Effects of pulsed electromagnetic fields on the A2A adenosine receptor in human degenerative nucleus pulposus cells
10.3760/cma.j.issn.0254-1424.2019.11.004
- VernacularTitle: 脉冲电磁场对人退变髓核细胞A2A腺苷受体的影响
- Author:
Weijun LIU
1
;
Wei WANG
;
Qingbo LI
;
Lei CAI
;
Zhengkun WANG
Author Information
1. Spine Department, Wuhan Puai Hospital, Wuhan 430030, China
- Publication Type:Journal Article
- Keywords:
Pulsed electromagnetic fields;
Adenosine receptors;
Nucleus pulposus cells;
Inflammatory cytokines
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2019;41(11):818-822
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the expression of the A2A adenosine receptor and the inflammatory cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) in human degenerative nucleus pulposus (NP) cells after they have been treated with a pulsed electromagnetic field (PEMF).
Methods:Human degenerative NP cells were cultured in vitro and treated using an 0.8mT PEMF with a pulse frequency of 50Hz. The pulse width was 150μs and the exposure time was 30min, repeated 5 times at 12 hour intervals. The expression of the A2A adenosine receptor in NP cells was determined using western blotting and reverse transcription polymerase chain reactions. The expression of the inflammatory cytokines IL-1β and TNF-α were detected using enzyme-linked immunosorbent assays (ELISA). The human degenerative NP cells were also treated with an antagonist and agonist of the A2A adenosine receptor, and the expression of IL-1β and TNF-α were also determined using ELISA.
Results:After the PEMF treatment the expression of the A2A adenosine receptor increased significantly, while the expression of IL-1β and TNF-α decreased significantly. However, the A2A adenosine receptor antagonist reversed the inhibitory effect of the PEMF on the expression of IL-1β and TNF-α, while the agonist played an opposite role.
Conclusion:A PEMF can significantly inhibit the expression of IL-1β and TNF-α in human degenerative NP cells, which could be related to up-regulation of the expression of the A2A adenosine receptor in those cells.
