RESUMEN
Objective: The barks, leaves, and branches of Cinnamomum cassia have been historically used as a traditional Chinese medicine, spice, and food preservative, in which phenylpropanoids are responsible compounds. However phenylpropanoid biosynthesis pathways are not clear in C. cassia. We elucidated the pathways by descriptive analyses of differentially expressed genes related to phenylpropanoid biosynthesis as well as to identify various phenylpropanoid metabolites. Methods: Chemical analysis, metabolome sequencing, and transcriptome sequencing were performed to investigate the molecular mechanisms underlying the difference of active components content in the barks, branches and leaves of C. cassia. Results: Metabolomic analysis revealed that small amounts of flavonoids, coumarine, and cinnamaldehyde accumulated in both leaves and branches. Transcriptome analysis showed that genes associated with phenylpropanoid and flavonoid biosynthesis were downregulated in the leaves and branches relative to the barks. The observed differences in essential oil content among the three tissues may be attributable to the differential expression of genes involved in the phenylpropanoid and flavonoid metabolic pathways. Conclusion: This study identified the key genes in the phenylpropanoid pathway controling the flavonoid, coumarine, and cinnamaldehyde contents in the barks, branches and leaves by comparing the transcriptome and metabolome. These findings may be valuable in assessing phenylpropanoid and flavonoid metabolites and identifying specific candidate genes that are related to the synthesis of phenylpropanoids and flavonoids in C. cassia.
RESUMEN
Cannabidiol (CBD) and cannabis-based medicines are potential therapeutic agents. Because the immune system has been widely demonstrated to be affected by psychoactive cannabinoids, such as Delta(9)-tetrahydrocannabinol, the objective of the present studies is to investigate the immunomodulatory effect of CBD, the major non-psychoactive cannabinoid in marijuana. BALB/c mice were intraperitoneally administered with a single dose of CBD (5-20 mg/kg) prior to ovalbumin (OVA) sensitization, and the serum production of antigen-specific antibodies was measured 7 days post OVA sensitization. The serum level of OVA-specific IgM was significantly attenuated by a high dose of CBD (20 mg/kg), and OVA-specific IgG(1) and IgG(2a) by all 3 doses of CBD. Concordantly, splenocytes of mice administered with CBD (5 or 20 mg/kg) produced less IL-2, IL-4 and IFN-gamma than those of vehicle-treated controls, upon ex vivo stimulation with phorbol ester plus calcium ionophore. Likewise, T-cell mitogen (concanavalin A)-induced proliferation of splenocytes was also markedly suppressed in mice administered with CBD. Furthermore, the observed ex vivo effects of CBD on cytokine production and T-cell proliferation were confirmed in splenocytes directly exposed to CBD (1-8 microM) in vitro, indicating a direct effect by CBD. Taken together, the results demonstrated that CBD markedly suppressed antigen-specific antibody production in OVA-sensitized mice, and suggest that CBD-mediated suppression of humoral immunity could be mediated by the impaired functions of splenocytes.