Pulsed Electromagnetic Fields Reduce Interleukin-6 Expression in Intervertebral Disc Cells Via Nuclear Factor-κβ and Mitogen-Activated Protein Kinase p38 Pathways.


Author: Tang X1, Coughlin D1, Ballatori A1, Berg-Johansen B1, Waldorff EI2, Zhang N2, Ryaby JT2, Aliston T1, Lotz JC1

Affiliation: <sup>1</sup>Department of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA.

<sup>2</sup>Orthofix Inc., Lewisville, TX.
Conference/Journal: Spine (Phila Pa 1976).
Date published: 2019 Nov 15
Other:
 Volume ID: 44   ,  Issue ID: 22   ,  Pages: E1290-E1297   ,  Special Notes: doi: 10.1097/BRS.0000000000003136.   ,  Word Count: 279  
    STUDY DESIGN: This is an in vitro study of bovine disc cells exposed to pulsed electromagnetic fields.



OBJECTIVE: The purpose of the present study was to investigate whether pulsed electromagnetic fields (PEMF) effects on the expression of interleukin-6 (IL-6) expression is mediated by two known inflammation regulators, nuclear factor-κB (NF-κβ) and phosphorylated mitogen-activated protein kinase p38 (p38-MAPK) signaling pathways SUMMARY OF BACKGROUND DATA.: Inflammatory cytokines play a dominant role in the pathogenesis of disc degeneration. Increasing evidence showed that PEMF, a noninvasive biophysical stimulation, can have physiologically beneficial effects on inflammation and tissue repair. Our previous research shows that PEMF treatment can reduce IL-6 expression by intervertebral disc cells. However, the underlying mechanisms of PEMF action are yet to be uncovered.



METHODS: Intervertebral disc nuclear pulposus cells were challenged with interleukin-1α (IL-1α) (for mimicking inflammatory microenvironment) and treated with PEMF simultaneously up to 4 hours. Cells were then collected for NF-κβ and phosphorylated p38-MAPK protein detection with Western blot. Additionally, the RelA (p65) subunit of NF-κβ was examined with immunostaining for assessment of NF-κβ activation.



RESULTS: As expected, Western blot results showed that both NF-κβ and phosphorylated p38 expression were significantly increased by IL-1α treatment. This induction was significantly inhibited to control condition levels by PEMF treatment. Immunostaining demonstrated similar trends, that PEMF treatment reduced the NF-κβ activation induced by IL-1α exposure.



CONCLUSION: Our data indicate that the previously-reported inhibitory effect of PEMF treatment on disc inflammation is mediated by NF-κβ and phosphorylated p38-MAPK signaling pathways. These results further establish PEMFs anti-inflammatory activity, and may inform potential future clinical uses for management of inflammation associated with disc degeneration.



LEVEL OF EVIDENCE: N/A.



PMID: 31689248  DOI: 10.1097/BRS.0000000000003136