期刊
JOURNAL OF NATURAL MEDICINES
卷 76, 期 1, 页码 268-275出版社
SPRINGER JAPAN KK
DOI: 10.1007/s11418-021-01564-4
关键词
Celastrol; Neuropathic pain; Inflammation; Cytokine; TLR4/NF-kappa B signaling
资金
- 2018 National Talent Training Project of Traditional Chinese Medicine Characteristic Technology Inheritance [T20184828005]
Celastrol, a compound from Tripterygium wilfordii Hook F., showed analgesic effects in rats with neuropathic pain by inhibiting the TLR4/NF-kappa B signaling pathway and exerting anti-inflammatory effects in the spinal cord.
Tripterygium wilfordii Hook F. is a well-known but poisonous traditional Chinese medicine used for treating a wide variety of inflammatory and autoimmune disorders. Celastrol, a quinone methyl triterpenoid compound and a representative component of T. wilfordii Hook F., shows a variety of pharmacological activities, such as anti-inflammatory and antitumor activities. Here, we investigated the antineuropathic pain (NP) effect of celastrol and its potential mechanisms. Rats with chronic constrictive injury (CCI)-induced NP were used to evaluate the analgesic effect of celastrol. Gabapentin was used as a reference compound (positive control). The results showed that gabapentin (100 mg/kg, i.p.) and multiple doses of celastrol (0.5, 1 and 2 mg/kg, i.p.) increased the threshold of mechanical and thermal pain in the rats with NP. Western blot results showed that celastrol significantly inhibited the activation of microglia and astrocytes in the spinal cord of rats with NP. Additionally, the levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta and interleukin 6, detected by ELISA in the spinal cord of the rats with NP, were significantly inhibited by celastrol. Furthermore, celastrol treatment dramatically inhibited the expression of the TLR4/NF-kappa B signaling pathway in the spinal cord. Taken together, our findings suggested that celastrol could attenuate mechanical and thermal pain in CCI-induced NP, and this protection might be attributed to inhibiting the TLR4/NF-kappa B signaling pathway and exerting anti-inflammatory effects in the spinal cord. [GRAPHICS] .
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