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Review paper

Snakehead fish extract as an enhancer of vascular endothelial growth factor and nitric oxide levels in cerebral angiogenesis: an insight of stroke therapy

By
Iskandar Nasution Orcid logo ,
Iskandar Nasution
Contact Iskandar Nasution

Department of Neurology, School of Medicine, Universitas Sumatera Utara, Medan, Indonesia

Hasan Sjahrir ,
Hasan Sjahrir

Department of Neurology, School of Medicine, Universitas Sumatera Utara, Medan, Indonesia

Syafruddin Ilyas ,
Syafruddin Ilyas

Department of Biology, Faculty of Mathematics and Natural Sciences, Universitas Sumatera Utara, Medan, Indonesia

Muhammad Ichwan
Muhammad Ichwan

Department of Pharmacology, School of Medicine, Universitas Sumatera Utara, Indonesia

Abstract

Aim
To assess the effect of snakehead fish extract administration in angiogenesis focusing on the level of vascular endothelial growth factor (VEGF), nitric oxide (NO) and VEGF receptor 2 (R2) expression is ischemic stroke models.
Methods
An experimental study was conducted on 5 groups of ischemic stroke rats models: Group K-without carotid artery ligation, Group K+ with artery ligation, Group P1 with artery ligation and administration of 200 mg/day extract, Group P2 with artery ligation and 400 mg/day extract, and Group P3 with artery ligation and 800 mg/day extract. The VEGF expression and NO levels were assessed on day 3.
Results
Snakehead fish extract significantly increased VEGF levels along with increasing doses, in which the highest VEGF level was observed in P3 group (361.7±40.2; p<0.001). The NO level also increased along with an increasing dose of snakehead fish extract, in which the highest NO level was found in P3 group (59.43±0.88 μmol/gr; p<0.001). The VEGFR2 expression also increased significantly after snakehead extract administration along with increasing doses (p<0.001) in which administration of 800 mg extract yielded the highest VEGFR2 expression compared with lower doses (17.7 vs. 15.6; p<0.001)
Conclusion
Snakehead fish extract administration increased angiogenesis process marked by an increased level of VEGF, NO and VEGFR2 expression in ischemic stroke rat models.

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