Toxicology Reports (Dec 2024)

Protective effect of Ficus capensis lyophilized extract against carboplatin-induced liver injury via inhibition of oxidative stress and inflammation in rats

  • Josiah Aja Nwadibia,
  • Ilemobayo Victor Fasogbon,
  • Angela Mumbua Musyoka,
  • Ezebuilo Ugbala Ekpono,
  • Udu Ama Ibiam,
  • Obasi Uche Orji,
  • Ejike Daniel Eze,
  • Olufunke Onaadepo,
  • Peter Chinedu Agu,
  • Patrick Maduabuchi Aja

Journal volume & issue
Vol. 13
p. 101734

Abstract

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Patients who are receiving carboplatin therapy for cancer often experience toxic side effects. This study examined the effects of lyophilized aqueous leaf extracts of F. capensis (LALEFC) on oxidative stress and inflammatory markers in albino rats with carboplatin-damaged livers. We randomly assigned 35 rats to five experimental groups. Groups 2–5 underwent liver injury induction using carboplatin, while groups 1 and 2 served as the normal and carboplatin control groups, respectively. Groups 3–5 were the treatment groups. Treatments were performed for 17 days. We analyzed the quantitative phytochemical constituents of LALEFC using standard procedures and analyzed the liver oxidative stress and inflammatory markers using liver homogenate. The phytochemical constituents of LALEFC (mg/100 g) occur in the following order: The most abundant compounds were phenols (1577.72 ± 0.008), flavonoids (1253.13 ± 0.007), tannins (878.97 ± 0.007), alkaloids (652.66 ± 0.007), glycosides (314.39 ± 0.011), and terpenoids (261.18 ± 0.154), while steroids (0.573 ± 0.062), saponins (0.370 ± 0.003), and HCN (0.254.00 ± 0.006) were found in trace amount. The study of oxidative stress and inflammatory markers showed that giving carboplatin to rats greatly increased the levels of interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-α), malondialdehyde (MDA), reactive oxygen species (ROS), and caspase-3 activity. It also decreased the levels of reduced glutathione (GSH) and the activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). D). However, coadministration of LALEFC significantly restored the altered oxidative and inflammatory responses. This finding suggested that carboplatin induced liver injury through redox imbalance, which elevated the expression of inflammatory markers. LALEFC's restoration of altered markers could be relevant in the treatment of carboplatin-induced liver injury.

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