摘要
Objective: To investigate the effect and significance of electroacupuncture (EA) on neuronal apoptosis and hindlimb motor and bladder functional improvement in rats with acute spinal cord injury (SCI). Methods: Sixty healthy Sprague Dawley rats were randomly assigned to sham, model, EA, and EA control groups (n = 15 each). EA group rats received EA treatment at Zhibian and Shuidao acupoints seven times daily, whereas EA control group rats received EA at two points, 0.5 cm away from Zhibian and Shuidao, respectively. Histomorphological changes in spinal cord tissue were examined using hematoxylin-eosin staining. Neuronal apoptosis was detected by TUNEL assay. Bcl-2, Bax, and Bad protein levels were detected using immunohistochemistry. Additionally, hindlimb motor function, residual urine volume and maximum bladder capacity were measured. Results: HE staining revealed a morphologically and structurally intact spinal cord in the EA group, and the tissue contained scattered blood cells without edema. In the EA control group, there were small morphological defects in the spinal cord, and the tissue contained fewer blood cells with local edema. Compared with the EA control and model groups, Bax and Bad levels were significantly decreased in the EA group and Bcl-2 expression was increased (P < 0.05). After SCI, hindlimb function scores, residual urine volume, and maximum bladder capacity in rats of the EA group significantly differed from those of the EA control group (P < 0.05). Conclusion: EA may induce SCI-induced improvements in hindlimb motor and bladder functions by affecting neuronal apoptosis and relevant gene expression changes.
Objective: To investigate the effect and significance of electroacupuncture (EA) on neuronal apoptosis and hindlimb motor and bladder functional improvement in rats with acute spinal cord injury (SCI). Methods: Sixty healthy Sprague Dawley rats were randomly assigned to sham, model, EA, and EA control groups (n = 15 each). EA group rats received EA treatment at Zhibian and Shuidao acupoints seven times daily, whereas EA control group rats received EA at two points, 0.5 cm away from Zhibian and Shuidao, respectively. Histomorphological changes in spinal cord tissue were examined using hematoxylin-eosin staining. Neuronal apoptosis was detected by TUNEL assay. Bcl-2, Bax, and Bad protein levels were detected using immunohistochemistry. Additionally, hindlimb motor function, residual urine volume and maximum bladder capacity were measured. Results: HE staining revealed a morphologically and structurally intact spinal cord in the EA group, and the tissue contained scattered blood cells without edema. In the EA control group, there were small morphological defects in the spinal cord, and the tissue contained fewer blood cells with local edema. Compared with the EA control and model groups, Bax and Bad levels were significantly decreased in the EA group and Bcl-2 expression was increased (P < 0.05). After SCI, hindlimb function scores, residual urine volume, and maximum bladder capacity in rats of the EA group significantly differed from those of the EA control group (P < 0.05). Conclusion: EA may induce SCI-induced improvements in hindlimb motor and bladder functions by affecting neuronal apoptosis and relevant gene expression changes.
