Abstract Neuropathic pain, resulting from damage or dysfunction of the nervous system, presents significant clinical challenges due to its chronic nature and resistance to treatment. This study compared the thermal nociception and inflammatory mechanisms of two neuropathic pain models: Sciatic nerve ligation (SNL) and oxaliplatin-induced peripheral neuropathy. Male Wistar Albino rats were randomly assigned to control, SNL, and oxaliplatin-induced neuropathy. The SNL model was established through partial sciatic nerve ligation, while oxaliplatin (4 mg/kg) was administered intraperitoneally twice weekly for four weeks. Thermal nociception was evaluated using tail-flick and hot-plate tests, and inflammatory markers (TNF-α and IL-1β) were measured in dorsal root ganglia(DRG) tissue and serum using ELISA. Thermal analgesia tests revealed that neuropathic pain symptoms appeared from the second week in the oxaliplatin group and from the fourth week in both models (p
Neuropathic pain, resulting from damage or dysfunction of the nervous system, presents significant clinical challenges due to its chronic nature and resistance to treatment. This study compared the thermal nociception and inflammatory mechanisms of two neuropathic pain models: Sciatic nerve ligation (SNL) and oxaliplatin- induced peripheral neuropathy. Male Wistar Albino rats were randomly assigned to control, SNL, and oxaliplatin- induced neuropathy. The SNL model was established through partial sciatic nerve ligation, while oxaliplatin (4 mg/kg) was administered intraperitoneally twice weekly for four weeks. Thermal nociception was evaluated using tail-flick and hot-plate tests, and inflammatory markers (TNF-α and IL-1β) were measured in dorsal root ganglia (DRG) tissue and serum using ELISA. Thermal analgesia tests revealed that neuropathic pain symptoms appeared from the second week in the oxaliplatin group and the fourth week in both models (p<0.05). TNF-α and IL-1β levels were significantly elevated in the SNL and oxaliplatin groups compared to controls, with the highest TNF-α levels observed in the oxaliplatin group (p<0.05). These findings indicate that both models effectively induce neuropathic pain, with notable increases in pro-inflammatory cytokines in DRG and serum. The study examines the inflammatory mechanisms underlying neuropathic pain, providing insights into its pathophysiology and potential therapeutic approaches.
