目的　探讨危重病性肌病大鼠骨骼肌自噬相关因子p62和泛素的表达情况。  方法　将健康SD大鼠分为对照组和实验组；实验组又分为7、9、11 d 3个时相点（n=10）。实验组采用5 mg/kg地塞米松连续腹腔注射，每天1次，对照组腹腔注射等量的生理盐水。采用肌功能缺损评分判定肌功能缺损情况。利用免疫组化和Western blot检测骨骼肌自噬相关因子p62和泛素的表达情况。  结果　与对照组相比，实验组大鼠出现不同程度肌肉功能缺损症状，以11 d时大鼠缺损程度最为严重。免疫组化检测结果显示，对照组骨骼肌纤维可见少量泛素阳性表达细胞，无p62阳性细胞表达，实验组肌纤维胞质中可见明显p62和泛素表达，随时间延长表达量逐渐减少，以11 d时相点降低表达最为明显。 Western blot也证实了同一趋势。  结论　地塞米松诱导的大鼠CIM可能通过抑制p62和泛素的表达从而发挥对细胞自噬的调节作用。

Objective　To investigate the expression of critical illness myopathy on autophagy-related factors p62 and ubiquitin in rat skeletal muscle.　Method　SD rats were divided into control and experimental groups; Experimental groups were divided into groups of 7, 9, 11d time points （n=10. Rats in experimental groups recerved intraperitoneal injection of dexamethasone 5 mg/kg once daily, and the healthy control group received intraperitoneal injection of normal saline. Muscle function were determined by muscle function impairment score. By immunohistochemistry and Western blot analysis the expression of skeletal muscle autophagy-related factors p62 and ubiquitin were determined.　Results　Compared with rats in the control group, rats in the experimental group demonstrated a varying degrees of muscle function impairment symptoms, with impairment most serious in rats in 11d point group. Immunohistochemistry showed visible expression of ubiquitin-positive cells and no p62-positive cells in a small group of skeletal muscle fibers. In the experimental group, a small amount of p62 and ubiquitin were expressed in the muscle fibers; the expression of p62 and ubiquitin was reduced the most obviously at 11d point. Western blot confirmed the same trend.　Conclusion　p62 and ubiquitin may play an important role in cell autophagy of skeletal muscle in critical illness myopathy in rats.