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Research Article | Open Access

Effects of apple polyphenols on oxidative stress and cerebral vasospasm after subarachnoid hemorrhage in a rabbit double hemorrhage model

Masato Naraoka( ), Yuchen Li, Takeshi Katagai, Hiroki Ohkuma
Department of Neurosurgery, Hirosaki University School of Medicine & Hospital, Hirosaki, Japan
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Abstract

Subarachnoid hemorrhage (SAH) is almost always caused by ruptured cerebral aneurysms, and the most serious complication after SAH is cerebral vasospasm. Oxidative stress due to free radicals released from subarachnoid hemorrhage clots causes cerebral vasospasm, as proven by animal experiments. Apple polyphenols have already been demonstrated to strongly suppress oxidized low-density lipoprotein (ox-LDL) and lectin-like oxidized LDL receptor-1 (LOX-1) derived from reactive oxygen species (ROS), and to improve cerebral vasospasm. However, it is unclear how apple polyphenol acts downstream of ROS. The purpose of this study is to reveal a more detailed mechanism of functioning for apple polyphenols in suppressing oxidative stress and cerebral vasospasm. Using the double-hemorrhage rabbit subarachnoid hemorrhage (SAH) model, we investigated the effect of apple polyphenols by measuring the basilar artery diameter, endothelial NO synthase (eNOS) expression, diacron reactive oxygen metabolites (d-ROM), biological antioxidant potential (BAP), and malondialdehyde (MDA). The mean diameter of the basilar artery in the apple polyphenol treatment group was significantly larger than in the SAH group (p < 0.01). The expression of endothelial nitric oxide synthase (eNOS), evaluated by immunohisto-chemistry in the apple polyphenol treatment group, was higher than in the SAH group (p < 0.05). The BAP test in the apple polyphenol treatment group showed a significant difference, while there was no significant difference in the values of d-ROM and MDA. The results of the present study revealed that apple polyphenol significantly improved cerebral vasospasm and eNOS. In spite of a significant increase in antioxidant power expressed by increased BAP, oxidative stress measured by the d-ROM value was not significantly suppressed. Either the number of experimental animals was not sufficient to reach statistical significance, or the eNOS increase due to apple polyphenols and suppression of vasospasm are attributable to pathways other than lipid oxidation detected by MDA.

Keywords

Oxidative stressSubarachnoid hemorrhageCerebral vasospasmApple polyphenols

References

1

Ecker A, Riemenschneiderr PA. Arteriographic demonstration of spasm of the intracranial arteries, with special reference to saccular arterial aneurysms. J Neurosurg. 1951;8:660–667.
Crossref Google Scholar
2

King JT. Epidemiology of aneurysmal subarachnoid hemorrhage. Neuroimaging Clin N Am. 1997;7:659–668.
Google Scholar
3

Pluta RM, Hansen-Schwartz J, Dreier J, et al.. Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought. Neurol Res. 2009;31:151–158.
Crossref Google Scholar
4

Vergouwen MDI, Vermeulen M, van Gijn J, et al.. Definition of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage as an outcome event in clinical trials and observational studies: proposal of a multidisciplinary research group. Stroke. 2010;41:2391–2395.
Crossref Google Scholar
5

Naraoka M, Munakata A, Matsuda N, Shimamura N, Ohkuma H. Suppression of the Rho/Rho-kinase pathway and prevention of cerebral vasospasm by combination treatment with statin and fasudil after subarachnoid hemorrhage in rabbit. Transl Stroke Res. 2013;4:368–374.
Crossref Google Scholar
6

Suzuki H. What is early brain injury?. Transl Stroke Res. 2015:1–3.
Crossref Google Scholar
7

Matsuda N, Ohkuma H, Naraoka M, Munakata a, Shimamura N, Asano K. Role of oxidized LDL and lectin-like oxidized LDL receptor-1 in cerebral vasospasm after subarachnoid hemorrhage. J Neurosurg. 2014;121:621–630.
Crossref Google Scholar
8

Foley PL, Caner HH, Kassell NF, Lee KS. Reversal of subarachnoid hemorrhage-induced vasoconstriction with an endothelin receptor antagonist. Neurosurgery. 1994;34:108–112. discussion 112-3.
Crossref Google Scholar
9

Cesarone MR, Belcaro G, Carratelli M, et al.. A simple test to monitor oxidative stress. Int Angiol. 1999;18:127–130.
Google Scholar
10

Trotti R, Carratelli M, Barbieri M, et al.. Oxidative stress and a thrombophilic condition in alcoholics without severe liver disease. Haematologica. 2001;86:85–91.
Google Scholar
11

Gerardi G, Usberti M, Martini G, et al.. Plasma total antioxidant capacity in hemodialyzed patients and its relationships to other biomarkers of oxidative stress and lipid peroxidation. Clin Chem Lab Med. 2002;40:104–110.
Crossref Google Scholar
12

Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: the FRAP assay. Anal Biochem. 1996;239:70–76.
Crossref Google Scholar
13

Faienza MF, Francavilla R, Goffredo R, et al.. Oxidative stress in obesity and metabolic syndrome in children and adolescents. Horm Res Paediatr. 2012;78:158–164.
Crossref Google Scholar
14

Antus B. Oxidative stress markers in sputum. Oxid Med Cell Longev. 2016;2016.
Crossref Google Scholar
15

Ho E, Karimi Galougahi K, Liu CC, Bhindi R, Figtree GA. Biological markers of oxidative stress: applications to cardiovascular research and practice. Redox Biol Elsevier. 2013;1:483–491.
Crossref Google Scholar
16

Pompella A, Corti A. Editorial: the changing faces of glutathione, a cellular protagonist. Front Pharmacol. 2015;6:4–7.
Crossref Google Scholar
17

Shoji T, Akazome Y, Kanda T, Ikeda M. The toxicology and safety of apple polyphenol extract. Food Chem Toxicol. 2004;42:959–967.
Crossref Google Scholar
18

Sabri M, Ai J, Knight B, et al.. Uncoupling of endothelial nitric oxide synthase after experimental subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2011;31:190–199.
Crossref Google Scholar
19

Kanaoka Y, Inagaki EI, Hamanaka S, Masaki H, Tanemoto K. Analysis of reactive oxygen metabolites (ROMs) after cardiovascular surgery as a marker of oxidative stress. Acta Med Okayama. 2010;64:323–330.
Google Scholar
20

Dohi K, Satoh K, Ohtaki H, Shioda S, Miyake Y, Shindo M, et al.. Elevated plasma levels of bilirubin in patients with neurotrauma reflect its pathophysiological role in free radical scavenging. In Vivo. 2005;19:855–860.
Google Scholar
21

Yoshida A, Watanabe K, Iwasaki A, Kimura C, Matsushita H, Wakatsuki A. Placental oxidative stress and maternal endothelial function in pregnant women with normotensive fetal growth restriction. J Matern Neonatal Med. 2018;31:1051–1057.
Crossref Google Scholar
Brain Hemorrhages
Volume 1 Issue 1,
March 2020
Pages 54-58
DOI: 10.1016/j.hest.2019.12.006
Cite this article:
Naraoka M, Li Y, Katagai T, et al. Effects of apple polyphenols on oxidative stress and cerebral vasospasm after subarachnoid hemorrhage in a rabbit double hemorrhage model. Brain Hemorrhages, 2020, 1(1): 54-58. https://doi.org/10.1016/j.hest.2019.12.006

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Received: 19 December 2019
Accepted: 19 December 2019
Published: 23 January 2020
© 2020

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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