Echinacea

 from Wikipedia

"The immunomodulatory effects of echinacea preparations are likely caused by fat-soluble alkylamides (alkamides), which occur mostly in E. angustifolia and E. purpurea but not in E. pallida.^[22] Alkylamides bind particularly to human CB2 and to a much lesser degree to CB1 cannabinoid receptors; as a result they are implicated in a variety of modulatory functions, including immune suppression, induction of apoptosis, cell migration and inhibition of tumor necrosis factor α TNF-alpha^[23] These Alkylamides have similar potency to that of THC at the CB2 receptor, with THC being around 1.5 times stronger (~40 nm vs ~60 nm affinities). However, potency is dramatically less than that of THC at the psychoactive CB1 receptor (~40 nm vs ~ >1500 nm affinities).
As with any herbal preparation, individual doses may vary significantly in active chemical composition. In addition to poor process control which may affect inter- and intra-batch homogeneity, species, plant part, extraction method, and contamination or adulteration with other products all lead to variability between products.^[24][25]"
 Echinacea extracts inhibited growth of three species of trypanosomatids: Leishmania donovani, Leishmania major, and Trypanosoma brucei.^{[35]
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Like the CB₁ receptors, CB₂ receptors inhibit the activity of adenylyl cyclase through their Gi/Go_α subunits.^[9][10] Through their G_βγ subunits, CB₂ receptors are also known to be coupled to the MAPK-ERK pathway,^[9][10][11] a complex and highly conserved signal transduction pathway, which critically regulates a number of important cellular processes in both mature and developing tissues.^[12] Activation of the MAPK-ERK pathway by CB₂ receptor agonists acting through the G_βγ subunit ultimately results in changes in cell migration^[13] as well as in an induction of the growth-related gene Zif268 (also known as Krox-24, NGFI-A, and egr-1).^[11] The Zifi268 gene encodes a transcriptional regulator implicated in neuroplasticity and long term memory formation.^[14]
At present, there are five recognized cannabinoids produced endogenously throughout the body: Arachidonoylethanolamine (anandamide), 2-arachidonoyl glycerol (2-AG), 2-arachidonyl glyceryl ether (noladin ether), virodhamine,^[9] as well as the recently-discovered N-arachidonoyl-dopamine (NADA).^[15] Many of these ligands appear to exhibit properties of functional selectivity at the CB₂ receptor: 2-AG preferentially activates the MAPK-ERK pathway, while noladin preferentially inhibits adenylyl cyclase.^[9] Like noladin, the synthetic ligand CP-55,940 has also been shown to preferentially inhibit adenylyl cyclase in CB₂ receptors.^[9] Together, these results support the emerging concept of agonist-directed trafficking at the cannabinoid receptors." wikipedia
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