Fenofibrate attenuates peripheral neuropathic pain by suppressing neuroinflammation in the anterior cingulate cortex

Background : Chemotherapy-induced neuropathy is a frequent complication of cancer treatment and significantly reduces patient quality of life. Neuroinflammatory processes in the anterior cingulate cortex (ACC) play a critical role in the modulation of pain sensitivity. Fenofibrate has demonstrated neuroprotective properties and has been proposed as a potential therapeutic agent for the management of peripheral neuropathy. Materials and methods : A total of 20 male BALB/c mice were divided into four groups (five per group): control, neuropathy (oxaliplatin, 3 mg/kg), neuropathy + fenofibrate (150 mg/kg), and neuropathy + fenofibrate (300 mg/kg). A behavioral test using von Frey filaments was used to assess mechanical allodynia. mRNA expression of ionized calcium-binding adapter molecule 1 (IBA-1), tumor necrosis factor-alpha (TNF-α), and caspase-3 in the ACC was measured using RT-qPCR. Results : Fenofibrate at doses of 150 and 300 mg/kg improved the mechanical withdrawal threshold, followed by significant alterations in the mRNA expression of IBA-1, TNF-α, and caspase-3. Conclusion : Fenofibrate ameliorates chemotherapy-induced neuroinflammation and neuronal apoptosis in the ACC.