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Siler divaricatum
Key TCM wind-releasing herb used for pain, spasm, skin conditions, and reducing fever.
Siler divaricatum (syn. Saposhnikovia divaricata) is a key wind-dispelling herb in Traditional Chinese Medicine, used for pain, spasms, skin conditions, and fever. Its primary active compounds include chromone glycosides (prim-O-glucosylcimifugin, cimifugin, sec-O-glucosylhamaudol) and polyacetylenes, which contribute to its anti-inflammatory, analgesic, and antispasmodic properties. Evidence is limited (Grade C) but supports its traditional applications.
The anti-inflammatory and analgesic effects of S. divaricatum are mediated through inhibition of COX-2 and 5-LOX pathways, reducing prostaglandin and leukotriene synthesis. The chromone glycosides, particularly prim-O-glucosylcimifugin, suppress NF-κB activation and downregulate pro-inflammatory cytokines (TNF-α, IL-6). Antispasmodic activity involves blockade of voltage-dependent calcium channels and modulation of GABAergic transmission. Immunomodulation occurs via enhancement of macrophage phagocytosis and regulation of Th1/Th2 balance.
Key TCM wind-releasing herb used for pain, spasm, skin conditions, and reducing fever.
Siler divaricatum (syn. Saposhnikovia divaricata) is a key wind-dispelling herb in Traditional Chinese Medicine, used for pain, spasms, skin conditions, and fever. Its primary active compounds include chromone glycosides (prim-O-glucosylcimifugin, cimifugin, sec-O-glucosylhamaudol) and polyacetylenes, which contribute to its anti-inflammatory, analgesic, and antispasmodic properties. Evidence is limited (Grade C) but supports its traditional applications.
The anti-inflammatory and analgesic effects of S. divaricatum are mediated through inhibition of COX-2 and 5-LOX pathways, reducing prostaglandin and leukotriene synthesis. The chromone glycosides, particularly prim-O-glucosylcimifugin, suppress NF-κB activation and downregulate pro-inflammatory cytokines (TNF-α, IL-6). Antispasmodic activity involves blockade of voltage-dependent calcium channels and modulation of GABAergic transmission. Immunomodulation occurs via enhancement of macrophage phagocytosis and regulation of Th1/Th2 balance.