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通过尿中3-甲基组氨酸排泄量测定大鼠类固醇肌病中的肌原纤维蛋白分解代谢。

Myofibrillar protein catabolism in rat steroid myopathy measured by 3-methylhistidine excretion in the urine.

作者信息

Shoji S

机构信息

Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan.

出版信息

J Neurol Sci. 1989 Nov;93(2-3):333-40. doi: 10.1016/0022-510x(89)90203-7.

Abstract

The fractional rate of breakdown of myofibrillar protein in rat skeletal muscle was measured during subcutaneous cortisone acetate treatment (10 mg/100 g body weight per day). The daily urinary excretion of 3-methylhistidine divided by the 3-methylhistidine pool of the skeletal muscle was used to determine the fractional breakdown rate of myofibrillar protein. The mean fractional breakdown rate remained within the normal range throughout the first 5 days, but decreased significantly from the 16th day of treatment. When the daily 3-methylhistidine excretion was divided by the creatinine excretion, the rate showed the same trend of change. These results strongly suggest that the loss of myofibrillar protein induced by cortisone administration is not caused by increased breakdown but by decreased synthesis.

摘要

在皮下注射醋酸可的松(每天10毫克/100克体重)治疗期间,测定了大鼠骨骼肌中肌原纤维蛋白的分解率。用骨骼肌中3-甲基组氨酸的每日尿排泄量除以3-甲基组氨酸池来确定肌原纤维蛋白的分解率。在前5天,平均分解率保持在正常范围内,但从治疗第16天起显著下降。当每日3-甲基组氨酸排泄量除以肌酐排泄量时,该比率呈现相同的变化趋势。这些结果有力地表明,可的松给药引起的肌原纤维蛋白丢失不是由分解增加所致,而是由合成减少所致。

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