Methyl cinnamate

Vasorelaxation induced by methyl cinnamate, the major constituent of the essential oil of Ocimum micranthum, in rat isolated aorta.[Pubmed: 25115734]

Clin Exp Pharmacol Physiol. 2014 Oct;41(10):755-62.

The aim of the present study was to investigate the vascular effects of the E-isomer of Methyl cinnamate (E-MC) in rat isolated aortic rings and the putative mechanisms underlying these effects.
METHODS AND RESULTS:
At 1-3000 μmol/L, Methyl cinnamate concentration-dependently relaxed endothelium-intact aortic preparations that had been precontracted with phenylephrine (PHE; 1 μmol/L), with an IC50 value (geometric mean) of 877.6 μmol/L (95% confidence interval (CI) 784.1-982.2 μmol/L). These vasorelaxant effects of Methyl cinnamate remained unchanged after removal of the vascular endothelium (IC50 725.5 μmol/L;In the presence of a saturating contractile concentration of K(+) (150 mmol/L) in Ca(2+) -containing medium combined with 3 μmol/L PHE, 1000 μmol/L Methyl cinnamate only partially reversed the contractile response. In contrast, under similar conditions, Methyl cinnamate nearly fully relaxed PHE-induced contractions in aortic rings in a Ba(2+) -containing medium. In preparations that were maintained under Ca(2+) -free conditions, 600 and 1000 μmol/L Methyl cinnamate significantly reduced the contractions induced by exogenous Ca(2+) or Ba(2+) in KCl-precontracted preparations, but not in PHE-precontracted preparations (in the presence of 1 μmol/L verapamil). In addition, Methyl cinnamate (1-3000 μmol/L) concentration-dependently relaxed the contractions induced by 2 mmol/L sodium orthovanadate.
CONCLUSIONS:
Based on these observations, Methyl cinnamate-induced endothelium-independent vasorelaxant effects appear to be preferentially mediated by inhibition of plasmalemmal Ca(2+) influx through voltage-dependent Ca(2+) channels. However, the involvement of a myogenic mechanism in the effects of Methyl cinnamate is also possible.

Optimization of antimicrobial and physical properties of alginate coatings containing carvacrol and methyl cinnamate for strawberry application.[Pubmed: 24405047]

J Agric Food Chem. 2014 Jan 29;62(4):984-90.

Increasing strawberry consumption has led to a growing safety concern because they are not washed after harvest.
METHODS AND RESULTS:
An antimicrobial edible coating could be an effective postharvest technique to ensure microbial safety and, at the same time, retain overall quality of the fruits. Response surface methodology was used to optimize the antimicrobial activity against Escherichia coli O157:H7 and Botrytis cinerea and several physical properties (turbidity, viscosity, and whitish index) of an alginate coating. A full factorial design was used to select the concentrations of carvacrol and Methyl cinnamate on the basis of their effect against E. coli and B. cinerea. A central composite design was then performed to evaluate the effects/interactions of the two antimicrobials on the coating characteristics.
CONCLUSIONS:
The results from analysis of variance showed the significant fitting of all responses to the quadratic model. To attain the desirable responses, the optimal concentrations were 0.98% (w/w) carvacrol and 1.45% (w/w) Methyl cinnamate.

Increasing strawberry shelf-life with carvacrol and methyl cinnamate antimicrobial vapors released from edible films.[Reference: WebLink]

Postharvest Biol. Tec., 2014, 89(3):11-8.

The effect of carvacrol and Methyl cinnamate vapors incorporated into strawberry puree edible films on the postharvest quality of strawberry fruit (Fragaria × ananassa) was investigated.
METHODS AND RESULTS:
Fresh strawberries were packed in clamshells and kept at 10 °C for 10 days with 90% RH. Strawberry puree edible films, applied in the clamshell, served as carriers for the controlled release of natural antimicrobial compounds without direct contact with the fruit. Changes in weight loss, visible decay, firmness, surface color, total soluble solids content, total soluble phenolics content and antioxidant capacity of strawberries during storage were evaluated. A significant delay and reduction in the severity of visible decay was observed in fruit exposed to antimicrobial vapors. Carvacrol and Methyl cinnamate vapors released from the films helped to maintain firmness and brightness of strawberries as compare to the untreated strawberries. The natural antimicrobial vapors also increased the total soluble phenolics content and antioxidant activity of fruit at the end of the storage period.

Myorelaxant effects of methyl cinnamate, the major constituent of the essential oil of Ocimum micranthum, on smooth muscle of the gastrointestinal tract of rats.[Reference: WebLink]

Planta Med., 2013, 79(13):PF5-6.

Methyl cinnamate (MC) is a flavoring compound naturally found in the essential oil of Ocimum micranthum Willd. (EOOM), but its effects on gastrointestinal tract are not known. This study aimed to characterize the pharmacological actions of the EOOM (˜40% of MC) and MC on the contractile behavior of strips from rat gastrointestinal smooth muscle disposed in bath chambers.
METHODS AND RESULTS:
EOOM (0.1 to 500 μg/ml) had antispasmodic effects against contractions induced by carbachol (CCh; 1μM; IC50 of 91.9 μg/ml) or KCl (60 mM; IC50 of 46.8 μg/ml) in strips of rat stomach fundus, whereas MC inhibited CCh with IC50 of 63.6 μg/ml (392.6 [227.8 – 675.9] μM; [geometric mean [95% C.I.]; n = 5) or KCl with IC50 of 34.5 μg/ml (213.0 [96.0 – 472.4] μM; n = 8). In strips of gastric antrum, duodenum or large intestine, the inhibitory actions of MC was not significantly different in comparison to that in fundic strips (p > 0.05, ANOVA). The myorelaxant effect of MC on CCh-induced contractions was not changed by pretreatment with L-NAME (300μM; IC50 of 382.9 [340.0 – 431.3] μM; n = 6) or tetraethylammonium (TEA; 3 mM; IC50 of 399.5 [149.8 – 1065.5] μM; n = 6). In presence of 0.2 mM sodium orthovanadate, a tyrosine phosphatase inhibitor, the CCh-induced contraction was reduced by MC (1 mM) to 43.8 ± 8.2% of the control (n = 11), value significantly higher than 26.7 ± 6.6% (n = 11) observed with MC alone (p < 0.05, Student's t test). In Fluo4-loaded freshly isolated smooth muscle cells from large intestine, MC (600μM) significantly decreased the cytoplasmic level of Ca2+ measured by confocal microscopy (p < 0.05, Holm-Sidak). Under Ca2+-free conditions, MC (300μM) also inhibited the intracellularly mediated transient contractions induced by acetylcholine (3μM) or caffeine (20 mM).
CONCLUSIONS:
In conclusion, MC appears involved in the relaxant effect of EOOM. The effects of MC recruit a decrease in the intracellular levels of Ca2+, being partially blunted by the inhibition of the protein tyrosine phosphatase.

Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.[Pubmed: 22273148]

J Agric Food Chem. 2012 Feb 1;60(4):955-63.

Methyl cinnamate, an active component of Zanthoxylum armatum , is a widely used natural flavor compound with antimicrobial and tyrosinase inhibitor activities. However, the underlying bioactivity and molecular mechanisms of Methyl cinnamate on adipocyte function and metabolism remain unclear. The aim of this study was to investigate the inhibitory effect of Methyl cinnamate on adipogenesis in 3T3-L1 preadipocytes.
METHODS AND RESULTS:
Methyl cinnamate markedly suppressed triglyceride accumulation associated with down-regulation of adipogenic transcription factor expression, including sterol regulatory element binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer-binding protein α (C/EBPα). Additionally, Methyl cinnamate-inhibited PPARγ activity and adipocyte differentiation were partially reversed by the PPARγ agonist troglitazone. Furthermore, Methyl cinnamate stimulated Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and phospho-AMP-activated protein kinase (AMPK) expression during adipogenesis.
CONCLUSIONS:
This study first revealed Methyl cinnamate has antiadipogenic activity through mechanisms mediated, in part, by the CaMKK2-AMPK signaling pathway in 3T3-L1 cells.