Journal of ethnopharmacology · 2026
Safflower yellow alleviates sciatic nerve crush injury in rats: associated with TRPV1-pERK signaling pathway.
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Wei Songyi, Pan Wuying, Liu Qinghua, Wang Jun
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Peripheral nerve injury (PNI) clinically resembles the traditional Chinese medical "Bi" and "Blood-Stasis" syndromes. Carthamus tinctorius L. (safflower) is a classic blood-activating and stasis-resolving herb commonly prescribed for PNI, whereas the protective effect of its major active component safflower yellow (SY) against PNI remains unclear.
AIM OF THE STUDY: To explore the efficacy and potential mechanisms of SY in ameliorating PNI using a rat sciatic nerve crush (SNC) model.
MATERIALS AND METHODS: Rats were randomly assigned to four groups (n=10): Sham, SNC model, SNC+SY 20 mg/kg, and SNC+SY 40 mg/kg. All rats were sacrificed 15 days after SNC surgery.
RESULTS: SY intervention significantly promoted sciatic nerve functional recovery, alleviated mechanical allodynia, reversed denervation-induced gastrocnemius atrophy, and ameliorated histopathological damage in SNC-injured nerve tissues. Mechanistically, SY suppressed neuroinflammation, as evidenced by reduced CD68-positive macrophage accumulation and decreased levels of tumor necrosis factor-α, interleukin-1β, prostaglandin E2, and cyclooxygenase-2, restored oxidative balance by regulating superoxide dismutase and malondialdehyde contents in injured nerves. Moreover, SY upregulated nerve regeneration markers (growth-associated protein 43, myelin basic protein, β3-tubulin). Molecular docking revealed strong binding of SY to transient receptor potential vanilloid 1 (TRPV1) (-7.7 kcal/mol); molecular dynamics simulation verified stable complex formation (RMSD 0.38±0.03 nm). Biological validation demonstrated that SY markedly inhibited SNC-induced upregulation of TRPV1-pERK1/2 in sciatic nerve and dorsal root ganglion.
CONCLUSIONS: SY alleviates peripheral nerve damage, neuroinflammation, oxidative stress, promotes nerve repair in SNC rats, and is associated with modulation of TRPV1-pERK1/2 signaling, revealing a novel neuroprotective role of SY for PNI.
AIM OF THE STUDY: To explore the efficacy and potential mechanisms of SY in ameliorating PNI using a rat sciatic nerve crush (SNC) model.
MATERIALS AND METHODS: Rats were randomly assigned to four groups (n=10): Sham, SNC model, SNC+SY 20 mg/kg, and SNC+SY 40 mg/kg. All rats were sacrificed 15 days after SNC surgery.
RESULTS: SY intervention significantly promoted sciatic nerve functional recovery, alleviated mechanical allodynia, reversed denervation-induced gastrocnemius atrophy, and ameliorated histopathological damage in SNC-injured nerve tissues. Mechanistically, SY suppressed neuroinflammation, as evidenced by reduced CD68-positive macrophage accumulation and decreased levels of tumor necrosis factor-α, interleukin-1β, prostaglandin E2, and cyclooxygenase-2, restored oxidative balance by regulating superoxide dismutase and malondialdehyde contents in injured nerves. Moreover, SY upregulated nerve regeneration markers (growth-associated protein 43, myelin basic protein, β3-tubulin). Molecular docking revealed strong binding of SY to transient receptor potential vanilloid 1 (TRPV1) (-7.7 kcal/mol); molecular dynamics simulation verified stable complex formation (RMSD 0.38±0.03 nm). Biological validation demonstrated that SY markedly inhibited SNC-induced upregulation of TRPV1-pERK1/2 in sciatic nerve and dorsal root ganglion.
CONCLUSIONS: SY alleviates peripheral nerve damage, neuroinflammation, oxidative stress, promotes nerve repair in SNC rats, and is associated with modulation of TRPV1-pERK1/2 signaling, revealing a novel neuroprotective role of SY for PNI.