Phytochemicals in Foods - 10 Health Benefits of Cinnamic acid

Cinnamic acid is a phytochemical in the class of Hydroxycinnamic acids, found abundantly in cinnamon, aloe. etc.

Health Benefits
1. Depigmenting activity
In the examination of the effects of cinnamic acid on melanin biosynthesis within the melanocytes and brown guinea pigs, found that cinnamic acid exhibited depigmenting activity on the UV-B-induced hyperpigmentation of brown guinea pig skin. Our results suggest that cinnamic acid might act as a skin whitening agent via inhibition of tyrosinase activity and expression within melanocytes, according to "Inhibitory effects of cinnamic acid on melanin biosynthesis in skin" by Kong YH, Jo YO, Cho CW, Son D, Park S, Rho J, Choi SY.(1)

2. Gastroprotective Effect
in the sudy of the ulcer-preventive properties of aqueous extract of ginger rhizome (GRAE) belonging to the family Zingiberceae, found that compositional analysis favored by determination of the efficacy of individual phenolic acids towards their potential ulcer-preventive ability revealed that between cinnamic (50%) and gallic (46%) phenolic acids, cinnamic acid appear to contribute to better H(+), K(+)-ATPase and Helicobacter pylori inhibitory activity, while gallic acid contributes significantly to anti-oxidant activity, according to "Gastroprotective Effect of Ginger Rhizome (Zingiber officinale) Extract: Role of Gallic Acid and Cinnamic Acid in H+, K+-ATPase/H. pylori Inhibition and Anti-oxidative Mechanism" by Nanjundaiah SM, Annaiah HN, M Dharmesh S.(2)

3. Antioxidant effects
found that TPP-OH protected cells against H(2)O(2) and linoleic acid hydroperoxide-induced oxidative stress. As mitochondrial oxidative damage is associated with a number of clinical disorders, TPP-OH may be a useful lead that could be added to the family of mitochondria-targeted antioxidants that can decrease mitochondrial oxidative damage, according to "Rational discovery and development of a mitochondria-targeted antioxidant based on cinnamic acid scaffold" by Teixeira J, Soares P, Benfeito S, Gaspar A, Garrido J, Murphy MP, Borges F.(3)

4. Prostate cancer
In the study, testing the effects of tetra-bromo-cinnamic acid (TBCA) as an effort to develop new chemotherapy for prostate cancers, found that TBCA blocked AR nuclear translocation and gene expression. To confirm the target specificity, we used gene-specific siRNAs for both CK2α and CK2α' subunits, and the results suggested that both CK2 catalytic subunits are involved in androgen-stimulated AR nuclear translocation and AR-mediated gene expression in prostate cancer cells, according to "Casein kinase 2 inhibition attenuates androgen receptor function and cell proliferation in prostate cancer cells" by Yao K, Youn H, Gao X, Huang B, Zhou F, Li B, Han H.(4)

5. Antimicrobial activity
In a series of cinnamic acid derivatives synthesized and then brominated with bromine in the presence of chloroform or acetic acid, found that the tested compounds had mainly antifungal activity and were moderately active against Gram-positive bacteria. Bromination of the double bond determined the enhancement of the antimicrobial activity for all the tested compounds, according to "[Antimicrobial activity of some cinnamic acid derivatives].[Article in Romanian]" by Jităreanu A, Tătărîngă G, Zbancioc AM, Tuchiluş C, Stănescu U.(5)

6. Insulin secretion
in the elucidation of the mechanisms by which p-Methoxycinnamic acid (p-MCA), a cinnamic acid increases [Ca2+]i and insulin secretion in INS-1 cells. p-MCA (100 μM) increased [Ca2+]i in INS-1 cells, found that 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. 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, according to "Mechanisms of p-methoxycinnamic acid-induced increase in insulin secretion" by
Adisakwattana S, Hsu WH, Yibchok-anun S.(6)

7. Lung cancer
In the development of a practicable method previously to transform and obtain pure c-CA, and the pure compound was used to evaluate the anti-invasive effect on human adenocarcinoma A549 cells, found that the invasive ability was significantly (p<0.05) reduced to 68% and 65%, respectively, relative to PMA treatment alone after treatment of PMA-treated A549 cells with either 50 μM c-CA or 100 μM t-CA for 24 h. The results suggest that both of the c-CA and t-CA are inhibitors for invasion of A549 cells and the activity of c-CA seems to be higher than t-CA, according to "A comparative study on the effectiveness of cis- and trans-form of cinnamic acid treatments for inhibiting invasive activity of human lung adenocarcinoma cells" by Yen GC, Chen YL, Sun FM, Chiang YL, Lu SH, Weng CJ.(7)

8. Anti-platelet aggregation
A series of novel ligustrazinyloxy-cinnamic acid derivatives were synthesized and evaluated for their inhibitory effect on adenosine diphosphate (ADP)-induced platelet aggregation in vitro,
found that compound 2e displayed the highest protective effect on the proliferation of the damaged ECV-304 cells (EC(50) = 0.020 mM), and compound 2f was the most active anti-platelet aggregation agent (EC(50) = 0.054 mM). Structure-activity relationships were briefly discussed, according to "Ligustrazine derivatives. Part 5: design, synthesis and biological evaluation of novel ligustrazinyloxy-cinnamic acid derivatives as potent cardiovascular agents" by Chen H, Li G, Zhan P, Liu X.(8)

9. Hypoglycemic effects
In the study of the effect of cinnamic acid, ferulic acid, p-coumaric acid, eugenol, chlorogenic acid, and caffeic acid, alone and in combination with two commercial oral hypoglycemic drugs (OHD), namely, thiazolidinedione (THZ) and metformin, on the uptake of 2-deoxyglucose (2DG) by 3T3-L1 adipocytes, found that Chlorogenic and cinnamic acids increased the expression of PPARγ, whereas other hydroxycinnamic acids enhanced the expression of PI3K, indicating different mechanisms of action between these compounds. These phytochemicals were able to reduce the expressions of the fatty acid synthase and HMG CoA reductase genes, indicating that they may be able to reduce the secondary complications caused by the accumulation of lipids, according to "Interaction of cinnamic acid derivatives with commercial hypoglycemic drugs on 2-deoxyglucose uptake in 3T3-L1 adipocytes' by Prabhakar PK, Doble M.(9)

10. Anti malarial activity
In the assessment, in vitro of antimalarial activity of four compounds isolated from Kigelia africana stem bark (atranorin - KAE1, specicoside - KAE7, 2β,3β,19α-trihydroxy-urs-12-20-en-28-oic acid - KAE3, and p-hydroxy-cinnamic acid - KAE10) and their drug interactions among themselves and their combination effects with quinine and artemetherinvestigation of the antiplasmodial activity and drug interactions against the multidrug-resistant W2mef strain of Plasmodium falciparum using the parasite lactate dehydrogenase assay, found that all the three compounds showed synergistic effects with artemether, unlike the slight antagonistic interactions of atranorin and 2β,3β,19α-trihydroxy-urs-12-en-28-oic acid in combination with quinine. K. africana compounds are therefore likely to serve as leads in the development of new partner drugs in artemether-based combination therapy, according to "Antimalarial drug interactions of compounds isolated from Kigelia africana (Bignoniaceae) and their synergism with artemether, against the multidrug-resistant W2mef Plasmodium falciparum strain" by Zofou D, Tene M, Tane P, Titanji VP.(10)

11. Etc.

Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/18451524
(2) http://www.ncbi.nlm.nih.gov/pubmed/19570992
(3) http://www.ncbi.nlm.nih.gov/pubmed/22292941
(4) http://www.ncbi.nlm.nih.gov/pubmed/22290244
(5) http://www.ncbi.nlm.nih.gov/pubmed/22046817
(6) http://www.ncbi.nlm.nih.gov/pubmed/22009371
(7) http://www.ncbi.nlm.nih.gov/pubmed/21871959
(8) http://www.ncbi.nlm.nih.gov/pubmed/21993151
(9) http://www.ncbi.nlm.nih.gov/pubmed/21870829
(10) http://www.ncbi.nlm.nih.gov/pubmed/21814840