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目的:观察严重烧伤后大鼠骨骼肌功能变化，探讨Janus激酶/信号转导与转录激活子3（JAK/STAT3）通路抑制剂对骨骼肌功能的影响及可能的机制。方法:采用实验研究方法。取120只8周龄雄性Wistar大鼠，按随机数字表法分为假伤组、单纯烧伤组和烧伤+JAK/STAT3抑制剂组，每组40只，后2组大鼠于背部、腹部造成50%体表总面积 Ⅲ度烫伤，假伤组大鼠致假伤。烧伤+JAK/STAT3抑制剂组大鼠腹腔注射JAK/STAT3抑制剂鲁索替尼。伤后0、1、4、7、14 d，每组取8只大鼠，采用多通道电生理仪测量脉冲频率20、40、60、80、100、120、140、160 Hz刺激最佳肌肉长度的趾长伸肌产生的比力，测量脉冲频率50 Hz刺激0、10、20、30、60、120、180、240、300 s的最佳肌肉长度的趾长伸肌疲劳期比力，采用紫外分光光度法检测趾长伸肌羰基化合物含量，采用微量法检测趾长伸肌ATP含量。对数据行析因设计方差分析、Bonferroni检验、n t检验。n 结果:（1）与假伤组比较，单纯烧伤组大鼠伤后0、1、7 d各脉冲频率，伤后4 d除20 Hz外，伤后14 d于20、40 Hz脉冲频率刺激后趾长伸肌比力均显著下降（n P＜0.05或n P＜0.01）。与单纯烧伤组相比，烧伤+JAK/STAT3抑制剂组大鼠伤后1 d除20 Hz外，伤后4、7、14 d各脉冲频率刺激后趾长伸肌比力显著升高（n P＜0.05或n P＜0.01）。（2）与假伤组比较，单纯烧伤组大鼠除伤后7 d刺激240 s外趾长伸肌疲劳期比力显著下降（n P＜0.05或n P＜0.01）。与单纯烧伤组比较，烧伤+JAK/STAT3抑制剂组大鼠伤后1 d除刺激60、300 s外，伤后4 d除刺激240 s外，伤后7、14 d所有刺激时间点疲劳期比力显著升高（n P＜0.05或n P＜0.01）。 （3）单纯烧伤组大鼠伤后0、1、4、7、14 d趾长伸肌羰基化合物含量为（0.651±0.155）（0.739±0.194）（0.618±0.086）（0.813±0.162）（0.615±0.115）nmol/mg，明显高于假伤组的（0.196±0.019）（0.156±0.004）（0.169±0.023）（0.156±0.027）（0.175±0.008）nmol/mg（n t=7.219、6.491、10.938、9.182、11.589，n P＜0.01）和烧伤+JAK/STAT3抑制剂组的（0.538±0.069）（0.369±0.059）（0.273±0.061）（0.334±0.109）（0.318±0.101）nmol/mg（n t=2.446、4.689、8.355、5.754、6.097，n P＜0.05或n P＜0.01）。（4）单纯烧伤组大鼠伤后1、4、7、14 d趾长伸肌中ATP含量明显低于假伤组（n t=7.159、7.591、7.473、4.026，n P＜0.01）和烧伤+JAK/STAT3抑制剂组（n t=2.295、2.575、2.453、2.997，n P＜0.05）。n 结论:严重烧伤后大鼠趾长伸肌在不同频率脉冲刺激后比力显著下降，且易于疲劳；阻断JAK/STAT3信号通路可通过降低肌蛋白氧化应激和增加ATP含量，进而减轻烧伤引起的肌力下降，改善其疲劳期肌力下降。“,”Objective:To observe the functional changes of skeletal muscle in severely burned rats, and investigate the possible effects and mechanisms of Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway inhibitors on skeletal muscle function.Methods:The experiment research method was applied. One hundred and twenty male Wistar rats of 8-weeks-old were divided into sham injury group, simple burn group, and burn+JAK/STAT3 inhibitor group according to the random number table, with 40 rats in each group. Rats in simple burn group and burn+JAK/STAT3 inhibitor group were inflicted with 50% total body surface area full-thickness scald in back and abdomen, and rats in sham injury group were sham injured. Rats in burn+JAK/STAT3 inhibitor group were intraperitoneally injected with JAK/STAT3 inhibitor ruxolitinib. On post injury day (PID) 0, 1, 4, 7, and 14, 8 rats in each group were used to measure the specific force generated by extensor digitorum longus in optimal length stimulated with pulse frequency of 20, 40, 60, 80, 100, 120, 140, 160 Hz using a multichannel electrophysiological instrument, and specific force in fatigue period of extensor digitorum longus in optimal length stimulated with pulse frequency of 50 Hz for 0, 10, 20, 30, 60, 120, 180, 240, 300 s. On PID 0, 1, 4, 7, and 14, carbonyl compound content of extensor digitorum longus was determined by ultraviolet spectrophotometry, and ATP content of extensor digitorum longus was determined by micrometry. Data were statistically analyzed with analysis of variance for factorial design, Bonferroni test, and n t test.n Results:(1) Compared with sham injury group, specific forces of extensor digitorum longus of rats in simple burn group were significantly decreased after stimulated with all the pulse frequency on PID 0, 1, 7, and all the pulse frequency except for 20 Hz on PID 4, and pulse frequency of 20 and 40 Hz on PID 14 (n P<0.05 orn P<0.01). Compared with simple burn group, specific forces of extensor digitorum longus of rats in burn+JAK/STAT3 inhibitor group were significantly increased after stimulated with all pulse frequency except for 20 Hz on PID 1 and all the pulse frequency on PID 4, 7, and 14 (n P<0.05 orn P<0.01). (2) Compared with sham injury group, specific forces of extensor digitorum longus of rats in simple burn group were significantly decreased in fatigue period at all the stimulation time points except for 240 s on PID 7 (n P<0.05 orn P<0.01). Compared with simple burn group, specific forces of extensor digitorum longus of rats in burn+JAK/STAT3 inhibitor group were significantly increased in fatigue period at all stimulation time points except for 240 s on PID 4, and all stimulation time points on PID 7 and 14 (n P<0.05 orn P<0.01). (3) The carbonyl compound content of extensor digitorum longus of rats in simple burn group on PID 0, 1, 4, 7, and 14 was (0.651±0.155), (0.739±0.194), (0.618±0.086), (0.813±0.162), (0.615±0.115) nmol/mg, which were significantly higher than (0.196±0.0190, (0.156±0.004), (0.169±0.023) (0.156±0.027), (0.175±0.008) nmol/mg of rats in simple burn group (n t=7.219, 6.491, 10.938, 9.182, 11.589, n P<0.01) and (0.538±0.069), (0.369±0.059), (0.273±0.061), (0.334±0.109), (0.318±0.101) nmol/mg of rats in burn+JAK/STAT3 inhibitor group (n t=2.446, 4.689, 8.355, 5.754, 6.097, n P<0.05 orn P<0.01). (4) The ATP content in extensor digitorum longus of rats in simple burn group on PID 1, 4, 7, and 14 was significantly lower than that in sham injury group (n t=7.159, 7.591, 7.473, 4.026, n P<0.01) and burn+JAK/STAT3 inhibitor group (n t=2.295, 2.575, 2.453, 2.997, n P<0.05).n Conclusions:After severe burn, the specific force of extensor digitorum longus in rat decreased significantly after stimulated with different pulse frequencies, and the extensor digitorum longus in rat was prone to fatigue. Blocking the JAK/STAT3 signaling pathway could reduce the oxidative stress of muscle protein and increase ATP content, thereby reducing the muscle strength decline caused by burn and improving the muscle strength decline during fatigue.