peel of Punica granatum L.
Tannic acid/Gallotannin,Tannin/Gallotannin Tannin/Glycerite
Methanol; Water; DMSO
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provides coniferyl ferulate(CAS#:1401-55-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The aim of the study was to determine the relationship between anti-inflammatory effects of the natural polyphenolic compound tannic acid (CAS number: 1401-55-4) and myeloperoxidase (MPO) enzyme activity in paw edema model. Thirty-five female rats were divided into five groups. The paws of rats were injected subcutaneously in the plantar surface with formalin except for the control group. Indomethacin and tannic acid were intraperitoneally administered 1 h after formalin injection. The paws volume was measured by using vernier caliper. MPO enzyme activity was determined using 4-aminoantipyrine-phenol solution as the substrate for MPO-mediated oxidation by H2O2. About 17% and 13% edema inhibition has detected in the indomethacin-applied group, at the measurements run every other hour right after the treatment. An inhibition of 16% was found at the group treated with 25 mg/kg tannic acid. However, in the group treated with 50 mg/kg tannic acid, 15% and 7% of the edema inhibition was observed. Serum and paw tissue MPO activities were decreased in treated groups with indomethacin and tannic acid according to formalin control group. Our study results suggest that tannic acid may contribute to the treatment of inflammation by decreasing MPO enzyme activity, but the molecular mechanism is still not clear.
% inhibition; Tannic acid; anti-inflammatory efficiency; formalin; myeloperoxidase; paw edema; rat
Tannic acid exhibits anti-inflammatory effects on formalin-induced paw edema model of inflammation in rats.
Soyocak A1, Kurt H2, Cosan DT2, Saydam F3, Calis IU2, Kolac UK2, Koroglu ZO4, Degirmenci I5, Mutlu FS6, Gunes HV2.
Catechol (CAS: 120-80-9), given in drinking water to rats, was the most effective of 5 phenols in enhancing [3H]thymidine incorporation [( 3H]dThd-l) into esophageal DNA. To test for esophageal cocarcinogenesis, groups of 30 male MRC-Wistar rats received 3 weekly ip injections of 25 mg methyl-n-amylnitrosamine [(MNAN) CAS: 13256-07-0]/kg. From the time of the first MNAN injection, each group also received catechol, tannic acid (CAS: 1401-55-4), dried leaves of Bidens pilosa L., or croton oil (CAS: 8001-28-3) (respectively, 2, 10, 50, and 2 g/kg semipurified diet), or were given 20 ip injections of 6 mg phorbol (CAS: 17673-25-5)/rat. The rats were killed after 20-45, 46-52, or 53-72 weeks (subgroups A, B, and C). In the group given MNAN alone, most esophageal papillomas developed during the first 45 weeks. Both catechol and B. pilosa significantly increased the esophageal papilloma multiplicity (No. of papillomas/rat) induced by MNAN, with a maximum tumor yield of 2.2 times that in the corresponding subgroup treated with MNAN alone. Papilloma multiplicity increased from subgroup A to subgroup C in the MNAN plus B. pilosa group but not in the MNAN plus catechol group. No tumors were induced by the test cocarcinogens given without MNAN. We concluded that a) an increased esophageal [3H]dThd-I indicates potential cocarcinogenicity and b) catechol and B. pilosa were weak esophageal cocarcinogens. These results support the view that catechol in cigarette smoke and B. pilosa as eaten in South Africa contribute to the etiology of human esophageal cancer.
Test of catechol, tannic acid, Bidens pilosa, croton oil, and phorbol for cocarcinogenesis of esophageal tumors induced in rats by methyl-n-amylnitrosamine.
Mirvish SS, Salmasi S, Lawson TA, Pour P, Sutherland D.
Amyloid precursor protein (APP) proteolysis is essential for production of amyloid-β (Aβ) peptides that form β-amyloid plaques in brains of Alzheimer disease (AD) patients. Recent focus has been directed toward a group of naturally occurring anti-amyloidogenic polyphenols known as flavonoids. We orally administered the flavonoid tannic acid (TA) to the transgenic PSAPP mouse model of cerebral amyloidosis (bearing mutant human APP and presenilin-1 transgenes) and evaluated cognitive function and AD-like pathology. Consumption of TA for 6 months prevented transgene-associated behavioral impairment including hyperactivity, decreased object recognition, and defective spatial reference memory, but did not alter nontransgenic mouse behavior. Accordingly, brain parenchymal and cerebral vascular β-amyloid deposits and abundance of various Aβ species including oligomers were mitigated in TA-treated PSAPP mice. These effects occurred with decreased cleavage of the β-carboxyl-terminal APP fragment, lowered soluble APP-β production, reduced β-site APP cleaving enzyme 1 protein stability and activity, and attenuated neuroinflammation. As in vitro validation, we treated well characterized mutant human APP-overexpressing murine neuron-like cells with TA and found significantly reduced Aβ production associated with less amyloidogenic APP proteolysis. Taken together, these results raise the possibility that dietary supplementation with TA may be prophylactic for AD by inhibiting β-secretase activity and neuroinflammation and thereby mitigating AD pathology.
Alzheimers Disease, Amyloid, Flavonoids, Plant, Transgenic Mice, Anti-amyloidogenic, Compound
Tannic Acid Is a Natural β-Secretase Inhibitor That Prevents Cognitive Impairment and Mitigates Alzheimer-like Pathology in Transgenic Mice*
Takashi Mori,a,b,1 Kavon Rezai-Zadeh,c Naoki Koyama,a Gary W. Arendash,d,e Haruyasu Yamaguchi,f Nobuto Kakuda,g Yuko Horikoshi-Sakuraba,g Jun Tan,h,i and Terrence Townc,j,k,2
2012 Jan 4.
Tannic acid is a novel hERG channel blocker with IC50 of 3.4 μM.