Pulsed electromagnetic field activation of the A2A adenosine receptors can retard intervertebral disc degeneration
10.3760/cma.j.issn.0254-1424.2023.09.001
- VernacularTitle:脉冲电磁场对椎间盘退行性病变大鼠A2A腺苷受体及p38 MAPK信号通路的影响
- Author:
Qingbo LI
1
;
Lei CAI
;
Zhengkun WANG
;
Weizhi FANG
;
Chuankun ZHOU
;
Yichi ZHOU
;
Zhi YAO
;
Mengcheng WEI
;
Shishuang ZHANG
;
Weijun LIU
Author Information
1. 武汉市第四医院脊柱科，武汉 430030
- Keywords:
Pulsed electromagnetic fields;
A2A adenosine receptor;
p38 MAPK;
Intervertebral discs;
Disc degeneration
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2023;45(9):769-775
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore any effect of pulsed electromagnetic field (PEMF) stimulation on intervertebral disc degeneration (IDD).Methods:Forty Sprague-Dawley rats were randomly divided into a control group, an IDD model group, a PEMF group and an observation group. An IDD model was induced in all except those in the control group. Both the PEMF and observation groups were given PEMF stimulation, while the latter was additionally injected with the A2AR agonist CGS-21680. Eight weeks after the modelling any pathological changes in the morphology of the rats′ intervertebral disc tissues were evaluated using saffron solid green staining. The expression of A2AR, cyclic adenosine phosphate (cAMP), protein kinase A (PKA), cysteine aspartate proteolytic enzyme-3 (Caspase-3), type II collagen (COL-II) and matrix metalloproteinase-3 (MMP3) in the intervertebral discs were evaluated.Results:The nucleus pulposus had shrunk, while fibrous tissues and chondrocytes had increased in the IDD model group. In the observation group the nucleus pulposus was intact and of basically normal shape. A2AR mRNA and protein levels were higher in the intervertebral disc tissue of the model group than among the control group, on average, while the levels in the observation group were significantly higher than in the other groups. In the PEMF and observation groups cAMP and PKA mRNA were significantly higher than in the IDD model group. The p38 MAPK and P-P38 MAPK levels of the IDD model group and its average P-P38 MAPK/p38 MAPK ratio were significantly higher than in the control group. In the PEMF and observation groups those indices had decreased to varying degrees, with those of the observation group significantly lower than among the model and PEMF groups on average, except for the p38 MAPK values. Caspase-3 and its mRNA were significantly higher in the model group than in the control group, on average, and those values were significantly lower in the PEMF and observation groups than in the IDD model group. The average MMP3 contents of the IDD model group had increased significantly compared with the control group, while the Col-Ⅱ level had decreased significantly. Compared with the IDD model group, the MMP3 level had decreased but Col-Ⅱ expression had increased in both the PEMF and observation groups, with significant differences between the IDD model and observation groups.Conclusions:The activation of the p38 MAPK signaling pathway by inflammatory factors to induce apoptosis is one of the important reasons for the aggravation of IDD lesions. PEMF combined with A2AR agonists can activate the A2AR/cAMP/PKA signaling pathway, inhibit p38 MAPK phosphorylation, reduce apoptosis of nucleus pulposus cells, and relieve IDD damage.
