Protective Effects of Luteolin in a Rat Model of Ischemic Stroke

Document Type : Original article

Authors

1 a.Assistant Professor, Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran b.Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran c.Shefa Neuroscience

2 a.Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. b.Medical student, Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

3 MSc, Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

4 Medical student, Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

5 a.Assistant Professor, Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran b.Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Abstract

Introduction: Recent studies have pointed to the protective effects of luteolin against inflammation and oxidative stress. The present study aimed to investigate the protective effect of luteolin on neurogenesis, behavioral deficits, and infarct volume in a rat model of ischemiastroke.
Materials and Methods: The present experimental study was conducted on eight rats in four groups of  sham, control, and two treatments. The treatment groups received luteolin (15 or 30 mg/kg body weight) following focal cerebral ischemia. To assess the efficacy of luteolin, some stroke pathological changes, such as infarct volume, roger behavioral test, and neurogenesis were evaluated after 24 h.
Results: Administration of luteolin at doses of 15 and 30 mg/kg body weight reduced the infarct volume and improved the behavioral test after stroke in a dose-dependent manner. In the present study, the mRNA expression of neurogenesis markers, such as sox2, Nestin, and Dcx was investigated. The results showed that luteolin did not exert any significant effects on neurogenesis markers.
Conclusion: As evidenced by the obtained results, luteolin has a strong potential in the prevention/neuroprotection of ischemiastroke. Further studies are needed to clearly define the neuroprotective effects of luteolin.

Keywords

References

  1. Ovbiagele B, Nguyen-Huynh MN. Stroke epidemiology: advancing our understanding of disease mechanism and therapy. Neurotherapeutics. 2011; 8(3):319.
  2. Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Béjot Y, et al. A comparison of two LDL cholesterol targets after ischemic stroke. N Engl J Med. 2020; 382(1):9-19.
  3. Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage. Neuropharmacology. 2008; 55(3):310-8.
  4. González RG. Acute ischemic stroke. Heidelberg, Germany: Springer Verlag GmbH; 2011.
  5. Frank J, Fukagawa NK, Bilia AR, Johnson EJ, Kwon O, Prakash V, et al. Terms and nomenclature used for plant-derived components in nutrition and related research: efforts toward harmonization. Nutr Rev. 2020; 78(6):451-8.
  6. Daglia M, Di Lorenzo A, Nabavi SF, Talas ZS, Nabavi SM. Polyphenols: well beyond the antioxidant capacity: gallic acid and related compounds as neuroprotective agents: you are what you eat! Curr Pharm Biotechnol. 2014; 15(4):362-72.
  7. Ashokkumar P, Sudhandiran G. Protective role of luteolin on the status of lipid peroxidation and antioxidant defense against azoxymethane-induced experimental colon carcinogenesis. Biomed Pharma-cother. 2008; 62(9):590-7.
  8. Qiao H, Dong L, Zhang X, Zhu C, Zhang X, Wang L, et al. Protective effect of luteolin in experimental ischemic stroke: upregulated SOD1, CAT, Bcl-2 and claudin-5, down-regulated MDA and Bax expression. Neurochem Res. 2012; 37(9):2014-24.
  9. Aziz N, Kim MY, Cho JY. Anti-inflammatory effects of luteolin: a review of in vitro, in vivo, and in silico studies. J Ethnopharmacol. 2018; 225:342-58.
  10. Longa EZ, Weinstein PR, Carlson S, Cummins R. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke. 1989; 20(1):84-91.
  11. Carmichael ST. Rodent models of focal stroke: size, mechanism, and purpose. NeuroRx. 2005; 2(3):
    396-409.
  12. Gutiérrez-Fernández M, Rodríguez-Frutos B, Ramos-Cejudo J, Vallejo-Cremades MT, Fuentes B, Cerdán S, et al. Effects of intravenous administration of allogenic bone marrow-and adipose tissue-derived mesenchymal stem cells on functional recovery and brain repair markers in experimental ischemic stroke. Stem Cell Res Ther. 2013; 4(1):11.
  13. Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM, et al. Heart disease and stroke statistics--2011 update: a report from the American Heart Association. Circulation. 2011; 123(4):e18-209.
  14. Forouzanfar F, Hosseinzadeh H, Ebrahimzadeh Bideskan A, Sadeghnia HR. Aqueous and Ethanolic Extracts of Boswellia serrata Protect Against Focal Cerebral Ischemia and Reperfusion Injury in Rats. Phytother Res.
  15. 2016 ; 30(12): 1954-67. Ginsberg MD. The new language of cerebral ischemia. AJNR Am J Neuroradiol. 1997; 18(8):1435-45.
  16. Ghazavi H, Hoseini SJ, Ebrahimzadeh-Bideskan A, Mashkani B, Mehri S, Ghorbani A, et al. Fibroblast growth factor type 1 (FGF1)-overexpressed adipose-derived mesenchaymal stem cells (AD-MSC FGF1) induce neuroprotection and functional recovery in a rat stroke model. Stem Cell Rev Rep. 2017; 13(5):670-85.
  17. Sinha K, Chaudhary G, Gupta YK. Protective effect of resveratrol against oxidative stress in middle cerebral artery occlusion model of stroke in rats. Life Sci. 2002; 71(6):655-65.
  18. Durukan A, Tatlisumak T. Acute ischemic stroke: overview of major experimental rodent models, pathophysiology, and therapy of focal cerebral ischemia. Pharmacol Biochem Behav. 2007; 87(1):
    179-97.
  19. Forouzanfar F, Hosseinzadeh H, Ebrahimzadeh Bideskan A, Sadeghnia HR. Aqueous and ethanolic extracts of boswellia serrata protect against focal cerebral ischemia and reperfusion injury in rats. Phytother Res. 2016; 30(12):1954-67.
  20. Coyle JT, Puttfarcken P. Oxidative stress, glutamate, and neurodegenerative disorders. 1993; 262(5134):
    684-95.
  21. Halliwell B. Free radicals, antioxidants, and human disease: curiosity, cause, or consequence? Lancet. 1994; 344(8924):721-4.
  22. Sugawara T, Chan PH. Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia. Antioxid Redox Signal. 2003; 5(5):597-607.
  23. Crack PJ, Taylor JM. Reactive oxygen species and the modulation of stroke. Free Radic Biol Med. 2005; 38(11):1433-44.
  24. Li M, Li Q, Zhao Q, Zhang J, Lin J. Luteolin improves the impaired nerve functions in diabetic neuropathy: behavioral and biochemical evidences. Int J Clin Exp Pathol. 2015; 8(9):10112-20.
  25. Kang SS, Lee JY, Choi YK, Kim GS, Han BH. Neuroprotective effects of flavones on hydrogen peroxide-induced apoptosis in SH-SY5Y neuroblostoma cells. Bioorg Med Chem Lett. 2004; 14(9):2261-4.
  26. Fu J, Sun H, Zhang Y, Xu W, Wang C, Fang Y, et al. Neuroprotective effects of luteolin against spinal cord ischemia–reperfusion injury by attenuation of oxidative stress, inflammation, and apoptosis. J Med Food. 2018; 21(1):13-20.
  27. Lindvall O, Kokaia Z. Neurogenesis following stroke affecting the adult brain. Cold Spring Harb Perspect Biol. 2015; 7(11):a019034.
  28. Xie F, Liu H, Liu Y. Adult neurogenesis following ischaemic stroke and implications for cell-based therapeutic approaches. World Neurosurg. 2020; 138:474-80.
Navid No
Volume 24, Issue 77
June 2021
Pages 11-19

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