title: Effect of ischemia post-conditioning on skeletal muscle oxidative injury, mTOR, Bax, Bcl-2 proteins expression, and HIF-1α/β-actin mRNA, IL-6/β-actin mRNA and caveolin-3/β-actin mRNA expression in ischemia-reperfusion rabbits.
abstract: This study is designed to investigate the effect of ischemia post-conditioning on IR-induced skeletal muscle injury in limbs of experimental rabbits. Rabbits are randomized to one of the following three groups: sham control, ischemic reperfusion, ischemic postconditioning. The lipid peroxidation level, antioxidant enzymes activities, skeletal muscle mammalian target of rapamycin (mTOR), Bax, Bcl-2 proteins expression and Bcl-2/Bax, and HIF-1α/β-actin mRNA, interleukin-6 (IL-6)/β-actin mRNA and caveolin-3/β-actin mRNA expression were tested in the current study. The results suggested that ischemic postconditioning might decrease lipid peroxidation level, lactic dehydrogenase (LDH), creatine kinase (CK) activities, Bcl-2 proteins expression and Bcl-2/Bax, HIF-1α/β-actin mRNA expression and increase skeletal muscle antioxidant enzymes activities, Bax protein expression and IL-6/β-actin mRNA and caveolin-3/β-actin mRNA expression. These indicated that protective effect of ischemic postconditioning against IR-induced skeletal muscle injury involve into a complex molecular mechanism. Our research results may offer a theoretical guidance for therapy of related clinical diseases.
authors.affiliation: Hands and Feet Microsurgery, Dalian Municipal Central Hospital, Dalian 116033, China. lianghdsyln@yahoo.com.cn
authors.forename: Haidong
authors.initials: H
authors.lastname: Liang
authors.forename: Fang
authors.initials: F
authors.lastname: Yu
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Tong
authors.forename: Bo
authors.initials: B
authors.lastname: Yuan
authors.forename: Chunsheng
authors.initials: C
authors.lastname: Wang
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D002374:Catalase / Q000378:metabolism; D051244:Caveolin 3 / Q000235:genetics; D005978:Glutathione / Q000378:metabolism; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D057775:Ischemic Postconditioning; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism*; D010084:Oxidation-Reduction; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D015427:Reperfusion Injury / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000199:Actins; D051244:Caveolin 3; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D015850:Interleukin-6; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D002374:Catalase; D013482:Superoxide Dismutase; D058570:TOR Serine-Threonine Kinases; D005978:Glutathione