Mangiferin - CAS 4773-96-0
Catalog number: 4773-96-0
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C19H18O11
Molecular Weight:
422.3
COA:
Inquire
Targets:
Others
Description:
Mangiferin prevents the renal glomerulus fibrosis of diabetic rats, which is realized through the suppression of osteopontin overproduction and inflammation likely via inactivation of NF-кB. Mangiferin regulates proliferation and apoptosis in glioma cells
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Purity:
≥95%
Appearance:
Solid powder
Synonyms:
1,3,6,7-tetrahydroxy-2-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]xanthen-9-one;
Solubility:
Soluble in DMSO
Storage:
Store at -20 °C
MSDS:
Inquire
Application:
Antioxidant.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Grams-Kilos
InChIKey:
AEDDIBAIWPIIBD-ZJKJAXBQSA-N
InChI:
1S/C19H18O11/c20-4-11-15(25)17(27)18(28)19(30-11)12-8(23)3-10-13(16(12)26)14(24)5-1-6(21)7(22)2-9(5)29-10/h1-3,11,15,17-23,25-28H,4H2/t11-,15-,17+,18-,19+/m1/s1
Canonical SMILES:
C1=C2C(=CC(=C1O)O)OC3=CC(=C(C(=C3C2=O)O)C4C(C(C(C(O4)CO)O)O)O)O
1.Mangiferin attenuates DSS colitis in mice: Molecular docking and in vivo approach.
Somani S1, Zambad S2, Modi K3. Chem Biol Interact. 2016 Apr 26;253:18-26. doi: 10.1016/j.cbi.2016.04.033. [Epub ahead of print]
Inflammation, oxidative stress and altered mucosal barrier permeability are potential etiopathological or triggering factors for inflammatory bowel disease (IBD). In this study, the therapeutic potential of Mangiferin was investigated in vivo in mouse model of colitis and also attempts were made to understand mechanistic insights of Mangiferin in IBD. In present study, colitis was induced by administration of 5% DSS for 11 days, followed by 3 days of DSS free period. On day 14, animals were sacrificed and colon tissues were taken for biochemical and histological analysis. Therapeutic treatment with Mangiferin after colitis induction (i.e. day 5) ameliorated symptoms of colitis (presence of blood in stools, body weight loss and diarrhea) as evidenced by reduced DAI score, attenuated the levels of catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO). It also decreased the colonic pro-inflammatory mediators tumor necrosis factor (TNF-α), interleukin 1β (IL-1β) levels, matrix metalloproteinase-9 (MMP-9) activity and histopathological score.
2.Mangiferin: a promising anticancer bioactive.
Khurana RK1, Kaur R1, Lohan S2, Singh KK3, Singh B1,2. Pharm Pat Anal. 2016 Apr 18. [Epub ahead of print]
Of late, several biologically active antioxidants from natural products have been investigated by the researchers in order to combat the root cause of carcinogenesis, in other words, oxidative stress. Mangiferin, a therapeutically active C-glucosylated xanthone, is extracted from pulp, peel, seed, bark and leaf of Mangifera indica. These polyphenols of mangiferin exhibit antioxidant properties and tend to decrease the oxygen-free radicals, thereby reducing the DNA damage. Indeed, its capability to modulate several key inflammatory pathways undoubtedly helps in stalling the progression of carcinogenesis. The current review article emphasizes an updated account on the patents published on the chemopreventive action of mangiferin, apoptosis induction made on various cancer cells, along with proposed antioxidative activities and patent mapping of other important therapeutic properties. Considering it as promising polyphenol, this paper would also summarize the diverse molecular targets of mangiferin.
3.Attenuative role of mangiferin in oxidative stress-mediated liver dysfunction in arsenic-intoxicated murines.
Saha S1, Rashid K1, Sadhukhan P1, Agarwal N1, Sil PC1. Biofactors. 2016 Mar 28. doi: 10.1002/biof.1276. [Epub ahead of print]
Mangiferin (MAG), a natural xanthone mainly derived from mangoes, possesses great antioxidative potentials. The present study has been carried out to investigate the hepato-protective role of MAG, against arsenic (As)-induced oxidative damages in the murine liver. As, a well-known toxic metalloid, is ubiquitously found in nature and has been reported to affect nearly all the organs of the human body via oxidative impairment. Administration of As in the form of sodium arsenite (NaAsO2 ) at a dose of 10 mg/kg body weight for 3 months abruptly increased reactive oxygen species (ROS) level, led to oxidative stress and significantly depleted the first line of antioxidant defense system in the body. Moreover, As caused apoptosis in hepatocytes. Treatment with MAG at a dose of 40 mg/kg for body weight for 30 days simultaneously and separately after NaAsO2 administration decreased the ROS production and attenuated the alterations in the activities of all antioxidant indices.
4.Pharmacokinetics of mangiferin and its metabolite-Norathyriol, Part 1: Systemic evaluation of hepatic first-pass effect in vitro and in vivo.
Tian X1, Gao Y1, Xu Z2, Lian S3, Ma Y3, Guo X1, Hu P1, Li Z1, Huang C1. Biofactors. 2016 Apr 30. doi: 10.1002/biof.1291. [Epub ahead of print]
Mangiferin (MGF), a glucoside of xanthone existing in phytomedicines and food, is increasingly attracting attention on diabetes treatment, while the underlying mechanism leading to its low oral bioavailability is unclear. Norathyriol (NTR), an active metabolite with hypoglycemic activity and its exposure after MGF dosing remains unclear. Hence, a rapid and sensitive LC-MS/MS method was established and validated to determine MGF and NTR and applied in the PK study in rats. Correspondingly, the in vitro experiments on temperature-dependent uptake, and MGF metabolism in hepatocyte and enterobacteria samples were performed. Results revealed that hepatic first-pass effect slightly contributed to the poor bioavailability of MGF, based on the MGF exposure in portal vein plasma was nearly similar to that in systemic plasma, and the MGF accumulation in the liver was limited, so was that of NTR. Correspondingly, the in vitro study revealed the MGF uptake was mainly dependent on poor passive transport, possibly leading to its limited hepatic metabolism and accumulation.
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CAS 4773-96-0 Mangiferin

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