4-Methoxycinnamic acid

Natural products modulate Shigella-host-cell interaction.[Pubmed: 21719574]

J Med Microbiol. 2011 Nov;60(Pt 11):1626-32.

This study focused on identifying possible new options derived from natural sources for the treatment of bacterial infections. Several natural products were investigated for their potential in modulating Shigella-host-cell interactions.
METHODS AND RESULTS:
The proliferation of Shigella sonnei was effectively inhibited inside HEp-2 cells in the presence of 4-Methoxycinnamic acid and propolin D. Propolin D also significantly reduced the apoptosis of infected macrophage-like U937 cells and moderately reduced the secretion of interleukin (IL)-1β and IL-18, which probably resulted from the inhibition of invasion plasmid antigen B secretion by this compound. Further characterization showed that propolin D did not prevent escape of Shigella from phagocytic vacuoles, as evidenced by actin-based motility and by the fact that addition of chloroquine did not further reduce the number of intracellular c.f.u. The role of propolin D in modulating autophagy could not be established under the experimental conditions used.
CONCLUSIONS:
As these compounds had no direct anti-Shigella activity in vitro, it was concluded that these compounds modulated Shigella-host-cell interactions by targeting yet-to-be defined mechanisms that provide benefits to host cells.

Photosensitive semiconductor nanocrystals, photosensitive composition comprising semiconductor nanocrystals and method for forming semiconductor nanocrystal pattern using the same[Reference: WebLink]

US 8758864 B2[P]. 2014.

4. The organic-inorganic hybrid electroluminescent device according to claim 1, wherein the compound containing a photosensitive functional group is selected from a group consisting of methacrylic acid, crotonic acid, vinylacetic acid, tiglic acid, 3,3-dimethylacrylic acid, trans-2-pentenoic acid, 4-pentenoic acid, trans-2-methyl-2-pentenoic acid, 2,2-dimethyl-4-pentenoic acid, trans-2-hexenoic acid, trans-3-hexenoic acid, 2-ethyl-2-hexenoic acid, 6-heptenoic acid, 2-octenoic acid, citronellic acid, undecylenic acid, myristoleic acid, palmitoleic acid, oleic acid, elaidic acid, cis-11-elcosenoic acid, euric acid, nervonic acid, trans-2,4-pentadienoic acid, 2,4-hexadienoic acid, 2,6-heptadienoic acid, geranic acid, linoleic acid, 11,14-eicosadienoic acid, cis-8,11,14-eicosatrienoic acid, arachidonic acid, cis-5,8,11,14,17-eicosapentaenoic acid, cis-4,7,10,13,16,19-docosahexaenoic acid, fumaric acid, maleic acid, itaconic acid, ciraconic acid, mesaconic acid, trans-glutaconic acid, trans-beta-hydromuconic acid, trans-traumatic acid, trans-muconic acid, cis-aconitic acid, trans-aconitic acid, cis-3-chloroacrylic acid, trans-3-chloroacrylic acid, 2-bromoacrylic acid, 2-(trifluoromethyl)acryl-ic acid, trans-styrylacetic acid, trans-cinnamic acid, alpha.-methylcinnamic acid, 2-methylcinnamic acid, 2-fluorocinnamic acid, 2-(trifluoromethyl)cinnamic acid, 2-chlorocinnamic acid, 2-methoxycinnamic acid, 2-hydroxycinnamic acid, 2-nitrocinnamic acid, 2-carboxycinnamic acid, trans-3-fluorocinnamic acid, 3-(trifluoromethyl)cinnamic acid, 3-chlorocinnamic acid, 3-bromocinnamic acid, 3-methoxycinnamic acid, 3-hydroxycinnamic acid, 3-nitrocinnamic acid, 4-methylcinnamic acid, 4-fluorocinnamic acid, trans-4-(trifluoromethyl)-cinnamic acid, 4-chlorocinnamic acid, 4-bromocinnamic acid, 4-Methoxycinnamic acid, 4-hydroxycinnamic acid, 4-nitrocinnamic acid, 3,3-dimethoxycinnamic acid, 4-vinylbenzoic acid, allyl methyl sulfide, allyl disulfide, diallyl amine, oleylamine, 3-amino-1-propanol vinyl ether, 4-chlorocinnamonitrile, 4-methoxycinnamonitrile, 3,4-dimethoxycinnamonitrile, 4-dimethylaminocinnamonitrile, acrylonitrile, allyl cyanide, crotononitrile, methacrylonitrile, cis-2-pentenenitrile, trans-3-pentenenitrile, 3,7-dimethyl-2,6-octadienenitrile, and 1,4-dicyano-2-butene.

Protective effect of p-methoxycinnamic acid, an active phenolic acid against 1,2-dimethylhydrazine-induced colon carcinogenesis: modulating biotransforming bacterial enzymes and xenobiotic metabolizing enzymes.[Pubmed: 24908112 ]

Mol Cell Biochem. 2014 Sep;394(1-2):187-98.

Objective of the study is to evaluate the modifying potential of p-methoxycinnamic acid (4-Methoxycinnamic acid,p-MCA), an active rice bran phenolic acid on biotransforming bacterial enzymes and xenobiotic metabolizing enzymes in 1,2-dimethylhydrazine-induced rat colon carcinogenesis.
METHODS AND RESULTS:
48 male albino wistar rats were divided into six groups. Group1 (control) received modified pellet diet and 0.1 % carboxymethylcellulose; group2 received modified pellet diet along with p-MCA (80 mg/kg b.wt. p.o.) everyday for 16 weeks; groups 3-6 received 1,2-dimethylhydrazine (DMH) (20 mg/kg b.wt.) subcutaneous injection once a week for the first 4 weeks, while groups 4-6 received p-MCA at three different doses of 20, 40 and 80 mg/kg b.wt. p.o. everyday for 16 weeks. A significant increase in carcinogen-activating enzymes (cytochrome P450, cytochrome b5, cytochrome P4502E1, NADH-cytochrome-b5-reductase and NADPH-cytochrome-P450 reductase) with concomitant decrease in phaseII enzymes, DT-Diaphorase, glutathione S-transferase, UDP-glucuronyl-transferase and gamma glutamyltransferase were observed in group3 compared to control. DMH treatment significantly increased the activities of feacal and colonic bacterial enzymes (β-glucosidase, β-galactosidase, β-glucuronidase, nitroreductase, sulphatase and mucinase). p-MCA supplementation (40 mg/kg b.wt) to carcinogen exposed rats inhibited these enzymes, which were near those of control rats.
CONCLUSIONS:
The formation of dysplastic aberrant crypt foci in the colon and the histopathological observations of the liver also supports our biochemical findings. p-MCA (40 mg/kg b.wt.) offers remarkable modulating efficacy of biotransforming bacterial and xenobiotic metabolizing enzymes in colon carcinogenesis.

Mechanisms of p-methoxycinnamic acid-induced increase in insulin secretion.[Pubmed: 22009371 ]

Inhibitory effects of cinnamic acid and its derivatives on the diphenolase activity of mushroom ( Agaricus bisporus ) tyrosinase.[Reference: WebLink]

Food Chem.,2005, 92(4):707-12.

The effects of cinnamic acid and its derivatives (2-hydroxycinnamic acid, 4-hydroxycinnamic acid and 4-Methoxycinnamic acid) on the activity of mushroom tyrosinase have been studied.
METHODS AND RESULTS:
Results showed that cinnamic acid, 4-hydroxycinnamic acid and 4-Methoxycinnamic acid strongly inhibited the diphenolase activity of mushroom tyrosinase and the inhibition was reversible. The IC 50 values were estimated to be 2.10, 0.50 and 0.42 mM, respectively. 2-Hydroxycinnamic acid had no inhibitory effect on the diphenolase activity of the enzyme. Kinetic analyses showed that the inhibition type of cinnamic acid and 4-Methoxycinnamic acid was noncompetitive with the constants ( K I) determined to be 1.994 and 0.458 mM, respectively.
CONCLUSIONS:
The inhibition type of 4-hydroxycinnamic acid was competitive, with the inhibition constant ( K I) was 0.244 mM.

Horm. Metab. Res.,2011 Oct;43(11): 766-73. 

p-Methoxycinnamic acid (4-Methoxycinnamic acid,p-MCA) is a cinnamic acid derivative that shows various pharmacologic actions such as hepatoprotective and antihyperglycemic activities.
METHODS AND RESULTS:
The present study was to elucidate the mechanisms by which p-MCA increases [Ca2⁺]i and insulin secretion in INS-1 cells. p-MCA (100 μM) increased [Ca2⁺]i in INS-1 cells. The p-MCA-induced insulin secretion and rise in [Ca2⁺]i were markedly inhibited in the absence of extracellular Ca2⁺ or in the presence of an L-type Ca2⁺ channel blocker nimodipine. These results suggested that p-MCA increased Ca2⁺ influx via the L-type Ca2⁺ channels. Diazoxide, an ATP-sensitive K⁺ channel opener, did not alter p-MCA-induced insulin secretion, nor [Ca2⁺]i response. In addition, p-MCA enhanced glucose-, glibenclamide-induced insulin secretion whereas it also potentiated the increase in insulin secretion induced by arginine, and Bay K 8644, an L-type Ca2⁺ channel agonist.
CONCLUSIONS:
Taken together, our results suggest that p-MCA stimulated insulin secretion from pancreatic β-cells by increasing Ca2⁺ influx via the L-type Ca2⁺ channels, but not through the closure of ATP-sensitive K⁺ channels.