| 摘要: |
| 目的：观察推拿按法对痉挛型脑瘫（cerebral palsy，CP）模型大鼠肌痉挛的影响及作用机制。方法：50只SD大鼠采用两阶段随机分组法分为空白组、模型组、按法组、抑制剂组、溶剂组，每组各10只。按法组造模后采用自制推拿按法刺激腱器官，抑制剂组造模后鞘内注射钙/钙调蛋白依赖性蛋白激酶 Ⅱ（calcium-calmodulin - dependent protein kinase Ⅱ，CaMK-Ⅱ）抑制剂，溶剂组造模后鞘内注射二甲基亚砜（dimethyl sulfoxide，DMSO）溶剂。使用改良Ashworth量表评估大鼠肢体痉挛程度，Zea Longa量表评估大鼠神经功能缺损程度，软组织张力仪测定各组大鼠软组织D0.2kg数值，苏木精-伊红染色（Hematoxylin and Eosin Staining，HE）观察大脑锥体束损毁情况和肌肉萎缩情况，免疫组化检测大脑锥体束和脊髓中γ-氨基丁酸（γ-aminobutyric acid，GABA）的平均光密度（average optical density，AOD）值。结果：1）Ashworth量表评分。干预后，与模型组相比，按法组、抑制剂组Ashworth量表评分均显著降低（P<0.01），且按法组、抑制剂组干预前后组内比较，差异有统计学意义（P<0.05）。2）Zea Longa量表评分。干预后，与模型组相比，按法组 Zea Longa量表评分显著降低（P<0.01），且按法组干预前后组内比较，差异有统计学意义（P<0.05）。3）软组织肌张力值。干预前，与空白组相比，模型组D0.2kg数值降低（P<0.01）；干预后，与模型组相比，按法组、抑制剂组、溶剂组D0.2kg数值均显著升高（P<0.01），抑制剂组和溶剂组D0.2kg数值低于按法组（P<0.01）。4）HE病理染色。除空白组外，其余组肌纤维排列紊乱，肌肉组织结构疏松，与正常肌肉组织的紧密排列形成对比，肌间隙稍增宽，肌间可见炎症细胞浸润。在萎缩的肌肉组织中，肌纤维直径变小，横截面积明显减少，细胞形态趋于圆形，伴有炎性细胞浸润。与模型组相比，按法组、抑制剂组、溶剂组锥体束部位神经束和细胞形态均有一定的改善，但仍有细胞肿胀、小囊腔形成，形态改善并不明显。5） GABA的AOD值。与模型组相比，按法组与抑制剂组大鼠锥体束和脊髓中GABA的AOD值均显著增加（P<0.01）。结论：推拿按法刺激腱器官能有效改善痉挛型CP模型大鼠的神经缺损症状和肌痉挛、肌肉萎缩情况，其作用机制可能与影响脑脊髓中抑制性神经递质GABA的含量相关。 |
| 关键词: 痉挛型脑瘫 推拿按法 腱器官 神经缺损 GABA 软组织肌张力 |
| DOI： |
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| Mechanism of action of massage and pressing manipulation in improving myospasm in rats with cerebral palsy based on the GABAergic pathway |
| FAN Hanbo,LAI Yitian,CHEN Heng,LI Jiangshan |
| (1. Hunan University of Chinese Medicine, Changsha 410208, Hunan, China; 2. Hunan Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Changsha 410006, Hunan, China;3. The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha 410005, Hunan, China;1. Hunan University of Chinese Medicine, Changsha 410208, Hunan, China;3. The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha 410005, Hunan, China) |
| Abstract: |
| Objective: To investigate the effect and mechanism of action of massage and pressing manipulation on muscle spasm in a rat model of cerebral palsy （CP）. Methods: A total of 50 Sprague-Dawley rats were divided into blank group, model group, pressing manipulation group, inhibitor group, and solvent group using a two-stage randomization method, with 10 rats in each group. After modeling, the rats in the pressing manipulation group were given stimulation of tendon organ using a self-designed method for massage and pressing manipulation, those in the inhibitor group were given intrathecal injection of calcium/calmodulin-dependent protein kinase II inhibitor, and those in the solvent group were given intrathecal injection of dimethyl sulfoxide solvent. Modified Ashworth Scale was used to assess the degree of limb spasm in rats; Zea Longa scale was used to assess the degree of neurological deficit; a soft tissue tensiometer was used to measure the D0.2kg value of rat soft tissue; HE staining was used to observe pyramidal tract damage and muscle atrophy; immunohistochemistry was used to measure the average optical density （AOD） of γ-aminobutyric acid （GABA） in the pyramidal tract and the spinal cord. Results: As for Ashworth Scale score, compared with the model group after intervention, the pressing manipulation group and the inhibitor group had a significant reduction in Ashworth Scale score （P<0.01）, as well as a significant change in this score after intervention （P<0.05）. As for the score of Zea Longa scale, compared with the model group after intervention, the pressing manipulation group had a significant reduction in the score of Zea Longa scale （P<0.01） and a significant change in this score after intervention （P<0.05）. As for soft tissue tension, before treatment, the model group had a significant reduction in D0.2kg value compared with the blank group （P<0.01）; compared with the model group after intervention, the pressing manipulation group, the inhibitor group, and the solvent group had a significant increase in D0.2kg value （P<0.01）, and the inhibitor group and the solvent group had a significantly lower D0.2kg value than the pressing manipulation group （P<0.01）. HE staining showed that all groups except the blank group had disordered arrangement of muscle fibers and a loose structure of muscle tissue （in comparison to the dense arrangement of normal muscle tissue）, as well as a slightly wider intermuscular space and the presence of intermuscular inflammatory cell infiltration; in the atrophic muscle tissue, there were reductions in the diameter and cross-sectional area of muscle fibers, and cells tended to have a round shape, with the presence of inflammatory cell infiltration; compared with the model group, the pressing manipulation group, the inhibitor group, and the solvent group had certain improvements in the morphology of nerve bundles and cells in the pyramidal tract, with the presence of cell swelling, the formation of small cystic cavity, and a lack of significant improvement in morphology. As for the AOD value of GABA, compared with the model group, the pressing manipulation group and the inhibitor group had a significant increase in the AOD value of GABA in both the pyramidal tract and the spinal cord （P<0.01）. Conclusion: Massage and pressing manipulation for stimulation of tendon organ can effectively improve neurological deficit, muscle spasm, and muscle atrophy in the rat model of spastic CP, possibly by affecting the content of the inhibitory neurotransmitter GABA in the brain and spinal cord. |
| Key words: spastic cerebral palsy massage and pressing manipulation tendon organ neurological deficit γ-aminobutyric acid soft tissue tension |
