目的观察推拿按法对慢性激痛点模型大鼠骨骼肌超微结构的影响,探讨推拿按法对慢性激痛点的治疗作用。方法将健康雄性SD大鼠随机分为空白组、模型组、按法组、利多卡因组,每组6只。采用钝性打击结合离心运动方式建立慢性激痛点大鼠模型...目的观察推拿按法对慢性激痛点模型大鼠骨骼肌超微结构的影响,探讨推拿按法对慢性激痛点的治疗作用。方法将健康雄性SD大鼠随机分为空白组、模型组、按法组、利多卡因组,每组6只。采用钝性打击结合离心运动方式建立慢性激痛点大鼠模型。按法组大鼠予按法刺激局部激痛点,隔天治疗1次,每次7.5 min,共治疗7次;利多卡因组大鼠予0.5 mL的1%利多卡因注射液治疗,6 d 1次,共治疗3次。2周干预结束后,采用HE染色观察各组大鼠骨骼肌显微结构变化;采用透射电镜观察各组大鼠骨骼肌组织超微结构变化。结果(1)光镜下,模型组可见异常梭形形态肌纤维,表现为中间膨大,两端变窄,伴大量炎症细胞浸润和核内移现象;与模型组比较,按法组和利多卡因组均可见肌纤维粗细均匀、排列较整齐,炎症细胞减少。(2)电镜下,模型组肌原纤维排列紊乱,大量肌纤维断裂、破损,线粒体数量减少,结构异常,出现肿胀变圆、嵴结构减少或呈空泡状;按法组和利多卡因组表现接近,与模型组比较,肌原纤维排列趋于整齐,线粒体数量增多,结构恢复正常,呈细长杆状和卵圆形,或出现融合形态。各组肌节长度测量结果显示,模型组与空白组比较,肌节长度明显缩短,差异有显著统计学意义(P<0.01);模型组与按法组、利多卡因组比较,差异有统计学意义(P<0.05)。结论慢性激痛点病理特征为骨骼肌肌节挛缩、线粒体结构和数量受损。按法治疗能够舒张挛缩的肌节、促进线粒体的损伤修复,起到对慢性激痛点的去活化作用。展开更多
目的通过观察按法干预对激痛点骨骼肌细胞骨架α微管蛋白(α-tubulin)和微管相关蛋白4(microtubule-associated protein 4,MAP-4)的影响,探讨按法的舒筋解结作用。方法40只SPF级雄性大鼠随机分为空白组10只和激痛点造模大鼠30只,采用钝...目的通过观察按法干预对激痛点骨骼肌细胞骨架α微管蛋白(α-tubulin)和微管相关蛋白4(microtubule-associated protein 4,MAP-4)的影响,探讨按法的舒筋解结作用。方法40只SPF级雄性大鼠随机分为空白组10只和激痛点造模大鼠30只,采用钝性打击结合离心运动的方法建立大鼠激痛点模型,模型评价后将符合标准的20只大鼠随机分为模型组和按法组,每组10只。空白组和模型组不予按法干预,仅正常观察,按法组以自制按法刺激器干预14 d。干预结束后在激痛点局部取材,用Western blot和免疫荧光双染法检测α-tubulin和MAP-4。结果α-tubulin和MAP-4在肌细胞和细胞外基质均有一定的共表达,空白组α-tubulin和MAP-4主要分布在肌细胞膜与细胞质,分布连续性较好,模型组α-tubulin分布连续性和完整性欠佳,在肌细胞内表达减少,在细胞外基质表达增加,MAP-4在肌细胞和细胞外基质表达均增加,两者在按法组有一定改善。与空白组相比,模型组α-tubulin表达下降、MAP-4表达升高(P<0.05);与模型组相比,按法组α-tubulin表达升高、MAP-4表达下降(P<0.05)。结论按法的舒筋解结作用可能与抑制微管蛋白解聚并促进其合成有关。展开更多
Objective To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points(MTrPs)by observing the effects of An-Pressing manipulation on adenosine triphosphate(ATP),...Objective To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points(MTrPs)by observing the effects of An-Pressing manipulation on adenosine triphosphate(ATP),adenosine 5′-monophosphate(AMP)-activated protein kinase(AMPK)/peroxisome proliferator-activated receptorγcoactivator 1α(PGC-1α)pathway and mitochondrial ultrastructure of skeletal muscle cells in MTrPs rats.Methods Forty-eight male Sprague-Dawley rats were randomly divided into a blank group,a model group,a lidocaine group,and an An-Pressing manipulation group,with 12 rats in each group.The model group,lidocaine group and An-Pressing manipulation group were used to replicate the MTrPs rat model by blunt shock and centrifugal motion method.After modeling,the An-Pressing manipulation group was subjected to 7 times An-Pressing manipulation,once every other day;the lidocaine group was treated with 3 times of injection of lidocaine at the MTrPs,once every 6 d.The blank group and the model group were fed normally without intervention.After the intervention,local muscle tissue was taken to detect the content of ATP and the expression of AMPK,phosphorylated AMPK(phospho-AMPK),PGC-1α,and glucose transporter 4(GluT4),and the ultrastructure of mitochondria was observed under an electron microscope.Results Compared with the blank group,the ATP content in the model group was decreased(P<0.05),the protein expression levels of phospho-AMPK,PGC-1α,and GluT4 and the ratio of phospho-AMPK to AMPK were decreased(P<0.05);under the electron microscope,the number of mitochondria decreased,and they were deformed,small in volume,and had deformed cristae.Compared with the model group,the ATP contents in the An-Pressing manipulation group and the lidocaine group were increased(P<0.05),and the protein expression levels of phospho-AMPK,PGC-1α,and GluT4 and the ratio of phospho-AMPK to AMPK were increased(P<0.05);under the electron microscope,the number of mitochondria increased,the shape and size of the mitochondria were basically normal,and the cristae could be seen.Compared with the lidocaine group,phospho-AMPK and the ratio of phospho-AMPK to AMPK in the An-Pressing manipulation group were increased(P<0.05);under the electron microscope,the numbers of mitochondria were similar,and the shape and size of the mitochondria were basically normal without swelling,and the cristae could be observed.Conclusion An-Pressing manipulation can increase the ATP content in MTrPs tissue,improve the expression levels of PGC-1α and GluT4 proteins and the ratio of phospho-AMPK to AMPK;its mechanism may relate to the activation of AMPK/PGC-1α signaling pathway to promote the repair of mitochondrial damages.展开更多
Objective:To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signa...Objective:To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signal-regulated kinase(ERK)/nuclear factor-κB(NF-κB)pathway.Methods:Fifty male Sprague-Dawley rats were randomly divided into a blank group,a model group,a pressing manipulation group,an ERK agonist group,and a pressing manipulation+ERK agonist group,with 10 rats in each group.Except for the blank group,rats in other groups were used to establish the trigger point rat model using the blunt blow combined with the eccentric exercise method.The pressing manipulation group underwent pressing manipulation intervention at the trigger points.The ERK agonist group received an injection of recombinant human epidermal growth factor via the tail vein.The pressing manipulation+ERK agonist group received interventions from both the pressing manipulation and ERK agonist groups.The pressure pain threshold(PPT)was measured by a mechanical pain threshold detector before and after the intervention.The histological changes were evaluated by hematoxylin-eosin staining after the intervention;the expression levels of ERK,phosphorylated ERK(p-ERK),NF-κB p65(p65),phosphorylated NF-κB p65(p-p65),and phosphorylated NF-κB inhibitor(p-IκB)were detected by Western blotting;the levels of interleukin(IL)-1β,IL-6,and tumor necrosis factor(TNF)-αwere detected by enzyme-linked immunosorbent assay.Results:The PPT increased(P<0.05);the inflammatory cells disappeared;the ratios of p-ERK/ERK,p-p65/p65,and p-IκB/β-actin,also the levels of IL-1β,IL-6,and TNF-αall decreased in the pressing manipulation group after the intervention compared with the model group(P<0.05).The PPT decreased significantly(P<0.05),the inflammatory cell presence increased,and the ratios of p-ERK/ERK and p-p65/p65 were elevated(P<0.05);additionally,the levels of IL-6 and TNF-αwere significantly higher in the pressing manipulation+ERK agonist group compared with the pressing manipulation group(P<0.05).The PPT was significantly lower(P<0.05),the inflammatory cell count was higher,the ratios of p-ERK/ERK and p-IκB/β-actin and the levels of IL-1βand TNF-αwere significantly higher in the ERK agonist group compared with the pressing manipulation+ERK agonist group(P<0.05).Conclusion:Pressing manipulation can effectively alleviate inflammation and pain in trigger point model rats,potentially by inhibiting the ERK/NF-κB signaling pathway.展开更多
文摘目的观察推拿按法对慢性激痛点模型大鼠骨骼肌超微结构的影响,探讨推拿按法对慢性激痛点的治疗作用。方法将健康雄性SD大鼠随机分为空白组、模型组、按法组、利多卡因组,每组6只。采用钝性打击结合离心运动方式建立慢性激痛点大鼠模型。按法组大鼠予按法刺激局部激痛点,隔天治疗1次,每次7.5 min,共治疗7次;利多卡因组大鼠予0.5 mL的1%利多卡因注射液治疗,6 d 1次,共治疗3次。2周干预结束后,采用HE染色观察各组大鼠骨骼肌显微结构变化;采用透射电镜观察各组大鼠骨骼肌组织超微结构变化。结果(1)光镜下,模型组可见异常梭形形态肌纤维,表现为中间膨大,两端变窄,伴大量炎症细胞浸润和核内移现象;与模型组比较,按法组和利多卡因组均可见肌纤维粗细均匀、排列较整齐,炎症细胞减少。(2)电镜下,模型组肌原纤维排列紊乱,大量肌纤维断裂、破损,线粒体数量减少,结构异常,出现肿胀变圆、嵴结构减少或呈空泡状;按法组和利多卡因组表现接近,与模型组比较,肌原纤维排列趋于整齐,线粒体数量增多,结构恢复正常,呈细长杆状和卵圆形,或出现融合形态。各组肌节长度测量结果显示,模型组与空白组比较,肌节长度明显缩短,差异有显著统计学意义(P<0.01);模型组与按法组、利多卡因组比较,差异有统计学意义(P<0.05)。结论慢性激痛点病理特征为骨骼肌肌节挛缩、线粒体结构和数量受损。按法治疗能够舒张挛缩的肌节、促进线粒体的损伤修复,起到对慢性激痛点的去活化作用。
文摘目的通过观察按法干预对激痛点骨骼肌细胞骨架α微管蛋白(α-tubulin)和微管相关蛋白4(microtubule-associated protein 4,MAP-4)的影响,探讨按法的舒筋解结作用。方法40只SPF级雄性大鼠随机分为空白组10只和激痛点造模大鼠30只,采用钝性打击结合离心运动的方法建立大鼠激痛点模型,模型评价后将符合标准的20只大鼠随机分为模型组和按法组,每组10只。空白组和模型组不予按法干预,仅正常观察,按法组以自制按法刺激器干预14 d。干预结束后在激痛点局部取材,用Western blot和免疫荧光双染法检测α-tubulin和MAP-4。结果α-tubulin和MAP-4在肌细胞和细胞外基质均有一定的共表达,空白组α-tubulin和MAP-4主要分布在肌细胞膜与细胞质,分布连续性较好,模型组α-tubulin分布连续性和完整性欠佳,在肌细胞内表达减少,在细胞外基质表达增加,MAP-4在肌细胞和细胞外基质表达均增加,两者在按法组有一定改善。与空白组相比,模型组α-tubulin表达下降、MAP-4表达升高(P<0.05);与模型组相比,按法组α-tubulin表达升高、MAP-4表达下降(P<0.05)。结论按法的舒筋解结作用可能与抑制微管蛋白解聚并促进其合成有关。
文摘Objective To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points(MTrPs)by observing the effects of An-Pressing manipulation on adenosine triphosphate(ATP),adenosine 5′-monophosphate(AMP)-activated protein kinase(AMPK)/peroxisome proliferator-activated receptorγcoactivator 1α(PGC-1α)pathway and mitochondrial ultrastructure of skeletal muscle cells in MTrPs rats.Methods Forty-eight male Sprague-Dawley rats were randomly divided into a blank group,a model group,a lidocaine group,and an An-Pressing manipulation group,with 12 rats in each group.The model group,lidocaine group and An-Pressing manipulation group were used to replicate the MTrPs rat model by blunt shock and centrifugal motion method.After modeling,the An-Pressing manipulation group was subjected to 7 times An-Pressing manipulation,once every other day;the lidocaine group was treated with 3 times of injection of lidocaine at the MTrPs,once every 6 d.The blank group and the model group were fed normally without intervention.After the intervention,local muscle tissue was taken to detect the content of ATP and the expression of AMPK,phosphorylated AMPK(phospho-AMPK),PGC-1α,and glucose transporter 4(GluT4),and the ultrastructure of mitochondria was observed under an electron microscope.Results Compared with the blank group,the ATP content in the model group was decreased(P<0.05),the protein expression levels of phospho-AMPK,PGC-1α,and GluT4 and the ratio of phospho-AMPK to AMPK were decreased(P<0.05);under the electron microscope,the number of mitochondria decreased,and they were deformed,small in volume,and had deformed cristae.Compared with the model group,the ATP contents in the An-Pressing manipulation group and the lidocaine group were increased(P<0.05),and the protein expression levels of phospho-AMPK,PGC-1α,and GluT4 and the ratio of phospho-AMPK to AMPK were increased(P<0.05);under the electron microscope,the number of mitochondria increased,the shape and size of the mitochondria were basically normal,and the cristae could be seen.Compared with the lidocaine group,phospho-AMPK and the ratio of phospho-AMPK to AMPK in the An-Pressing manipulation group were increased(P<0.05);under the electron microscope,the numbers of mitochondria were similar,and the shape and size of the mitochondria were basically normal without swelling,and the cristae could be observed.Conclusion An-Pressing manipulation can increase the ATP content in MTrPs tissue,improve the expression levels of PGC-1α and GluT4 proteins and the ratio of phospho-AMPK to AMPK;its mechanism may relate to the activation of AMPK/PGC-1α signaling pathway to promote the repair of mitochondrial damages.
文摘Objective:To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signal-regulated kinase(ERK)/nuclear factor-κB(NF-κB)pathway.Methods:Fifty male Sprague-Dawley rats were randomly divided into a blank group,a model group,a pressing manipulation group,an ERK agonist group,and a pressing manipulation+ERK agonist group,with 10 rats in each group.Except for the blank group,rats in other groups were used to establish the trigger point rat model using the blunt blow combined with the eccentric exercise method.The pressing manipulation group underwent pressing manipulation intervention at the trigger points.The ERK agonist group received an injection of recombinant human epidermal growth factor via the tail vein.The pressing manipulation+ERK agonist group received interventions from both the pressing manipulation and ERK agonist groups.The pressure pain threshold(PPT)was measured by a mechanical pain threshold detector before and after the intervention.The histological changes were evaluated by hematoxylin-eosin staining after the intervention;the expression levels of ERK,phosphorylated ERK(p-ERK),NF-κB p65(p65),phosphorylated NF-κB p65(p-p65),and phosphorylated NF-κB inhibitor(p-IκB)were detected by Western blotting;the levels of interleukin(IL)-1β,IL-6,and tumor necrosis factor(TNF)-αwere detected by enzyme-linked immunosorbent assay.Results:The PPT increased(P<0.05);the inflammatory cells disappeared;the ratios of p-ERK/ERK,p-p65/p65,and p-IκB/β-actin,also the levels of IL-1β,IL-6,and TNF-αall decreased in the pressing manipulation group after the intervention compared with the model group(P<0.05).The PPT decreased significantly(P<0.05),the inflammatory cell presence increased,and the ratios of p-ERK/ERK and p-p65/p65 were elevated(P<0.05);additionally,the levels of IL-6 and TNF-αwere significantly higher in the pressing manipulation+ERK agonist group compared with the pressing manipulation group(P<0.05).The PPT was significantly lower(P<0.05),the inflammatory cell count was higher,the ratios of p-ERK/ERK and p-IκB/β-actin and the levels of IL-1βand TNF-αwere significantly higher in the ERK agonist group compared with the pressing manipulation+ERK agonist group(P<0.05).Conclusion:Pressing manipulation can effectively alleviate inflammation and pain in trigger point model rats,potentially by inhibiting the ERK/NF-κB signaling pathway.
