Effect of Dose-Related Astaxanthin on Rats with Cerebral Ischemia-Reperfusion

Bengi Yeğin; Semih Öz; Dilek Burukoğlu Dönmez; Hilmi Özden; Mehmet Cengiz Üstüner; Sibel Canbaz Kabay; Ferruh Yücel

Research Article

Astaksantin'in Serebral İskemi-Reperfüzyonlu Sıçanlarda Doza Bağlı Etkisi

Year 2023, Volume: 4 Issue: 2, 42 - 49, 13.09.2023

Bengi Yeğin Semih Öz Dilek Burukoğlu Dönmez Hilmi Özden Mehmet Cengiz Üstüner Sibel Canbaz Kabay Ferruh Yücel

Abstract

İskemiye karşı en hassas organ olan beyinde iskemiden kaynaklanan hastalıklar artık yaygınlaşarak sosyal ve ekonomik sorunlara yol açmaktadır. Organizmanın oluşturduğu antioksidan savunma sisteminin yetersizliği sonucu artan serbest radikaller, serbest radikallerin artmasına neden olur ve bu da başta kanser olmak üzere çeşitli hastalıkların ve yaşlanma süreçlerinin gelişmesine katkıda bulunur. Çalışmamızda güçlü bir antioksidan olan Astaksantinin (AST) antioksidan sistem ile beyin üzerindeki koruyucu etkisinin araştırılması amaçlandı.
Araştırmamız Eskişehir Osmangazi Üniversitesi Tıp Fakültesi Anatomi Anabilim Dalı'nda gerçekleştirildi. Deneyde toplam 32 adet erkek sıçan kullanıldı ve sıçanlar her grupta 8 adet olmak üzere 4 gruba ayrıldı. Çalışmamızda sıçanlara farklı dozlarda AST verilerek a. carotis communis iskemi-reperfüzyon modeli üzerindeki koruyucu etkisi araştırıldı. Sıçanlara ameliyattan 30 dakika önce intraperitoneal olarak AST verildi. Sonrasında 15 dakika süreyle iskemi uygulandı. İskeminin ardından sıçanlar 24 saat reperfüzyonda bırakıldı. Sonrasında intrakardiyak perfüzyonla kan örnekleri alındı; Malondialdehit (MDA), Süperoksit dismutaz (SOD), Katalaz (CAT) düzeyleri belirlendi.
Biyokimyasal sonuçlara göre Sham grubunda SOD ve CAT düzeylerinde anlamlı derecede azalma gözlemlenmiştir. Bu da iskemi sonrası artan serbest radikaller karşısında antioksidan savunma sisteminin yetersiz olduğunu göstermektedir. Öte yandan AST ile tedavi edilen grupta anlamlı bir artış gözlemlenmiştir. Bu sonuç bize AST'nin antioksidan sistem üzerinde önemli bir koruyucu etkiye sahip olduğunu göstermektedir. Sham grubunda görülen MDA düzeylerindeki anlamlı artış iskemi sonrası beyinde oksidatif hasarın oluştuğunu göstermektedir. AST25 grubuna baktığımızda anlamlı bir düzeyde azalma gözlemledik. Bu sonuçta AST'nin beyin üzerinde önemli bir koruyucu etkisinin olduğunu destekler niteliktedir. AST 75 grubuna baktığımızda ise kontrol grubunun düzeylerinin altına düştüğünü gözlemledik. Bu da bize bu dozun AST'nin beyin üzerinde tam bir koruyucu etkiye sahip olduğunu göstermektedir.
Sham grubu, kontrol grubuyla karşılaştırıldığında serebral kortekste önemli hasar ve yüksek sayıda nekrotik nöron gözlemlenmiştir. AST verilen gruplarda oldukça sağlam bir görünüme sahip ve hasar seviyeleri azalmış nöronların varlığı tespit edilmiştir. Bu bulgu AST'nin sınırlı derecede nörolojik koruma sağlayabileceğini göstermektedir.
Histolojik veriler, AST'nin beyin hasarına karşı bir dereceye kadar önleyici etkinlik sergilediğini göstermektedir. Astaksantin, oksidatif hasarı azaltmada, özellikle 75 mg/kg dozajında, antioksidan savunma sistemi üzerinde dikkate değer bir koruyucu etki sergilemektedir. Histolojik değerlendirmelerin objektifliğini ve netliğini arttırmak için niceliksel analizler ve değerlendirmeler yapmak ve tespit edilen değişiklikleri kategorize etmek faydalı olacaktır.

Keywords

İskemi-reperfüzyon, a. carotis communis, serbest radikaller, antioksidanlar, astaksantin, serebral iskemi modelleri, doku hasarı

References

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Effect of Dose-Related Astaxanthin on Rats with Cerebral Ischemia-Reperfusion

Year 2023, Volume: 4 Issue: 2, 42 - 49, 13.09.2023

Bengi Yeğin Semih Öz Dilek Burukoğlu Dönmez Hilmi Özden Mehmet Cengiz Üstüner Sibel Canbaz Kabay Ferruh Yücel

Abstract

The prevalence of cerebral ischemia-related diseases, which mostly affect the brain, has become pervasive and is associated with significant societal and economic challenges. The deficiency of the organism's antioxidant defense system results in an elevation of free radicals, which in turn contributes to the development of a range of illnesses and aging processes, with a particular emphasis on cancer. The objective of our research was to examine the potential protective impact of astaxanthin (AST), a potent antioxidant, on the antioxidant system inside the brain.
The research was carried out in the Department of Anatomy, Faculty of Medicine, Eskisehir Osmangazi University. Within the experimental framework, a total of 32 male rats were utilized, with each group consisting of 8 rats separated into 4 subgroups. The present work aimed to examine the potential protective impact of AST, delivered at varying dosages, in a rat model of carotid artery ischemia-reperfusion. DMSO and AST were delivered intraperitoneally to the rats 30 minutes before to the surgery. A 15-minute period of ischemia was conducted. After a period of 24 hours of reperfusion, the rats underwent decapitation. The researchers obtained intracardiac blood samples and subsequently analyzed the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT).
According to the biochemical results, a significant decrease in the levels of SOD and CAT in the sham group indicates that the antioxidant defense system was inadequate in the face of increased free radicals after ischemia. A significant increase in the AST-treated group indicates that AST has a significant protective effect on the antioxidant system. A significant increase in MDA levels in the Sham group indicates that oxidative damage occurred in the cerebrum after ischemia. A significant decrease in the AST 25 group indicates that AST has a significant protective effect on the brain. When the levels of AST 75 group fall below the levels of the control group, this dose indicates that AST has a complete protective effect on the brain.
The Sham group had significant damage and a high number of necrotic neurons in the cerebral cortex in comparison to the control group. The groups who received AST exhibited the presence of neurons with a rather intact appearance and reduced levels of damage. This finding suggests that AST may confer a limited degree of neuroprotection.
The histological data indicate that AST exhibits a degree of preventive efficacy against cerebral injury. Astaxanthin (AST) exhibits a notable protective impact on the antioxidant defense system, particularly at a dosage of 75mg/kg, in mitigating oxidative damage. To enhance the objectivity and clarity of histological evaluations, it is beneficial to conduct quantitative analyses and assessments, as well as categorize the detected alterations.

Keywords

Ischemia-reperfusion, common carotid artery, free radicals, antioxidants, astaxanthin, cerebral ischemia models, tissue damage

References

1. Mehta SL, Manhas N, Raghubir R. Molecular targets in cerebral ischemia for developing novel therapeutics. Brain Res Rev. 2007;54:34–66. https://doi. org/10.1016/j.brainresrev.2006.11.003
2. Majino G, Jorris I. Apopitosis, oncosis, and necrosis –an overview of the cell death. Am J Pathol. 1995;146:3–15. Available at: https://pubmed.ncbi.nlm.nih.gov/7856735/
3. Zimmerman BJ, Granger DN. Reperfusion injury. Surg Clin North Am. 1992;72:65–83. https://doi.org/10.1016/S0039-6109(16)45628-8
4. Collard CD, Gelman S, Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology. 2001;94:1133– 1138. https://doi.org/10.1097/00000542-200106000-00030
5. Vardanian AJ, Busuttil RW, Kepiec-Weglinski J. Molecular mediators of liver ischemia and reperfusion injury: a brief review. Mol Med. 2008;14(5-6):337– 345. https://doi.org/10.2119/2007-00134.Vardanian
6. Wahul AB, Joshi PC, Kumar A, Chakravarty S. Transient global cerebral ischemia differentially affects cortex, striatum and hippocampus in bilateral common carotid arterial occlusion (BCCAo) mouse model. J Chem Neuroanat. 2018;92:1–15. https://doi.org/10.1016/j.jchemneu.2018.04.006
7. Ma M, Uekawa K, Hasegawa Y, Nakagawa T, Katayama T, Sueta D, et al. Pretreatment with rosuvastatin protects against focal cerebral ischemia/reperfusion injury in rats through attenuation of oxidative stress and inflammation. Brain Res. 2013;1519:87–94. https://doi.org/10.1016/j.brainres.2013.04.040
8. Chen H, Yoshioka H, Kim GS, Jung JE, Okami N, Sakata H, et al. Oxidative stress in ischemic brain damage: Mechanisms of cell death and potential molecular targets for neuroprotection. Antioxid Redox Signal. 2011;14:1505–1517. https://doi.org/10.1089/ars.2010.3576
9. Eltzschig HK, Eckle T. Ischemia and reperfusion-from mechanism to translation. Nat Med. 2011;17:1391–1401. https://doi.org/10.1038/nm.2507
10. Daverey A, Agrawal SK. Neuroprotective effects of Riluzole and Curcumin in human astrocytes and spinal cord white matter hypoxia. Neurosci Lett. 2020;738:135351. https://doi.org/10.1016/j.neulet.2020.135351
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13. Zeng X, Wang H, Xing X, Wang Q, Li W. Dexmedetomidine protects against transient global cerebral ischemia/reperfusion-induced oxidative stress and inflammation in diabetic rats. PLoS One. 2016;11:e0151620. https://doi.org/10.1371/journal.pone.0151620
14. Zheng YF, Bae SH, Kwon MJ, Park JB, Choi HD, Shin WG, et al. Inhibitory effects of astaxanthin, β-cryptoxanthin, canthaxanthin, lutein, and zeaxanthin on cytochrome P450 enzyme activities. Food Chem Toxicol. 2013;59:78–85.https://doi.org/10.1016/j.fct.2013.04.053
15. Zarneshan SN, Fakhri S, Farzaei MH, Khan H, Saso L. Astaxanthin targets PI3K/Akt signaling pathway toward potential therapeutic applications. Food Chem Toxicol. 2020;145. https://doi.org/10.1016/j.fct.2020.111714
16. Bjerkeng B, Peisker M, von Schwartzenberg K, Ytrestyl T, Åsgård T. Digestibility and muscle retention of astaxanthin in Atlantic salmon, Salmo salar, fed diets with the red yeast Phaffia rhodozyma in comparison with synthetic formulated astaxanthin. Aquaculture. 2007;269:476–489. https://doi.org/10.1016/j.aquaculture.2007.04.070
17. Akkoyun HT, Uyar A, Bengu AŞ, Bayramoglu-Akkoyun M, Arihan O, Keles OF. Protective effect of astaxanthin in the lung injury caused by ischemiareperfusion of the lower extremities. J Anim Plant Sci. 2019;29(1):82–90.
18. Zuluaga M, Barzegari A, Letourneur D, Gueguen V, Pavon-Djavid G. Oxidative stress regulation on endothelial cells by hydrophilic astaxanthin complex: chemical, biological, and molecular antioxidant activity evaluation. Oxid Med Cell Longev. 2017;2017:8073798. https://doi.org/10.1155/2017/8073798
19. Yamagishi R, Aihara M. Neuroprotective effect of astaxanthin against rat retinal ganglion cell death under various stresses that induce apoptosis and necrosis. Mol Vis. 2014;20:1796–1805.
20. Zhang XS, Zhang X, Wu Q, Li W, Wang CX, Xie GB, et al. Astaxanthin offers neuroprotection and reduces neuroinflammation in experimental subarachnoid hemorrhage. J Surg Res. 2014;192(1):206–213. https://doi.org/10.1016/j.jss.2014.05.029
21. Galasso C, Orefice I, Pellone P, Cirino P, Miele R, Ianora A, et al. On the neuroprotective role of astaxanthin: new perspectives? Mar Drugs. 2018;16:247. https://doi.org/10.3390/md16080247
22. Lee DH, Lee YJ, Kwon KH, Neuroprotective effects of astaxanthin in oxygen-glucose deprivation in SH-SY5Y cells and global cerebral ischemia in rat. J Clin Biochem Nutr. 2010;47(2):121–129. https://doi.org/10.3164/ jcbn.10-29
23. Taksima T, Chonpathompikunlert P, Sroyraya M, Hutamekalin P, Limpawattana M, Klaypradit W. Effects of astaxanthin from shrimp shell on oxidative stress and behavior in animal model of Alzheimer’s disease. Mar Drugs. 2019;17:628. https://doi.org/10.3390/md17110628
24. Shen DF, Qi HP, Ma C, Chang MX, Zhang WN, Song RR. Astaxanthin suppresses endoplasmic reticulum stress and protects against neuron damage in Parkinson’s disease by regulating miR-7/SNCA axis. Neurosci Res. 2021;165:51–60. https://doi.org/10.1016/j.neures.2020.04.003
25. Sun Y, Oberley LW, Li Y. A simple method for clinical assay of superoxide dismutase. Clin Chem. 1988;34:497–500. https://doi.org/10.1093/ clinchem/34.3.497
26. Esterbauer H, Cheeseman KH. Determination of aldehydic lipid peroxidation products: malonaldehyde and 4-hidroxynonenal. Methods Enzymol. 1990;186:407–421. https://doi.org/10.1016/0076-6879(90)86134-H
27. Aebi H. Catalase. In: Bergmeyer U, editor. Methods of enzymatic analysis. NY & London: Academic Press; 1974. pp. 673–680. https://doi.org/10.1016/B978- 0-12-091302-2.50032-3
28. Kietzmann T, Knabe W, Schmidt-Kastner R. Hypoxia and hypoxia-inducible factor modulated gene expression in brain: involvement in neuroprotection and cell death. Eur Arch Psychiatry Clin Neurosci. 2001;251:170–178. https://doi.org/10.1007/s004060170037
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Details

Primary Language	English
Subjects	Clinical Sciences (Other)
Journal Section	Araştırma makalesi
Authors	Bengi Yeğin 0000-0003-0730-5627 Semih Öz 0000-0002-1543-2223 Dilek Burukoğlu Dönmez 0000-0002-6454-4424 Hilmi Özden 0000-0003-2466-2757 Mehmet Cengiz Üstüner 0000-0001-9802-3988 Sibel Canbaz Kabay 0000-0003-4808-2191 Ferruh Yücel 0000-0002-1238-1483
Publication Date	September 13, 2023
Submission Date	August 28, 2023
Published in Issue	Year 2023 Volume: 4 Issue: 2

Cite

AMA	Yeğin B, Öz S, Burukoğlu Dönmez D, Özden H, Üstüner MC, Canbaz Kabay S, Yücel F. Effect of Dose-Related Astaxanthin on Rats with Cerebral Ischemia-Reperfusion. YIU Saglik Bil Derg. September 2023;4(2):42-49.

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