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目的:通过测试萎缩骨骼肌细胞Caspase-3、SOD活性和MDA含量,观察补充扇贝肽对运动大鼠停训导致骨骼肌萎缩后肌细胞Caspase-3活性及其抗氧化能力的影响,研究扇贝肽对停训后骨骼肌萎缩的干预作用。方法:40只SD雄性大鼠以15 m/min的速度,持续性水平跑台训练30 min开始进行递增负荷运动,运动6 d/周,休息1 d/周,速度递增3 m/min/周,时间递增30 min/周,运动3周后即刻处死10只大鼠为基础对照组,其余大鼠随机分组为补充安慰剂阴性对照组、补充牛乳阳性对照组和补充扇贝肽实验组,30只大鼠左侧后肢实施石膏固定模拟停训模型,并进行扇贝肽补充实验。实验组和对照组所有动物每天分别进行灌胃15%扇贝肽饮料2mL、等量的安慰剂和牛乳。结果:发现补充扇贝肽可显著减低停训后萎缩骨骼肌细胞MDA含量增加,增加SOD活性,提高细胞内抗氧化能力,可显著抑制停训后萎缩骨骼肌细胞Caspase-3的活性,从而抑制骨骼肌收缩蛋白和结构蛋白的降解,促进萎缩骨骼肌的恢复。  相似文献   
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Several genetic loci have been associated with risk of Achilles tendon pathology (ATP) within South African and Australian populations. The aim of this study was, therefore, to evaluate eight previously implicated genetic variants in an independent British population. A total of 130 asymptomatic controls (CON) and 112 participants clinically diagnosed with ATP comprising 87 individuals with chronic Achilles tendinopathy (TEN) and 25 with Achilles tendon ruptures (RUP) were included. All participants were genotyped for variants within the COL5A1, MIR608, IL-1β, IL-6 and CASP8 genes. Primary findings implicated COL5A1 and CASP8. Three inferred allele combinations constructed from COL5A1 rs12722, rs3196378 and rs71746744 were identified as risk modifiers. The T–C–D combination was associated with increased risk of ATP (= 0.023) and RUP (< 0.001), the C–A–I combination was associated with increased risk of ATP (= 0.011), TEN (P = 0.011) and RUP (= 0.011) and the C–C–D combination was associated with decreased risk of ATP (= 0.011) and RUP (= 0.004). The CASP8 rs3834129 DD genotype was associated with decreased risk of TEN (= 0.020, odds ratio: 0.45, 95% confidence interval: 0.22–0.90) and the CASP8 I–G (rs3834129–rs1045485) inferred allele combination was associated with increased risk of TEN (= 0.031). This study further highlights the importance of polymorphisms within COL5A1 and CASP8 in the aetiology of ATP.  相似文献   
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