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Background <p>Pain is an unpleasant experience associated with tissue damage, peripheral inflammation, and central sensitization. The pain-related pathological signs in the acute or chronic phase may be influenced by natural compounds such as sesamin. Therefore, we aimed to subject pretreated rats to formalin administration and evaluate pain-related genes in brain tissue.</p> Method <p>Animals were divided into six groups: Sham, formalin (100 µL, 2.5%), Sesamin (15, 30, and 60&#xa0;mg/kg in 5 mL, IP; vehicle: DMSO/Saline (1:1), administered over three days) + formalin, and morphine (2.5&#xa0;mg/kg) + formalin. After injections, pain scores, acute/chronic pain, oxidative stress markers (Superoxide dismutase, Glutathione peroxidase, and malondialdehyde), as well as gene expression of Toll-like receptor4 (TLR4), nuclear factor kappa B (NF-κB), and Nod-like receptor protein 3 (NLRP3) were evaluated in the brain.</p> Results <p>The results indicated that pretreatment with Sesamin, particularly at the effective dose of 30&#xa0;mg/kg, significantly reduced acute and chronic pain, oxidative stress markers, and the TLR4/NF-κB/NLRP3 signaling pathway in the brain tissue.</p> Conclusion <p>Sesamin may serve as a potential therapeutic agent for pain disorders by downregulating the inflammatory signaling pathway without the side effects associated with chemical drugs.</p>

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The role of sesamin in alleviating acute and chronic pain: a focus on the TRL4-NF-KB-NLRP3 signaling pathway

  • 期刊论文

  • 发表日期：

    2025年8月2日

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  • Farima Malekinia,
  • Alireza Sarkaki,
  • Yaghoob Farbood,
  • Seyed Esmaeil Khoshnam,
  • Seyedeh Parisa Navabi

摘要

Background

Pain is an unpleasant experience associated with tissue damage, peripheral inflammation, and central sensitization. The pain-related pathological signs in the acute or chronic phase may be influenced by natural compounds such as sesamin. Therefore, we aimed to subject pretreated rats to formalin administration and evaluate pain-related genes in brain tissue.

Method

Animals were divided into six groups: Sham, formalin (100 µL, 2.5%), Sesamin (15, 30, and 60 mg/kg in 5 mL, IP; vehicle: DMSO/Saline (1:1), administered over three days) + formalin, and morphine (2.5 mg/kg) + formalin. After injections, pain scores, acute/chronic pain, oxidative stress markers (Superoxide dismutase, Glutathione peroxidase, and malondialdehyde), as well as gene expression of Toll-like receptor4 (TLR4), nuclear factor kappa B (NF-κB), and Nod-like receptor protein 3 (NLRP3) were evaluated in the brain.

Results

The results indicated that pretreatment with Sesamin, particularly at the effective dose of 30 mg/kg, significantly reduced acute and chronic pain, oxidative stress markers, and the TLR4/NF-κB/NLRP3 signaling pathway in the brain tissue.

Conclusion

Sesamin may serve as a potential therapeutic agent for pain disorders by downregulating the inflammatory signaling pathway without the side effects associated with chemical drugs.