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Abstract Title:

The cannabinoid beta-caryophyllene (BCP) induces neuritogenesis in PC12 cells by a cannabinoid-receptor-independent mechanism.

Abstract Source:

Chem Biol Interact. 2017 Jan 5 ;261:86-95. Epub 2016 Nov 18. PMID: 27871898

Abstract Author(s):

Neife Aparecida Guinaim Santos, Nádia Maria Martins, Flávia Malvestio Sisti, Laís Silva Fernandes, Rafaela Scalco Ferreira, Osvaldo de Freitas, Antônio Cardozo Santos

Article Affiliation:

Neife Aparecida Guinaim Santos

Abstract:

Beta-caryophyllene (BCP) is a phytocannabinoid whose neuroprotective activity has been mainly associated with selective activation of cannabinoid-type-2 (CB2) receptors, inhibition of microglial activation and decrease of inflammation. Here, we addressed the potential of BCP to induce neuritogenesis in PC12 cells, a model system for primary neuronal cells that express trkA receptors, respond to NGF and do not express CB2 receptors. We demonstrated that BCP increases the survival and activates the NGF-specific receptor trkA in NGF-deprived PC12 cells, without increasing the expression of NGF itself. The neuritogenic effect of BCP in PC12 cells was abolished by k252a, an inhibitor of the NGF-specific receptor trkA. Accordingly, BCP did not induce neuritogenesis in SH-SY5Y neuroblastoma cells, a neuronal model that does not express trkA receptors and do not respond to NGF. Additionally, we demonstrated that BCP increases the expression of axonal-plasticity-associated proteins (GAP-43, synapsin and synaptophysin) in PC12 cells. It is known that these proteins are up-regulated by NGF in neurons and neuron-like cells, such as PC12 cells. Altogether, these findings suggest that BCP activates trka receptors and induces neuritogenesis by a mechanism independent of NGF or cannabinoid receptors. This is the first studyto show such effects of BCP and their beneficial role in neurodegenerative processes should be further investigated.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Neuritogenic : CK(185) : AC(101)

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