Sunday 3 November 2013

Phytochemicals in Foods - 9 Health Benefits of Gallic acid

Gallic acid is a phytochemical in the class of Phenolic acids, found abundantly in tea, mango, strawberries, rhubarb, soy, etc.

Health Benefits
1. Cytotoxic and antioxidative activities
In the investigation of the bioactivity guided isolation and characterization of phytoconstituents, indicated the extract showed strong radical scavenging effects against DPPH, nitric oxide (NO) and superoxide (SO) radicals comparable to that of known antioxidants 3-t-butyl-4-hydroxyanisole, ascorbic acid (vitamin C), and quercetin in addition to its cytotoxic activities against HEP-2 (human larynx epidermoid carcinoma) and RD (human rhabdomyosarcoma) cell lines based on MTT assay for growth inhibition. The gallic acid equivalent total phenolic content of the plant was found to be 79.94mg/g dry extract. Phenylethanoid glycosides, verbascoside and calceorioside A were isolated from the most active fraction and both compounds showed strong radical scavenging activity against tested radicals and cytotoxicity against HEP-2, RD and MCF-7 (human breast adenocarcinoma) cell line, according to "Cytotoxic and antioxidative activities of Plantago lagopus L. and characterization of its bioactive compounds" by Sebnem Harput U, Genc Y, Saracoglu I.(1)

2. Breast cancer
In the analyzing
the Sanguisorba officinalis L. (SA) effects on human breast cancer utilizing in vitro and in vivo methodologies, found that SA inhibited proliferation, induced S phase arrest and triggered mitochondrial pathway apoptosis in both cancer cells. Angiogenesis experiments revealed that SA inhibited VEGF expression in both cancer cell lines. Meanwhile, the proliferation, tube formation and migration abilities of endothelial cells were also inhibited. In vivo experiments demonstrated that SA reduced tumor size and neoangiogenesis in both cancer xenografts. Gallic acid and ellagic acid were finally identified as bioactive compounds in SA, according to "Effect of Sanguisorba officinalis L on breast cancer growth and angiogenesis" by Wang Z, Loo WT, Wang N, Chow LW, Wang D, Han F, Zheng X, Chen JP.(2)

3. Anti-leukemic effects
In the investigation of the apoptotic activity induced by GA on chronic myeloid leukemia (CML) cell line-K562 and the underlying mechanism, found that GA inhibited BCR/ABL tyrosine kinase and NF-κB. In conclusion, GA induced apoptosis in K562 cells involves death receptor and mitochondrial-mediated pathways by inhibiting BCR/ABL kinase, NF-κB activity and COX-2, according to "Anti-leukemic effects of gallic acid on human leukemia K562 cells: Downregulation of COX-2, inhibition of BCR/ABL kinase and NF-κB inactivation" by
Chandramohan Reddy T, Bharat Reddy D, Aparna A, Arunasree KM, Gupta G, Achari C, Reddy GV, Lakshmipathi V, Subramanyam A, Reddanna P.(3)

4. Antioxidants
In the evaluation of the antioxidant, anti-inflammatory, and antiproliferative activities of organic fractions from Cystoseira sedoides (Desfontaines) C. Agardh, indicated that the F-CHCl(3) and F-AcOEt fractions showed significant total phenolic content at 55.09 and 61.30 mg gallic-acid equivalent/g dried sample, respectively. Using the DPPH method, the F-CHCl(3) and the F-AcOEt fractions exhibited the strongest radical scavenging activity, with IC(50) 120 µg/mL for F-CHCl(3) and 121 µg/mL for F-AcOEt, which approaches the activity of the powerful antioxidant standard, Trolox (IC(50) = 90 µg/mL), according to "Antioxidant, anti-inflammatory, and antiproliferative activities of organic fractions from the Mediterranean brown seaweed Cystoseira sedoides" by Mhadhebi L, Laroche-Clary A, Robert J, Bouraoui A.(4)

5. Anti cancers
In the identification of gallic acid (GA) as a major bioactive cytotoxic constituent of a polyherbal Ayurvedic formulation - triphala (TPL) on (AR)(+) LNCaP prostate cancer and normal epithelial cells, found that TPL contains 40% unidentified polyphenolic acids, of which 2.4% comprised GA. GA induced severe morphological alterations and was about 3-fold more cytotoxic towards cancer cells than TPL. This activity increased further in the presence of dihydrotestosterone. GA toxicity on normal cells was low at 72 h. Combination of GA with flutamide caused higher toxicity to cancer cells than either of the compounds alone, according to "Differential cytotoxicity of triphala and its phenolic constituent gallic acid on human prostate cancer LNCap and normal cells" by Russell LH Jr, Mazzio E, Badisa RB, Zhu ZP, Agharahimi M, Millington DJ, Goodman CB.(5)

6. Leukemia
In the investigation of the apoptotic effects induced by GA in human promyelocytic leukemia HL-60 cells, and clarify the underlying mechanism, found that GA-mediated apoptosis of HL-60 cells mainly depended on up-regulation of the mRNA of caspase-8, caspase-9, caspase-3, AIF and Endo G. In conclusion, GA-induced apoptosis occurs through the death receptor and mitochondria-mediated pathways, according to "Gallic acid induces G₀/G₁ phase arrest and apoptosis in human leukemia HL-60 cells through inhibiting cyclin D and E, and activating mitochondria-dependent pathway" by Yeh RD, Chen JC, Lai TY, Yang JS, Yu CS, Chiang JH, Lu CC, Yang ST, Yu CC, Chang SJ, Lin HY, Chung JG(6)

7. Colon cancer
found that
In vivo, GT (25 mg/kg body weight) injected intraperitoneally (i.p.) prior to or after tumor inoculation significantly decreased the volume of human colon cancer xenografts in NOD/SCID mice. GT-treated xenografts showed significantly lower microvessel density (CD31) as well as lower mRNA expression levels of IL-6, TNF-α and IL-1α and of the proliferation (Ki-67) and angiogenesis (VEGFA) proteins, which may explain GTs in vivo anti-tumorigenic effects, according to "Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts" by Al-Halabi R, Bou Chedid M, Abou Merhi R, El-Hajj H, Zahr H, Schneider-Stock R, Bazarbachi A, Gali-Muhtasib H.(7)

8. Anti-neoplastic effects
In the investigation of the effects of TS on various human oral squamous carcinoma cell lines (HOSCC), including UM1, UM2, SCC-4, and SCC-9, found that FACScan analysis revealed that the leaf extract induced apoptosis or a combination of apoptosis and necrosis, depending on cell type. Microarray and semi-quantitative RT-PCR analysis for apoptotic-related gene expression revealed that 3,4,5-trihydroxybenzoic acid (gallic acid, one of the major bioactive compounds purified from TS extract) up-regulated pro-apoptotic genes such TNF-α, TP53BP2, and GADD45A, and down-regulated the anti-apoptotic genes Survivin and cIAP1, resulting in cell death. This study suggests that gallic acid, the major bioactive compound present, is responsible for the anti-neoplastic effect of Toona sinensis leaf extract, according to "Anti-neoplastic effects of gallic acid, a major component of Toona sinensis leaf extract, on oral squamous carcinoma cells" by Chia YC, Rajbanshi R, Calhoun C, Chiu RH.(8)

9. Anti cancers, anti inflammatory and anti diabetic effects
In the review of 1, 2, 3, 4, 6-penta-O-galloyl-beta-D-glucose (PGG) is a polyphenolic compound highly enriched in a number of medicinal herbals, indicated that Chemically and functionally, PGG appears to be distinct from its constituent gallic acid or tea polyphenols. For anti-cancer activity, three published in vivo preclinical cancer model studies with PGG support promising efficacy to selectively inhibit malignancy without host toxicity. Potential mechanisms include anti-angiogenesis; anti-proliferative actions through inhibition of DNA replicative synthesis, S-phase arrest, and G(1) arrest; induction of apoptosis; anti-inflammation; and anti-oxidation. Putative molecular targets include p53, Stat3, Cox-2, VEGFR1, AP-1, SP-1, Nrf-2, and MMP-9. For anti-diabetic activity, PGG and analogues appear to improve glucose uptake, according to "Anti-cancer, anti-diabetic and other pharmacologic and biological activities of penta-galloyl-glucose" by Zhang J, Li L, Kim SH, Hagerman AE, Lü J(9)

10. Etc.


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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/22289578
(2) http://www.ncbi.nlm.nih.gov/pubmed/22316502
(3) http://www.ncbi.nlm.nih.gov/pubmed/22245431
(4) http://www.ncbi.nlm.nih.gov/pubmed/22115493
(5) http://www.ncbi.nlm.nih.gov/pubmed/22110195
(6) http://www.ncbi.nlm.nih.gov/pubmed/21868525
(7) http://www.ncbi.nlm.nih.gov/pubmed/21532339
(8) http://www.ncbi.nlm.nih.gov/pubmed/21081858
(9) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2822717/

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