| Literature DB >> 24291393 |
Jae Sue Choi1, Md Nurul Islam2, Md Yousof Ali2, Eon Ji Kim2, Young Myeong Kim3, Hyun Ah Jung4.
Abstract
Apigenin has gained particular interests in recent years as a beneficial and health promoting agent because of its low intrinsic toxicity. Vitexin and isovitexin, naturally occurring C-glycosylated derivatives of apigenin, have been known to possess potent anti-diabetic, anti-Alzheimer's disease (anti-AD), and anti-inflammatory activities. The present study was designed to investigate the anti-diabetic, anti-AD, and anti-inflammatory potential of apigenin and its two C-glycosylated derivatives, vitexin and isovitexin by in vitro assays including rat lens aldose reductase (RLAR), human recombinant aldose reductase (HRAR), advanced glycation endproducts (AGEs), protein tyrosine phosphatase 1B (PTP1B), acetylcholinesterase (AChE), butyrylcholinesterase (BChE), β-site amyloid precursor (APP) cleaving enzyme 1 (BACE1), and nitric oxide (NO), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Among them, isovitexin was found as the most potent inhibitor against RLAR, HRAR, AGE, AChE, and BChE while vitexin showed the most potent PTP1B inhibitory activity. Despite the relatively weak anti-diabetic and anti-AD potentials, apigenin showed powerful antiinflammatory activity by inhibiting NO production and iNOS and COX-2 expression while vitexin and isovitexin were inactive. Therefore, it could be speculated that C-glycosylation of apigenin at different positions might be closely linked to relative intensity of anti-diabetic, anti-AD, and anti-inflammatory potentials.Entities:
Keywords: 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine hydrochloride; 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide; 5,5′-dithiobis [2-nitrobenzoic acid]; ACh; AChE; AD; AGEs; AMT; APP; AR; ARI; Alzheimer’s disease; Apigenin derivative; Aβ; BACE1; BCh; BChE; COX-2; ChAT; DMEM; DTNB; Diabetic complication; Dulbecco’s Modified Eagle’s Medium; EDTA; FBS; Flavonoid; HRAR; HRP; Inflammation; LPS; MTT; NADPH; NO; NOS; PTP1B; PVDF; RLAR; ROS; acetylcholinesterase; acetylthiocholine iodide; advanced glycation endproducts; aldose reductase; aldose reductase inhibitor; amyloid-β peptides; butyrylcholinesterase; butyrylthiocholine chloride; choline acetyltransferase; cyclooxygenase-2; ethylenediaminetetraacetic acid; fetal bovine serum; horseradish peroxidase; human recombinant aldose reductase; iNOS; inducible nitric oxide synthase; lipopolysaccharide; nitric oxide; nitric oxide synthase; p-nitrophenyl phosphate; pNPP; polyvinylidene fluoride; protein tyrosine phosphatase 1B; rat lens aldose reductase; reactive oxygen species; β-nicotinamide adenine dinucleotide phosphate; β-site amyloid precursor; β-site amyloid precursor cleaving enzyme 1
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Year: 2013 PMID： 24291393 DOI： 10.1016/j.fct.2013.11.020
Source DB: PubMed Journal: Food Chem Toxicol ISSN： 0278-6915 Impact factor: 6.023