Soltow Quinlyn A, Betters Jenna L, Sellman Jeff E, Lira Victor A, Long Jodi H D, Criswell David S
Center for Exercise Science, University of Florida, Gainesville, 32611, USA.
Med Sci Sports Exerc. 2006 May;38(5):840-6. doi: 10.1249/01.mss.0000218142.98704.66.
We sought to determine whether cyclooxygenase (COX) activity is necessary for overload-induced growth of adult rat skeletal muscle, and whether nitric oxide synthase (NOS) activity is involved in upregulation of COX messenger RNA (mRNA) expression in skeletal muscle.
Unilateral surgical removal of the gastrocnemius and soleus was performed on the right hindlimb of 16 female Sprague-Dawley rats (approximately 230 g) to induce chronic overload (OL) of the plantaris for 14 d, with sham surgeries performed on the contralateral leg as a normally loaded (NL) control. Half of the rats were treated with the nonspecific COX inhibitor, ibuprofen (0.2 mg.mL(-1) in drinking water; approximately 20 mg.kg(-1).d(-1)). In a second experiment, the plantaris was unilaterally overloaded for 5 or 14 d in male rats (approximately 350 g; N = 16 rats per time point) and half of the animals were treated with the NOS inhibitor, L-NAME (0.75 mg.mL(-1) in drinking water; approximately 90 mg.kg(-1).d(-1)).
Ibuprofen treatment inhibited plantaris hypertrophy by approximately 50% (P < 0.05) following 14 d of OL, as did L-NAME treatment (P < 0.05). COX-1 and COX-2 mRNA did not differ between any groups at 5 d. At 14 d, however, L-NAME caused a 30-fold increase in plantaris COX-1 mRNA expression independent of loading condition. Additionally, OL induced a 20-fold increase in COX-2 mRNA expression compared with NL (P < 0.05) at 14 d, without affecting COX-1 mRNA level. L-NAME treatment significantly inhibited OL-induced expression of COX-2 mRNA.
COX activity is important for in vivo muscle hypertrophy, and plantaris overload is associated with NOS activity-dependent COX-2 expression.
我们试图确定环氧化酶（COX）活性对于成年大鼠骨骼肌超负荷诱导生长是否必要，以及一氧化氮合酶（NOS）活性是否参与骨骼肌中COX信使核糖核酸（mRNA）表达的上调。
对16只雌性斯普拉格-道利大鼠（约230克）的右后肢进行腓肠肌和比目鱼肌的单侧手术切除，以诱导跖肌慢性超负荷（OL）14天，对侧腿进行假手术作为正常负荷（NL）对照。一半的大鼠用非特异性COX抑制剂布洛芬（饮用水中0.2毫克·毫升⁻¹；约20毫克·千克⁻¹·天⁻¹）治疗。在第二个实验中，雄性大鼠（约350克；每个时间点n = 16只大鼠）的跖肌单侧超负荷5天或14天，一半的动物用NOS抑制剂L-NAME（饮用水中0.75毫克·毫升⁻¹；约90毫克·千克⁻¹·天⁻¹）治疗。
OL 14天后，布洛芬治疗使跖肌肥大抑制约50%（P < 0.05），L-NAME治疗也有同样效果（P < 0.05）。5天时，各实验组间COX-1和COX-2 mRNA无差异。然而，14天时，L-NAME使跖肌COX-1 mRNA表达增加30倍，且与负荷情况无关。此外，与NL相比，OL在14天时使COX-2 mRNA表达增加20倍（P < 0.05），而不影响COX-1 mRNA水平。L-NAME治疗显著抑制OL诱导的COX-2 mRNA表达。
COX活性对体内肌肉肥大很重要，跖肌超负荷与NOS活性依赖性COX-2表达相关。
