Journals / European Journal of Therapeutics / 2020 / Cilt: 26 - Sayı: 1

Immunosuppressants and Ischemic Postconditioning in the Management of Brain Ischemia in Rats: The Role of Pharmacologic and Nonpharmacologic Treatments

Pages
53–60
Publication Date
2022-10-12
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Although the curative effects of postconditioning treatment on brain injury were documented, the lengths of the postconditioning cycles are important for its efficacy.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Ischemic postconditioning in limb skeletal muscle may decrease the size of the cerebral hypoperfused area after stroke.
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Key Findings & Data:Global cerebral ischemia was induced by clamping the bilateral common carotid arteries for 20 min, and subsequently reperfusion was allowed for 2 h.
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Conclusion & Impact:Although the curative effects of postconditioning treatment on brain injury were documented, the lengths of the postconditioning cycles are important for its efficacy.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Ischemic postconditioning in limb skeletal muscle may decrease the size of the cerebral hypoperfused area after stroke. We compared the effects of ischemic postconditioning with the effects of the pharmacologic agents infliximab and leflunomide in the management of stroke.Methods: Thirty-two rats were divided into four groups: postconditioning, infliximab, leflunomide, and saline (control). Global cerebral ischemia was induced by clamping the bilateral common carotid arteries for 20 min, and subsequently reperfusion was allowed for 2 h. Rats in the infliximab group received 7 mg/kg of infliximab immediately after and 6 h after the induction of stroke. Rats in the leflunomide group received 10 mg/kg of leflunomide immediately after and 6 h after the induction of stroke. In the postconditioning group, the unilateral limb muscle was clamped for 180 min immediately after the induction of stroke, and subse-quently reperfusion was allowed for 120 min. Rats in the control group received saline immediately after and 6 h after the induc-tion of stroke. Glutathione peroxidase, malondialdehyde, and ischemia-modified albumin were measured, and histopathologic evaluation of cerebral tissue was performed.Results: The area of hemorrhage was significantly decreased in the infliximab group. Loss of the gray matter–white matter bound-ary was significantly decreased in the infliximab and leflunomide groups. Brain glutathione peroxidase was significantly increased in the infliximab group. There were no significant differences between the infliximab, leflunomide, and postconditioning groups and the control group in serum malondialdehyde and ischemia-modified albuminConclusion: Immunosuppression by infliximab and leflunomide, but not ischemic postconditioning, may attenuate brain isch-emia–reperfusion injury. Although the curative effects of postconditioning treatment on brain injury were documented, the lengths of the postconditioning cycles are important for its efficacy.

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Cite This Article

KOCA, T., AYKAN, D. A., KAZANCI, Ü., URAL, A., SEYİTHANOĞLU, M., YILDIZ, B. T. (2022). Immunosuppressants and Ischemic Postconditioning in the Management of Brain Ischemia in Rats: The Role of Pharmacologic and Nonpharmacologic Treatments. European Journal of Therapeutics, Cilt: 26 - Sayı: 1, 53–60. https://ajindex.com/articles/511795

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References (1)

  1. Deb P, Sharma S, Hassan KM. Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis. Pathophysiology 2010; 17: 197-218. [CrossRef ] 2. Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage. Neuropharmacology 2008; 55: 310-8. [CrossRef ] 3. Yang J, Liu C, Du X, Liu M, Ji X, Du H, et al. Hypoxia Inducible Factor 1α Plays a Key Role in Remote Ischemic Preconditioning Against Stroke by Modulating Inflammatory Responses in Rats. J Am Heart Assoc 2018; 7: pii e007589.[CrossRef ] 4. Wegener S, Gottschalk B, Jovanovic V, Knab R, Fiebach JB, Schellinger PD, et al; MRI in Acute Stroke Study Group of the German Compe-tence Network Stroke. Transient ischemic attacks before ischemic stroke: preconditioning the human brain? A multicenter magnetic resonance imaging study. Stroke 2004; 35: 616-21. [CrossRef ] 5. Keep RF, Wang MM, Xiang J, Hua Y, Xi G. Is there a place for cere-bral preconditioning in the clinic? Transl Stroke Res 2010; 1: 4-18. [CrossRef ] 6. Zhou HJ, Li H, Shi MQ, Mao XN, Liu DL, Chang YR, et al. Protective Effect of Klotho against Ischemic Brain Injury Is Associated with Inhibition of RIG-I/NF-κB Signaling. Front Pharmacol 2018; 8: 950. [CrossRef ] 7. Ergün Y, Üremiş M, Kılınç M, Alıcı T. Antioxidant effect of Legalon(r) SIL in ischemia-reperfusion injury of rat skeletal muscle. Acta Cir Bras 2016; 31: 264-70. [CrossRef ] 8. Arango-Dávila CA, Vera A, Londoño AC, Echeverri AF, Cañas F, Cardo-zo CF, et al. Soluble or soluble/membrane TNF-α inhibitors protect the brain from focal ischemic injury in rats. Int J Neurosci 2015; 125: 936-40.[CrossRef ] 9. Maddahi A, Kruse LS, Chen QW, Edvinsson L. The role of tumor ne-crosis factor-α and TNF-α receptors in cerebral arteries following ce-rebral ischemia in rat. J Neuroinflammation 2011; 8: 107. [CrossRef ] 10. Sumbria RK, Boado RJ, Pardridge WM. Brain protection from stroke with intravenous TNFα decoy receptor-Trojan horse fusion protein. J Cereb Blood Flow Metab 2012; 32: 1933-8. [CrossRef ] 11. Barygina W, Becatti M, Soldi G, Prignano F, Lotti T, Nassi P, et al. Al-tered redox status in the blood of psoriatic patients: involvement of NADPH oxidase and role of anti TNF- α theraphy. Redox Rep 2013; 18: 100-6. [CrossRef ] 12. Guven C, Borcek AO, Cemil B, Kurt G, Yildirim Z, Ucankus NL, et al. Neuroprotective effects of infliximab in experimental spinal cord ischemic injury. J Clin Neurosci 2010; 17: 1563-7. [CrossRef ]