Journal of Rehabilitation Medicine 51-11 | Page 40

J Rehabil Med 2019; 51: 854–860 ORIGINAL REPORT EVALUATION OF THE EFFECTS OF EXTREMELY LOW FREQUENCY ELECTROMAGNETIC FIELD ON THE LEVELS OF SOME INFLAMMATORY CYTOKINES IN POST-STROKE PATIENTS Natalia CICHON, PhD 1 , Joanna SALUK-BIJAK, PhD 1 , Elzbieta MILLER, MD 2 , Tomasz SLIWINSKI, PhD 3 , Ewelina SYNOWIEC, PhD 3 , Paulina WIGNER, MSc 3 and Michal BIJAK, MD 1 From the 1 Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, 2 Department of Neurological Rehabilitation, Medical University of Lodz and 3 Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland Background: Activation of immunologically compe- tent cells results in the overproduction of pro-in- flammatory factors, and causes progression of nerve tissue damage. However, the potential neuroprotec- tive effects of these factors in brain damage have not been well investigated. Objective: To evaluate the effect of extremely low frequency electromagnetic field (ELF-EMF) treat- ment on the molecular mechanism of inflammatory cytokine activity in post-stroke patients. Methods: All patients underwent the same rehabili- tation program, but the ELF-EMF group were also gi- ven ELF-EMF treatment. Both groups have been used in our previous studies. In order to determine the plasma level of cytokines, the levels of interleukin 1β (IL-1β), interleukin 2 (IL-2), interferon-γ (INF-γ) and transforming growth factor β (TGF-β) were eva- luated, and the level of IL-1β mRNA expression was determined. Results: After ELF-EMF treatment, both IL-1β plasma level and IL-1β mRNA expression level, as well as IL-2 plasma level increased, while IFN-γ and TGF-β levels did not change. Conclusion: The increased expression of IL-1β found in this study may be a response to ELF-EMF stimula- tion. It is hypothesized that a neuroprotective role of this cytokine may occur due to IL-1β-dependent regulation of neurotrophic factors. Further research is needed to explore this hypothesis. Key words: extremely low frequency electromagnetic field treatment; interleukin 1; stroke; rehabilitation. Accepted Oct 29, 2019; Epub ahead of print Nov 5, 2019 J Rehabil Med 2019: 51: 854–860 Correspondence address: Michal Bijak, Department of General Bio- chemistry, University of Lodz, Pomorska 141/143 90-236 Lodz, Poland. E-mail: [email protected] R ehabilitation is probably one of the most important phases of recovery for many stroke patients. The effect of stroke usually enforces the necessity of the relearning process. Rehabilitation can improve basal functions after stroke because of the neuroplastic abi- lity of the brain. The term “brain plasticity” encompas- ses all the modifications in the organization of neural components occurring in the central nervous system. LAY ABSTRACT During stroke, overproduction of pro-inflammatory fac- tors occurs, which leads to the progression of brain da- mage. However, current knowledge indicates that these factors may also impact on protective processes in brain tissue, but this has not been well investigated. This stu- dy evaluated the effect of extremely low frequency elec- tromagnetic field treatment on the molecular mecha- nism of inflammatory cytokine activity in patients after stroke. A total of 48 patients were included in the study and were divided into 2 groups. Both groups have been used in our previous studies. All patients underwent the same rehabilitation program, but the study group also given magnetotherapy. Levels of interleukin 1β plas- ma, interleukin 1β mRNA expression, and interleukin 2 plasma increased after magnetotherapy. The increased expression of interleukin 1β may be a response to elec- tromagnetic field stimulation, and it is possible that this cytokine has a neuroprotective role; however, further research is needed to explore this hypothesis Neuronal plastic phenomena is likely to be at the basis of learning and adaptive modifications in response to anatomical or functional deficit or brain damage (1). The destruction of neural networks stimulates reorgani- zation of the connections and this modification process is regulated by neurotrophic factors (2). The mechanisms underlying network reorganization and regaining of basal functions in stroke patients are incompletely understood. The process of neurogenesis is regulated by many factors, including neurotrophins, growth factors, neurotransmitters and microenvironmen­ tal factors (3). Recent investigations have reported that these mechanisms could involve immune responses. The inflammatory reaction that is initiated in the peripheral blood immediately after stroke, due to the response to phenomena occurring in the area of acute ischaemia, affects the normal development of plastic changes (4). It is known that the activation of immunologically competent cells results in the overproduction of pro- inflammatory factors, which are responsible for pro- gression of neurodegenerative diseases (5), but their potential effects on neuroprotection have not been well investigated in neurodegenerative diseases. Little is known about endogenous regulatory immune mecha- nisms involved in neuro-restoration. However, some re- This is an open access article under the CC BY-NC license. www.medicaljournals.se/jrm doi: 10.2340/16501977-2623 Journal Compilation © 2019 Foundation of Rehabilitation Information. ISSN 1650-1977