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Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

机译:手动治疗可降低复杂区域疼痛综合征类型的小鼠模型中的疼痛行为和氧化应激

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Complex regional pain syndrome type I (CRPS-I) is a chronic painful condition. We investigated whether manual therapy (MT), in a chronic post-ischemia pain (CPIP) model, is capable of reducing pain behavior and oxidative stress. Male Swiss mice were subjected to ischemia-reperfusion (IR) to mimic CRPS-I. Animals received ankle joint mobilization 48h after the IR procedure, and response to mechanical stimuli was evaluated. For biochemical analyses, mitochondrial function as well as oxidative stress thiobarbituric acid reactive substances (TBARS), protein carbonyls, antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were determined. IR induced mechanical hyperalgesia which was subsequently reduced by acute MT treatment. The concentrations of oxidative stress parameters were increased following IR with MT treatment preventing these increases in malondialdehyde (MDA) and carbonyls protein. IR diminished the levels of SOD and CAT activity and MT treatment prevented this decrease in CAT but not in SOD activity. IR also diminished mitochondrial complex activity, and MT treatment was ineffective in preventing this decrease. In conclusion, repeated sessions of MT resulted in antihyperalgesic effects mediated, at least partially, through the prevention of an increase of MDA and protein carbonyls levels and an improvement in the antioxidant defense system.
机译:复杂的区域疼痛综合征I型(CRPS-I)是一种慢性痛苦的病情。我们研究了在慢性缺血疼痛(CPIP)模型中的手动治疗(MT)是否能够降低疼痛行为和氧化应激。将雄性瑞士小鼠进行缺血再灌注(IR)以模仿CRPS-I。动物在IR程序后48h接受踝关节动员,并评估对机械刺激的反应。对于生物化学分析,测定了测定了线粒体功能以及氧化应激硫酸酸反应性物质(TBARS),蛋白质羰基,抗氧化酶超氧化物歧化酶(SOD)和过氧化氢酶(猫)水平。 IR诱导机械痛觉过敏,随后通过急性Mt治疗减少。随着MT处理的氧化胁迫参数的浓度增加,防止丙二醛(MDA)和羰基蛋白增加这些增加。 IR减少了SOD和猫活性的水平,并且MT治疗可防止猫的减少,但不存在于SOD活动中。 IR还减少了线粒体复合物活性,并且MT治疗在预防这种下降方面是无效的。总之,MT的重复会话导致至少部分地通过预防MDA和蛋白质羰基水平的增加和抗氧化防御系统的改善而介导的抗震术效应。

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