地塞米松诱导的危重病性肌病大鼠骨骼肌p62和泛素的表达

doi:10.13418/j.issn.1001-165x.2014.05.021

中国临床解剖学杂志 ›› 2014, Vol. 32 ›› Issue (5): 599-603.doi: 10.13418/j.issn.1001-165x.2014.05.021

地塞米松诱导的危重病性肌病大鼠骨骼肌p62和泛素的表达

屈惠莹¹，　包翠芬¹，　于迪²，　李季¹，　宋欧荻¹，　秦书俭¹

1.辽宁医学院人体解剖与组织胚胎学教研室，辽宁锦州 121000； 2辽宁医学院畜牧兽医学院，辽宁锦州　121000

收稿日期:2014-04-25 出版日期:2014-09-25 发布日期:2014-10-14
通讯作者: 秦书俭，教授，博士生导师，E-mail： qinshujian@lnmu.edu.cn E-mail:qhy811@qq.com
作者简介:屈惠莹（1987-）女，辽宁本溪人，在读研究生，研究方向：危重病性肌病发病机制，Tel：18640616351
基金资助:
辽宁省教育厅科学技术创新团队课题 (2009A462）；国家自然科学基金（31170930， 81202783）

Expression of p62 and ubiquitin in dexamethasone-induced rat critical illness myopathy

QU Hui-ying¹, BAO Cui-fen¹, YU Di², LI Ji ¹, SONG Ou-di ¹, QIN Shu-jian ¹

1.Department of Human Anatomy & Histology and Embryology, Liaoning Medical University, Jinzhou 121000, Liaoning Province, China；2.Animal Husbandry and Veterinary College，Liaoning Medical University, Jinzhou 121000, Liaoning Province, China

Received:2014-04-25 Online:2014-09-25 Published:2014-10-14

摘要/Abstract

摘要：

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。

关键词: 地塞米松, 危重病性肌病, p62, 泛素

Abstract:

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.

Key words: Dexamethasone, Critical illness myopathy, p62, Ubiquitin

中图分类号:

R746
R977.1

屈惠莹, 包翠芬, 于迪, 李季, 宋欧荻, 秦书俭. 地塞米松诱导的危重病性肌病大鼠骨骼肌p62和泛素的表达[J]. 中国临床解剖学杂志, 2014, 32(5): 599-603.

JUE Hui-Ying, BAO Cui-Fen, XU Di, LI Ji, SONG Ou-Di, QIN Shu-Jian. Expression of p62 and ubiquitin in dexamethasone-induced rat critical illness myopathy[J]. Chinese Journal of Clinical Anatomy, 2014, 32(5): 599-603.

参考文献

[1]Baum P，Bercker S，Villmann T，et al. Critical illness myopathy and neuropathy (CR -IMYN). Electroneurographic classification
[J].Nervenarzt, 2011, 82(4):468-474.

[2]Stevens R D，Hart N，de-Jonghe B，et al. Weakness in the ICU:a call to action
[J].Crit Care, 2009,13(6):1002.

[3] Schefold JC，Bierbrauer J，Weber-Carstens S. Intensive care unit-acquired weak -ness (ICUAW) and muscle wasting in critically ill patients with severe sepsis and septic shock
[J]. J Cachexia Sarcopenia Muscle,2010,1(2):147-157.

[4] Yewdell JW，Antonl C，Bennink JR. Defective ribosomal products (DRiPs): a major source of antigenic peptides for MHC classⅠmolecules
[J] ? J Immunol,1996,157(5):1823-1826.

[5] Rich MM，Pinter MJ. Crucial role of sodium channel fact inactivation in muscle fibre inexcitability in a rat model of critical illness myopathy
[J].J Physiol, 2003, 547(Pt 2):555-566.

[6]袁静，梁佳，赵颂, 等.地塞米松诱导的危重病性肌病的细胞死亡方式
[J].第三军医大学学报，2012，34（5）：453-455.

[7]袁静，梁佳，赵颂, 等.地塞米松诱导的危重病性肌病中PKC、PKB/Akt 及NF-κB p65 的表达
[J].广东医学，2012，33（14）:2065-2067.

[8] 包翠芬, 袁静，梁佳等. 大剂量地塞米松诱导的脑细胞死亡机制
[J]. 中国临床解剖学杂志, 2013 , 31(2):184-187.

[9] Ichimura Y, Komatsu M. Selective degradation of p62 by autophagy
[J]. Semin Immunopathol , 2010, 32(4):431-436.

[10] 黄新敏，张艳霞，万小荣,等.泛素蛋白的研究进展
[J].广东农业科学，2010,37(6):191-197.

[11] Myeku N, Figueiredo-Pereira ME. Dynamics of the degradation of ubiquitinated proteins by proteasomes and autophagy: association with sequestosome1/p62
[J]. J Biol Chem, 2011, 286(25): 22426-22440.

[12]靳航.自噬与泛素-蛋白酶体系统在实验性脑出血灶周组织损伤中作用的研究
[D].吉林长春：吉林大学，2013.

地塞米松诱导的危重病性肌病大鼠骨骼肌p62和泛素的表达

Expression of p62 and ubiquitin in dexamethasone-induced rat critical illness myopathy

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