Electroacupuncture attenuates degeneration by upregulating of aquaporins via the cAMP/PKA pathway in a rabbit model of disc degeneration

Abstract

Abstract Background Intervertebral disc degeneration(IVDD) is characterized extracellular matrix (ECM) decrease and water loss which is one of the main causes of LBP. Electroacupuncture (EA) has long been used to release low back pain with IVDD. To investigate whether EA can upregulate aquaporins(APQs) in IVDD via the cAMP/PKA pathway in a rabbit model of disc degeneration. methods A homemade loading device was adapted to induce a disc degeneration model. After 28 days, EA treatment was performed. Magnetic resonance imaging (MRI), diffusion weighted imaging (DWI), and diffusion tensor imaging (DTI) were performed to evaluate the AQP content and water diffusion.The AQP protein expression in discs was observed by Western blotting and immunofluorescence staining (IFC). Using linear correlation analysis, the relationship between radiology images and AQPs contains was measured. The levels of cAMP and PKA were examined by using ELISA, and the expressions of AQPs and the cAMP/PKA signaling pathway and its related molecules were examined by using quantitative reverse transcription PCR (qRT-PCR) and Western blot analysis. Results EA intervention decreased the MRI grades, fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values. IFC showed an apparent increase in AQP 1 and 3 immunoreactions after EA intervention. MRI grades negatively correlated with the AQP1, 3 protein content, but a positive correlation was found between FA and ADC value and AQP protein expression. The levels of cAMP and PKA were significantly increased after EA intervention in rabbits with IDD. The mRNA and protein expression levels of AQP1 and 3, p-CREB, eIF-2, Actin, MAP1A, MAP1B, MAP2, MAP4, and Tau were significantly decreased in the model group as compared with the sham group, and the expression levels were partially restored after EA intervention. Conclusion EA may attenuate degeneration through regulating the AQPs expression, which may be mediated by the cAMP/PKA pathway.