التفاصيل البيبلوغرافية
| العنوان: |
银质针导热治疗肌筋膜疼痛综合征大鼠骨骼肌线粒体和 SIRT3 表达的变化. (Chinese) |
| العنوان البديل: |
Effects of silver needle-thermal conduction therapy on skeletal muscle mitochondria and silent information regulator homolog 3 expression in a rat model of myofascial pain syndrome. (English) |
| المؤلفون: |
王 玥, 张玉函, 王家益, 黄媛馨, 沃春新, 王彩霞, 周沛然, 王 林 |
| المصدر: |
Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 5/18/2024, Vol. 28 Issue 14, p2202-2208, 7p |
| مصطلحات موضوعية: |
PAIN threshold, MYOFASCIAL pain syndromes, TRANSMISSION electron microscopes, TRANSMISSION electron microscopy, SPRAGUE Dawley rats, METABOLIC disorders |
| الملخص (بالإنجليزية): |
BACKGROUND: Clinical studies have found good analgesic effects of silver needle-thermal conduction therapy in patients with myofascial pain syndrome, but the exact mechanism remains unclear. OBJECTIVE: To observe the effect of silver needle-thermal conduction therapy on silent information regulator homolog 3 (SIRT3) changes and mitochondrial ultrastructure in a rat model of myofascial pain syndrome. METHODS: Twenty rats were randomly selected from 26 Sprague-Dawley rats and were subjected to percussion combined with motor fatigue for replicating the rat model of myofascial pain syndrome. Sixteen rats that were successfully modeled were randomly divided into model group and silver needle-thermal conduction therapy group (treatment group), with eight rats in each group. The remaining rats were used as controls (normal group). The treatment group was treated with silver needle-thermal conduction therapy. Mechanical withdrawal threshold and thermal withdrawal latency of rats were measured at 1 day before modeling, 1 day after modeling and 14 days after treatment. Electromyographic activities of the right medial femoral muscle were measured at 14 days after treatment. The right medial femoral muscle tissue was taken for hematoxylin-eosin staining to observe the local morphology and for transmission electron microscopy to observe the mitochondrial ultrastructure. Western blot assay was performed to detect SIRT3 expression. RESULTS AND CONCLUSION: Pain threshold: The mechanical withdrawal threshold and thermal withdrawal latency of the model and treatment groups were significantly decreased compared with those in the normal group and before modeling (P < 0.01). After treatment, the mechanical withdrawal threshold and thermal withdrawal latency of rats were significantly higher in the treatment group compared with the model group (P < 0.01). Electromyography: The rats in the model group showed spontaneous electrical activity in the right medial femur, while the rats in the treatment group showed reduced spontaneous electrical activity, longer time frame (P < 0.01) and lower wave amplitude (P < 0.05) compared with the model group. Hematoxylin-eosin staining: In the normal group, rat muscle fibers arranged closely and regularly. In the model group, the muscle fibers of rats were atrophied, degenerated, and disordered in arrangement. In the treatment group, rat muscle structure disorder improved. Mitochondrial microstructure: Under the transmission electron microscope, mitochondrial structure in the normal group was normal; mitochondrial swelling with broken or disappeared cristae appeared in the model group; mitochondrial swelling in the treatment group was obviously relieved or tended to be normal. SIRT3 expression: SIRT3 expression was significantly downregulated in the model group compared with the normal group, but was significantly upregulated in the treatment group compared with the model group (P < 0.05). To conclude, abnormalities in local muscle mitochondria and downregulation of SIRT3 expression suggest the presence of impaired energy metabolism in the rat model of myofascial pain syndrome. Mitochondrial changes recover and are close to normal after the silver needle-thermal conduction therapy, and the expression of SIRT3 is also upregulated close to the normal group, indicating the silver needle-thermal conduction therapy may play a therapeutic role by promoting mitochondrial repair and improving energy metabolism disorder. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
背景: 临床研究发现银质针导热治疗对肌筋膜疼痛综合征患者具有良好镇痛作用, 但其具体机制仍不清楚. 目的: 观察银质针导热治疗对肌筋膜疼痛综合征大鼠线粒体超微结构和沉默信息调节因子同源蛋白3变化的影响. 方法: 26只大鼠随机取20只予以打击结合运动疲劳的方法复制肌筋膜疼痛综合征大鼠模型, 造模成功的16只大鼠随机分为模型组和银质 针导热组, 每组各8只; 银质针导热组给予银质针导热处理; 剩余6只为正常对照. 分别于造模前1 d、造模完成后第1天、银质针导热处理 后第14天检测大鼠机械刺激缩足阈值、热缩足潜伏期; 银质针导热处理后第14天检测大鼠股内侧肌肌电图电活动, 取大鼠右侧股内侧肌分 别进行苏木精-伊红染色观察局部形态、透射电镜观察线粒体超微结构、Western blot检测沉默信息调节因子同源蛋白3表达. 结果与结论: ①痛阈值: 与正常组和造模前相比, 模型组、银质针导热组造模后机械刺激缩足阈值和热缩足潜伏期显著缩短(P < 0.01); 经 银质针导热处理后, 与模型组相比, 银质针导热组机械刺激缩足阈值和热缩足潜伏期显著延长(P < 0.01); ②肌电图: 模型组大鼠右侧股内 侧出现自发电活动, 银质针导热组自发电活动较模型组减少, 时限较模型组延长(P < 0.01), 波幅较模型组降低(P < 0.05); ③苏木精-伊红 染色: 正常组大鼠肌纤维排列紧密规则, 模型组大鼠肌纤维萎缩、变性, 排列紊乱, 银质针导热组大鼠肌肉结构紊乱改善; ④骨骼肌线粒 体微观结构: 透射电镜显示正常组肌组织线粒体结构正常; 模型组肌组织线粒体肿胀, 嵴断裂或消失; 银质针导热组肌组织线粒体肿胀明 显缓解或趋于正常; ⑤沉默信息调节因子同源蛋白3表达: 模型组较正常组明显下调, 银质针导热组较模型组明显上调(P < 0.05); ⑥结果 表明: 肌筋膜疼痛综合征大鼠局部肌肉线粒体出现异常, 沉默信息调节因子同源蛋白3的表达下调, 提示存在能量代谢障碍; 银质针导热 处理后线粒体变化恢复, 接近正常, 且沉默信息调节因子同源蛋白3的表达上调接近正常组, 推测银质针导热疗法可能通过促进线粒体修 复而改善能量代谢障碍发挥治疗作用. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
