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Low Dose Aspirin and COX Inhibition in Human Skeletal Muscle
Journal of Applied Physiology ( IF 3.3 ) Pub Date : 2020-10-01 , DOI: 10.1152/japplphysiol.00512.2020
William A Fountain 1 , Masatoshi Naruse 1 , Alex Claiborne 1 , Andrew M Stroh 1 , Kevin J Gries 1 , Andrew M Jones 1 , Kiril Minchev 1 , Bridget E Lester 1 , Ulrika Raue 1 , Scott Trappe 1 , Todd A Trappe 1
Affiliation  

Skeletal muscle health has been shown to benefit from regular consumption of cyclooxygenase (COX) inhibiting drugs. Aspirin, especially at low doses, is one of the most commonly consumed COX inhibitors, yet investigations of low dose aspirin effects on skeletal muscle are nonexistent. The goal of this study was to examine the efficacy of low dose aspirin on skeletal muscle COX production of the inflammatory regulator prostaglandin (PG) E2 at rest and following exercise. Skeletal muscle biopsies (vastus lateralis) were taken from eight individuals (4M, 4W; 25±1y; 81.4±3.4kg; VO2max: 3.33±0.21L/min) before and 3.5 hours after 40 minutes of cycling at 70% of VO2max for the measurement of ex vivo PGE2 production. Muscle strips were incubated in Krebs-Henseleit buffer (control) or supplemented with one of two aspirin concentrations that reflected blood levels following a low (10µM; typical oral dose: 75-325mg) or standard (100µM; typical oral dose: 975-1000mg) dose. Low (-22±5%) and standard (-28±5%) dose aspirin concentrations both reduced skeletal muscle PGE2 production, independent of exercise (P<0.05). There was no difference in PGE2suppression between the two doses (P>0.05). In summary, low dose aspirin levels are sufficient to inhibit the COX enzyme in skeletal muscle and significantly reduce production of PGE2, a known regulator of skeletal muscle health. Aerobic exercise does not appear to alter the inhibitory efficacy of aspirin. These findings may have implications for the tens of millions of individuals that chronically consume low dose aspirin.

中文翻译:

低剂量阿司匹林和COX在人体骨骼肌中的抑制作用

骨骼肌健康已被证明可从定期服用环氧合酶(COX)抑制药物中受益。阿司匹林,尤其是低剂量的阿司匹林,是最常用的COX抑制剂之一,但尚无关于阿司匹林对骨骼肌影响的研究。这项研究的目的是检查低剂量阿司匹林在休息和运动后对炎性调节剂前列腺素(PG)E 2的骨骼肌COX产生的功效。在以40%的心率循环40分钟之前和之后的3.5小时内,从八个人(4M,4W; 25±1y; 81.4±3.4kg; VO 2 max:3.33±0.21L / min)进行骨骼肌活检(外侧血管)。 VO 2 max用于离体PGE 2的测量生产。在Krebs-Henseleit缓冲液(对照)中孵育肌条,或补充两种阿司匹林浓度之一,以反映低(10µM;典型口服剂量:75-325mg)或标准(100µM;典型口服剂量:975-1000mg)后的血液水平)剂量。低剂量(-22±5%)和标准剂量(-28±5%)的阿司匹林浓度均降低了骨骼肌PGE 2的产生,与运动无关(P <0.05)。两种剂量之间的PGE 2抑制没有差异(P> 0.05)。总之,低剂量的阿司匹林水平足以抑制骨骼肌中的COX酶并显着降低PGE 2的产生,骨骼肌健康的已知调节剂。有氧运动似乎并未改变阿司匹林的抑制作用。这些发现可能对数千万长期服用低剂量阿司匹林的个体有影响。
更新日期:2020-10-02
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