1Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
2Neuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran, Iran
3Radiation Biology Research Center, Iran University of Medical Sciences, Tehran, Iran
4Evidence-based Phytotherapy and Complementary Medicine Research Center, Alborz University of Medical Sciences, Karaj, Iran
5Department of Pharmacognosy, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran
چکیده
Chronic constriction injury (CCI) is a well‑established experimental model to induce neuropathic pain (NP). Evidence demonstrates that pro‑inflammatory cytokines (IL - 1 β, TNF-α) and beta nerve growth factor (β NGF) are key contributors to the initiation and maintenance of NP. Melissa officinalis (MO) is a medicinal plant with recognized anti‑inflammatory properties. In this investigation, we examine the neuroprotective effects of MO after CCI. The 32 rats were randomly assigned to four groups of eight animals per group, as follows: Sham (no surgery), CCI, CCI + vehicle (saline), and CCI + MO (150 mg/kg/day, p.o. gavage for 14 days after surgery). To evaluate NP, behavioral assessments of thermal hyperalgesia and Cold allodynia (N=8) were conducted on days 7, 14, and 21 after injury. Furthermore, H&E staining (N=5) was used to assess histopathological alterations within the dorsal horn of the spinal cord. Finally, the levels of IL - 1 β, TNF-α, β NGF, hepatotoxicity (ALT, AST), and nephrotoxicity (creatinine, Urea) markers were measured using standard biochemical and ELISA kits (N=3). MO Treatment significantly attenuated thermal hyperalgesia and cold allodynia at 14 and 21 days after CCI (Respectively, p<0.05, p<0.01). Furthermore, pro-inflammatory cytokine levels and β NGF expression were significantly decreased in the MO-treated group compared to the CCI groups (p<0.05). Furthermore, histological analyzes revealed that MO significantly decreased the number of dark neurons in the dorsal horn of the spinal cord (p<0.001). MO exerted possible protective effects in an animal model of CCI by improving behavioral tests, by reducing neuronal loss in the spinal dorsal horn, and by suppressing the expression of β‑NGF protein and pro‑inflammatory cytokines (TNF‑α, IL‑1β) in the spinal cord.