可能代表一种新型的非侵入性辅助治疗急性缺血性中风，提供神经保护和减少缺血后的功能缺陷。