scholarly journals AMELIORATIVE EFFECT OF ASTAXANTHIN ON ISCHEMIA-REPERFUSION INJURY OF SKELETAL MUSCLES

2022 ◽  
Vol 32 (4) ◽  
Keyword(s):  
Reperfusion Injury ◽  
Skeletal Muscles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ameliorative Effect

scholarly journals TLR4/NF-κB-Responsive MicroRNAs and Their Potential Target Genes: A Mouse Model of Skeletal Muscle Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Johnson Chia-Shen Yang ◽  
Shao-Chun Wu ◽  
Cheng-Shyuan Rau ◽  
Yi-Chun Chen ◽  
Tsu-Hsiang Lu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Skeletal Muscles ◽  
Target Genes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Whole Genome ◽  
Potential Target ◽  
Whole Genome Microarray ◽  
Innate Immunity Pathway

Background. The aim of this study was to profile TLR4/NF-κB-responsive microRNAs (miRNAs) and their potential target genes in the skeletal muscles of mice following ischemia-reperfusion injury.Methods. Thigh skeletal muscles of C57BL/6,Tlr4−/−, andNF-κB−/−mice isolated based on femoral artery perfusion were subjected to ischemia for 2 h and reperfusion for 0 h, 4 h, 1 d, and 7 d. The muscle specimens were analyzed with miRNA arrays. Immunoprecipitation with an argonaute 2- (Ago2-) specific monoclonal antibody followed by whole genome microarray was performed to identify mRNA associated with the RNA-silencing machinery. The potential targets of each upregulated miRNA were identified by combined analysis involving the bioinformatics algorithm miRanda and whole genome expression.Results. Three TLR4/NF-κB-responsive miRNAs (miR-15a, miR-744, and miR-1196) were significantly upregulated in the muscles following ischemia-reperfusion injury. The combined in silico and whole genome microarray approaches identified 5, 4, and 20 potential target genes for miR-15a, miR-744, and miR-1196, respectively. Among the 3 genes (Zbed4, Lrsam1,andDdx21) regulated by at least 2 of the 3 upregulated miRNAs,Lrsam1andDdx21are known to be associated with the innate immunity pathway.Conclusions. This study profiled TLR4/NF-κB-responsive miRNAs and their potential target genes in mouse skeletal muscle subjected to ischemia-reperfusion injury.

scholarly journals Tourniquet-induced acute ischemia–reperfusion injury in mouse skeletal muscles: Involvement of superoxide

2011 ◽  
Vol 650 (1) ◽  
pp. 328-334 ◽  
Author(s):  
Thai P. Tran ◽  
Huiyin Tu ◽  
Iraklis I. Pipinos ◽  
Robert L. Muelleman ◽  
Hassan Albadawi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Skeletal Muscles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Ischemia

The effects of iloprost on ischemia-reperfusion injury in skeletal muscles in a rodent model

2014 ◽  
Vol 187 (1) ◽  
pp. 162-168 ◽  
Author(s):  
Tuba Avci ◽  
Dilek Erer ◽  
Aysegul Kucuk ◽  
Yasin Oztürk ◽  
Murat Tosun ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Skeletal Muscles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rodent Model

scholarly journals The ameliorative effect of lutein on ovarian ischemia-reperfusion injury in rats

2018 ◽  
Vol 119 (11) ◽  
pp. 713-717
Author(s):  
C. Turkler ◽  
N. G. Kulhan ◽  
N. Ata ◽  
T. Kiremitli ◽  
F. Keskin Cimen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ameliorative Effect

Role of xanthine oxidase in reperfusion injury of ischemic skeletal muscles in the pig and human

1993 ◽  
Vol 75 (1) ◽  
pp. 246-255 ◽  
Author(s):  
D. Dorion ◽  
A. Zhong ◽  
C. Chiu ◽  
C. R. Forrest ◽  
B. Boyd ◽  
...  
Keyword(s):  
Uric Acid ◽  
Reperfusion Injury ◽  
Xanthine Oxidase ◽  
Acid Content ◽  
Skeletal Muscles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Warm Ischemia ◽  
Muscle Necrosis

We investigated whether xanthine oxidase (XO) is a major source of oxygen-derived free radicals (oxy-radicals) in the pig and human skeletal muscles. It was observed that xanthine dehydrogenase and XO activities in nonischemic pig latissimus dorsi (LD) and gracilis muscles and human LD and rectus abdominis (RA) muscles were < 0.5 mU/g wet wt. The pig LD muscle hypoxanthine content increased significantly from 0.33 +/- 0.02 to 2.33 +/- 0.44 mumol/g dry wt after 5 h of warm ischemia, but the muscle uric acid content remained unchanged up to 2 h of reperfusion. Similarly, the hypoxanthine content in the human LD and RA muscles increased from 0.33 +/- 0.03 to 0.84 +/- 0.23 mumol/g dry wt after 2.0–3.5 h of warm ischemia, and the muscle uric acid content remained unchanged at the end of 15–90 min of reperfusion. Furthermore, 5 days of allopurinol treatment (25 mg/kg iv twice daily) starting 2 days before ischemia or 3 days of oxypurinol treatment (25 mg/kg iv twice daily) starting 15 min before reperfusion did not attenuate the extent of skeletal muscle necrosis in pig LD muscles subjected to 5 h of ischemia and 48 h of reperfusion. However, deferoxamine treatment (250 mg/kg iv twice daily) starting before or after ischemia, as described above, significantly reduced the extent of pig LD muscle necrosis. Finally, at 2 and 48 h of reperfusion significantly higher muscle neutrophil contents were seen in ischemic than in nonischemic control pig LD muscles. Neutrophil depletion with mechlorethamine (0.75 mg/kg iv) significantly reduced the extent of necrosis in pig LD muscles. These observations indicate that XO is not a major source of oxy-radicals in ischemia/reperfusion injury in the pig gracilis and LD muscles and human RA and LD muscles.

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