Iranian Journal of Basic Medical Sciences (May 2024)

Therapeutic potential of virgin coconut oil in mitigating sodium benzoate- model of male infertility: Role of Nrf2/Hmox-1/NF-kB signaling pathway

  • Ayodeji Ajibare,
  • Olabode Akintoye,
  • Moshood Folawiyo,
  • Kabirat Babalola,
  • Olaposi Omotuyi,
  • Busayo Oladun,
  • Kafilat Aransi-ola,
  • Lukman Olayaki,
  • Adeyemi Fatai Odetayo

DOI
https://doi.org/10.22038/ijbms.2024.71288.15484
Journal volume & issue
Vol. 27, no. 5
pp. 543 – 551

Abstract

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Objective(s): Male infertility is a major public health issue due to increased prevalence, so there is an urgent need for a therapeutic solution. The search for a natural dietary substance that could modulate redox balance and inflammation and protect testicular function is in demand. Virgin Coconut Oil (VCO) has found use in the treatment of diabetes, and cancer owing to the presence of polyphenols. However, there is a dearth of information on its effect on testicular toxicity. The present study investigated VCO as a possible treatment for testicular toxicity in the Sodium Benzoate (SB) model of male infertility by evaluating the oxidative and inflammatory status, circulating hormonal levels, and key sperm indices.Materials and Methods: Twenty adult male rats were randomly assigned to four groups of 5 rats each and were treated with normal saline, sodium benzoate, sodium benzoate+5% VCO, and sodium benzoate+15% VCO for 30 days respectively. Biochemical analysis of reproductive hormones was assessed. Sperm parameters assessed include sperm function tests and sperm kinematics. One-way analysis of variance (ANOVA) followed by post hoc Tukey tests was performed.Results: 5% VCO reverts the deranged serum reproductive hormones caused by sodium benzoate. 5% VCO was more potent as an antioxidant and anti-inflammatory treatment than 15% VCO. However, both doses prevented SB’s effect on the sperm function test and kinematics.Conclusion: VCO-supplemented diet can ameliorate SB-induced testicular toxicity by inhibiting its mechanisms of toxicity that are related to oxidative stress, apoptosis, and inflammation.

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