Asiatic acid increased locomotor and head width by inducing brain-derived neurotrophic factor in intrauterine hypoxia-exposed zebrafish

Abstract

Background: Hypoxia ischemia leads to abnormal behavior and growth. Prenatal hypoxia also decreases brain adaptive
potential, which can cause fatal effects such as cell death. Asiatic acid (AA) in Centella asiatica is a neuroprotector through antioxidant and anti-inflammatory activities.

Aim: This study aimed to analyze the effect of AA as a neuroprotector against hypoxia during intrauterine development
on locomotor activity, head width, and brain-derived neurotrophic factor (BDNF) expression.

Methods: The true experimental laboratory research used a posttest control-only design. Zebrafish embryos (Danio
rerio) aged 0–2 dpf (days postfertilization) were exposed to hypoxia with oxygen levels reaching 1.5 mg/l. Then, AA
was administered at successive concentrations, namely, 0.36, 0.72, and 1.45 μg/ml, at 2 hpf (hours postfertilization), 3,
6, and 9 dpf. Head width, velocity activity, and BDNF expression were observed.

Results: Intrauterine hypoxia significantly decreased head width, velocity rate, and BDNF expression (<0.001). Administration of AA at all concentrations and age 9 dpf to zebrafish larvae with intrauterine hypoxia exposure increased head width (p < 0.0001), velocity (p < 0.05), and relative mRNA expression of BDNF (p < 0.05).

Conclusion: AA is  potentially neuroprotective to the brain in zebrafish larvae exposed to hypoxia during intrauterine development