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首页> 外文期刊>Endocrine Research >Effects of alpha-tocopherol on diabetes-induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle.
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Effects of alpha-tocopherol on diabetes-induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle.

机译：α-生育酚对糖尿病诱导的鼠背屈肌突触传递和收缩功能改变的影响。

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Diabetes mellitus affects skeletal muscle and free radicals may be implicated in the manifestation of diabetes complications. The present study investigated effects of alpha-tocopherol on diabetic dorsiflexor muscle via recording resting membrane potentials (RMPs), endplate potentials (EPPs), miniature endplate potentials (MEPPs) and isometric twitch tensions. Forty mice were divided randomly into two groups (n = 20). One group served as control and the other was injected once with streptozotocin (STZ) solution (60 mg/kg, i.p) to induce diabetes. The animals were then divided further into two subgroups (n = 10). Alpha-tocopherol (100 mg/kg, i.p) was administered daily to one control and one diabetic group for 3 weeks prior to recording day. Experiments were conducted 4 weeks following diabetes induction. Isometric twitch tension was measured in anaesthetized mice (2 mg/g urethane, i.p) via a transducer connected to a computer system. Resting membrane potentials and MEPPs were measured by utilizing the intracellular recording method. Compared to control, diabetic mice showed reduced twitch tension (4.4 +/- 0.4 g control vs. 2.5 +/- 0.3 g diabetic) and demonstrated delayed half time of decay. Diabetic flexor muscle also displayed significant reduction in MEPPs frequencies with no changes in RMPs. Alpha-tocopherol reversed tension reduction in diabetic mice (from 2.5 +/- 0.3 to 3.8 +/- 0.4 g), impacted delayed half time of decay and reversed reduction in MEPPs frequencies. Alpha-tocopherol exerts a protective role against diabetes-induced peripheral muscle dysfunction. This effect is probably mediated via a free radical scavenging mechanism or modification of Ca2+ homeostasis.
机译：糖尿病影响骨骼肌，自由基可能与糖尿病并发症的表现有关。本研究通过记录静息膜电位（RMPs），终板电位（EPPs），微型终板电位（MEPPs）和等距抽搐张力来研究α-生育酚对糖尿病背屈肌的影响。 40只小鼠随机分为两组（n = 20）。一组作为对照，另一组注射一次链脲佐菌素（STZ）溶液（60 mg / kg，腹腔注射）以诱发糖尿病。然后将动物进一步分为两个亚组（n = 10）。在记录日之前的3周内，每天向1个对照组和1个糖尿病组施用α-生育酚（100 mg / kg，腹膜内）。诱导糖尿病后4周进行实验。通过连接到计算机系统的传感器，在麻醉的小鼠（2 mg / g氨基甲酸酯，腹腔内）中测量等距抽搐张力。利用细胞内记录法测量静息膜电位和MEPPs。与对照组相比，糖尿病小鼠的抽搐张力降低（对照组为4.4 +/- 0.4 g，而糖尿病为2.5 +/- 0.3 g），并且衰减了一半。糖尿病屈肌也显示出MEPP频率显着降低，而RMP没有变化。 α-生育酚可逆转糖尿病小鼠的张力降低（从2.5 +/- 0.3到3.8 +/- 0.4 g），影响延迟的半衰期延迟和MEPPs频率的降低。 α-生育酚对糖尿病引起的周围肌肉功能障碍具有保护作用。此作用可能是通过自由基清除机制或Ca2 +稳态的修饰介导的。

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