PUBLICATION

Centella asiatica extract ameliorates deoxygenation-induced neurological dysfunction in zebrafish larvae

Authors
Ariani, A., Khotimah, H., Sulistyarini, A., Daniaridevi, A.S.
ID
ZDB-PUB-240628-11
Date
2024
Source
Open veterinary journal   14: 115411601154-1160 (Journal)
Registered Authors
Keywords
Centella asiatica, Neuroplasticity, Neuroprotective, Neurotoxicity
MeSH Terms
  • Animals
  • Brain-Derived Neurotrophic Factor*/genetics
  • Brain-Derived Neurotrophic Factor*/metabolism
  • Centella*/chemistry
  • Fish Diseases/chemically induced
  • Fish Diseases/drug therapy
  • Hypoxia/drug therapy
  • Hypoxia/veterinary
  • Larva*/drug effects
  • Larva*/growth & development
  • Neuroprotective Agents/pharmacology
  • Oxygen/metabolism
  • Plant Extracts*/administration & dosage
  • Plant Extracts*/pharmacology
  • Triterpenes*/administration & dosage
  • Triterpenes*/pharmacology
  • Zebrafish*
PubMed
38938421 Full text @ Open Vet J
Abstract
Oxygen deprivation (OD) is a critical condition that can lead to brain damage and even death. Current hypoxia management approaches are limited in effectiveness. Centella asiatica (CA), known for its neuroprotective properties, offers a potential alternative for OD treatment.
This study aims to investigate the neuroprotective effects of CA on the expression of brain-derived neurotrophic factor (BDNF) and vesicular glutamate transporter 1 (VGLUT1) in zebrafish larvae under oxygen-deficient conditions.
Zebrafish embryos were subjected to low oxygen levels (1.5 mg/l) 0-2 hours post-fertilization (hpf) until 3 days post-fertilization (dpf), simulating the early stages of OD. Subsequent treatment involved varying concentrations of CA (1.25-5 µg/ml) up to 9 days post-fertilization. The expression levels of BDNF and VGLUT1 were measured using PCR methods. Statistical analysis was conducted using a two-way analysis of variance to evaluate the impact of CA on the expression of BDNF and VGLUT1 in zebrafish larvae aged 3 and 9 dpf in oxygen-deprived conditions.
CA significantly influenced the expression of BDNF and VGLUT1 under OD (p < 0.001). An increase in BDNF expression (p < 0.001) and a decrease in VGLUT1 (p < 0.01) were observed in zebrafish larvae experiencing OD and treated with CA. There was no significant difference in BDNF and VGLUT1 expression across age variations in zebrafish larvae at 3 dpf and 9 dpf in the treatment groups (p > 0.05). CA concentration of 2.5 µg/ml effectively enhanced BDNF and reduced VGLUT1 in 3-9 dpf zebrafish larvae.
CA demonstrates potential as a neuroprotective agent, modulating increased BDNF expression and reduced VGLUT1 under OD conditions. These findings lay a foundation for further research in developing therapies for oxygen deficiency.
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