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Makale detayı · 2007 · article

Effects of Ascorbic Acid, Alpha-Tocopherol and Allopurinol on Ischemia-Reperfusion Injury in Rabbit Skeletal Muscle: An Experimental Study

Dergi Drug Target Insights
OpenAlex Açık erişim · gold
Yıl2007
Atıf23OpenAlex
Atıf25Semantic Scholar · 1 etkili
Yüzdelik%17,9
FWCI0,01,00 = dünya ortalaması
Scopus (SJR)Q4

Veri kaynağı ayrımı

  • YÖKSİS dergi adıDrug Target Insights
  • OpenAlexOpenAlex zenginleştirmesi (özet, atıf, konular)
  • Semantic Scholaratıf sayısı (OpenAlex ile birleştirilmez)

Özet

OpenAlex İngilizce

PURPOSE: Ischemia reperfusion injury to skeletal muscle, following an acute arterial occlusion is important cause of morbidity and mortality. The aim of the present study was to determine and evaluate the effects of ascorbic acide, alpha-tocopherol and allopurinol on ischemia reperfusion injury in rabbit skeletal muscle. METHODS: Forty-eight New Zealand white rabbits, all male, weighing between 2.5 to 3.0 (mean 2.8) kg, were used in the study. They were separated into four groups. Group I was the control group without any drugs. The other groups were treatment groups (groups II, III, and IV). Group II rabbits administrated 50 mg/kg ascorbic acide and 100 mg/kg alpha-tocopherol 3 days prior to ischemia, group III rabbits received 50 mg/kg allopurinol 2 days prior to ischemia, and group IV rabbits were administrated both 50 mg/kg ascorbic acide, 100 mg/kg alpha-tocopherol 3 days prior to ischemia and 50 mg/kg allopurinol 2 days prior to ischemia. Two hours ischemia and 2 hours reperfusion were underwent to the treatment groups. At the end of the reperfusion periods, muscle samples were taken from rectus femoris muscle for determination of superoxide dismutase, catalase and glutathione peroxidase activities as antioxidant enzymes, and malondialdehyde as an indicator of lipid peroxidation and xanthine oxidase levels as source hydroxyl radical. Besides, histopathological changes (edema, inflammation, ring formation and splitting formation) were evaluated in the muscle specimens. RESULTS: In the treatment groups; superoxide dismutase (U/mgprotein), catalase (U/mgprotein), and glutathione peroxidase (U/mgprotein) levels increased, malondialdehyde (nmol/mgprotein) and xanthine oksidase (mU/mgprotein) levels decreased compared to control I ( p < 0.05). Increase of superoxide dismutase, catalase, and glutathione peroxidase levels were the highest and decrease of malondialdehyde and xanthine oxidase levels were the highest in group IV compared to groups II and III, but no significant as statistically. Also amount of cellular injury in group II, III, and IV were lower than group I. CONCLUSIONS: Antioxidant medication may help lowering ischemia reperfusion injury. In our study, all drug medications are shown to be able to have an effective role for preventing ischemia reperfusion injury. Moreover, ascorbic acide + alpha-tocopherol + allopurinol group (group IV) may have a beneficial effect to decrease the local and systemic damage due to ischemia-reperfusion injury.

Konular

Atıflar

OpenAlex cited_by_count. WoS veya Scopus atıf sayısı değildir; o kaynaklar için ayrı kolon yoktur.

23atıfOpenAlex · cited_by_count (önbellek / veritabanı)

Yerel katalogda bu makaleye atıf yapan 5 yayın (OpenAlex referans eşleşmesi; tam dünya listesi değildir).

  1. 2015 Effect of N acetylcysteine and allopurinol combination to protect spinal cord ischemia reperfusion injury induced by aortic cross clamping in rat modelAtıf 12 · OpenAlex
  2. 2019 Neuroprotective Effects of Allopurinol On Spinal Cord Injury in Rats: A Biochemical and Immunohistochemical StudyAtıf 9 · OpenAlex
  3. 2022 Effects of Ascorbic Acid and Sodium Selenite on Inflammatory Response and Apoptosis in Renal Ischemia-Reperfusion InjuryAtıf 0 · OpenAlex
  4. 2022 Effects of Ascorbic Acid and Sodium Selenite on Inflammatory Response and Apoptosis in Renal Ischemia-Reperfusion InjuryAtıf 0 · OpenAlex
  5. 2022 Effects of Ascorbic Acid and Sodium Selenite on Inflammatory Response and Apoptosis in Renal Ischemia-Reperfusion InjuryAtıf 0 · OpenAlex

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