Evaluation of Palm Kernel Oil on Some Pro-inflammatory Markers in Lipopolysaccharide and Kainic acid Seizures-Induced Wistar Rats

Abstract

Background: Febrile seizures are common in early childhood and may involve measurable neuroinflammatory responses. Aims: This study evaluated whether palm kernel oil (PKO) modifies selected pro-inflammatory and damage-associated markers in Wistar rat pups exposed to lipopolysaccharide (LPS)- and kainic acid-induced seizures. Materials and Methods: Forty (40) Wistar rat pups were allocated into eight (8) groups of five (5) rats each. Group A was not induced and received normal saline (negative control). Group B was induced with seizures and received normal saline (positive control). Group C was induced with seizures and treated with the standard drug, diazepam (10 mg/kg), as described by Wang et al. (2018). Groups D, E, F and G were induced with seizures and treated with 5, 10, 15 and 20 mg/kg of palm kernel oil, respectively. Group H was pre-treated with 5 mg/kg palm kernel oil for three days and then induced with seizure on the fourth day. Data were analysed using GraphPad Prism version 8.02 (California, USA). Analysis of variance (ANOVA) and Tukey’s comparative analysis were used to compare group means. Results were expressed as mean ± standard deviation. Statistical significance was set at p < 0.05. Results: In the pretreatment exposure, HMGB1 in the palm-kernel-oil-pretreated group was significantly lower than that in the diazepam-treated group. In the post-treatment groups, TNF-α values in the 15 and 20 mg/kg groups were significantly lower than those in the 5 and 10 mg/kg groups. Similarly, IL-1β and HMGB1 values in the 15 and 20 mg/kg groups were significantly lower than those in the 5 and 10 mg/kg groups and in the diazepam-treated group. Conclusion: Palm kernel oil administered after seizure induction did not significantly reduce the inflammatory markers across the 5-20 mg/kg dose range, indicating limited acute anti-inflammatory efficacy in this rat model. However, PKO pretreatment at 5 mg/kg was associated with a substantial reduction in HMGB1, despite only modest changes in TNF-α and IL-1β. This finding suggests that PKO may exert a protective influence on damage-associated signalling when administered prophylactically, possibly by modulating cellular resilience or baseline inflammatory priming.