Impact of Virgin Coconut Oil (VCO) on Locomotor Speed and Bax Expression in Zebrafish (Danio rerio) Larvae Stunting Model

Abstract

Stunting is a chronic growth disorder caused by prolonged nutritional deficiencies and environmental stress, resulting in reduced height for age. Oxidative stress-induced apoptosis, involving the pro-apoptotic gene B-cell lymphoma 2-associated X protein (Bax), is a key molecular mechanism. Antioxidant-rich virgin coconut oil (VCO) with lauric acid and phenolic compounds has the potential to mitigate oxidative damage. The objective of this study is to evaluate the effect of VCO on locomotor speed and Bax gene expression of zebrafish larvae (Danio rerio) in a rotenone-induced stunting model. The larvae were divided into five groups: negative control (NC), positive control given rotenone (PC), and three treatment groups with rotenone and VCO at concentrations of 6.25% (V1), 3.125% (V2), and 1.625% (V3). Locomotor speed was measured at 3, 6, and 9 days post-fertilization (dpf), while Bax expression was analyzed using Reverse Transcription quantitative Polymerase Chain Reaction (RT-qPCR) at 9 dpf. The results showed that VCO increased larval locomotor speed, with the V1 group showing the best recovery compared to PC. In addition, Bax expression significantly increased in the PC group compared to NC (p < 0.05). VCO administration significantly decreased Bax expression in a dose-response manner for V1, V2, and V3. These findings indicate that VCO provides a protective effect against rotenone-induced apoptosis and motor impairment through modulation of oxidative stress. Thus, VCO has the potential as a natural therapeutic agent to reduce cellular damage and functional deficits associated with stunting.