Presence Of Naringin Research Articles

Flavonoids Promote Cell Migration in Nontumorigenic Colon Epithelial Cells Differing in Apc Genotype: Implications of Matrix Metalloproteinase Activity

Colonic epithelial cell migration is required for movement up to the apex of the crypt and, hence, normal differentiated cell function. This migratory phenotype is dependent upon wild-type adenomatous polyposis coli (Apc) expression. The purpose of this study is to determine whether specific flavonoids induce cell migration in colon epithelial cells either wild type or heterozygous for Apc genotype. Nontumorigenic murine colon epithelial cell lines with distinct Apc genotypes, young adult mouse colon (YAMC; Apc+/+) cells, and Immortomouse/Min colon epithelial (IMCE; ApcMin/+) cells were used to assess the ability of specific flavonoids to induce cell migration relative to migration induced by hepatocyte growth factor (HGF). The citrus flavanones naringenin and hesperetin did not induce cell migration comparable with HGF in either cell type. However, the glycosylated forms of these flavanones, naringin and hesperidin, induced migration differentially in YAMC and IMCE cells. Specifically, naringin and hesperidin induced the greatest migratory response in IMCE cells at 1 μM (P < 0.01) and induced migration greater than untreated control cells (P < 0.05) but equal to HGF-treated cells. In YAMC cells, hesperidin did not induce migration except at the 100-mM concentration. Apigenin induced migration in IMCE cells at 1 (P < 0.05) and 50 μM (P < 0.01) and did not induce migration in the YAMC cells. Catechin induced migration at the highest concentration (300 μM) only in the IMCE cells, whereas epicatechin induced migration at the lowest concentration only (1 mM) in IMCE cells. Overall, the glycosylated citrus flavanones induced the greatest migratory response at the lowest concentration in IMCE cells. Co-treatment of IMCE cells with the global matrix metalloproteinase (MMP) inhibitor Ilomastat® in the presence of naringin, hesperidin, or apigenin demonstrated that flavonoid-induced migration was dependent on MMP activity. Induction of the migratory phenotype by flavonoids in these models of preneoplastic epithelial cells suggests a novel mechanism for colon cancer prevention.

Alpha-L-rhamnosidase of Sphingomonas sp. R1 producing an unusual exopolysaccharide of sphingan.

A soil bacterium with alpha-L-rhamnosidase was isolated from a cumulative mixed culture containing a polysaccharide of gellan as a carbon source and identified to be Sphingomonas paucimobilis, known as a potent producer of gellan. The isolate (designated Sphingomonas sp. R1) produced an unusual exopolysaccharide of sphingan (denoted HWR1) distinct from gellan. The rhamnose in gellan was replaced with mannose in HWR1. The bacterium had a peculiar cell surface covered with many complicated plaits. alpha-L-Rhamnosidase purified from Sphingomonas sp. R1 grown in the presence of naringin was a monomer with a molecular mass of 110 kDa and most active at pH 8.0 and 50 degrees C. The enzyme required divalent metal ions for the activity and released L-rhamnose from various rhamnosyl glycosides.

The character of inhibition of the metabolism of 1,2-benzopyrone (coumarin) by grapefruit juice in human.

Constituents of grapefruit juice are known to interfere with mammalian cytochrome P450 isozymes such as intestinal CYP3A4 and hepatic CYP2A6, lowering the biotransformation of drugs and increasing their bioavailability. The aim of this study was to investigate whether the presence of naringin is demanded for the inhibition of the coumarin 7-hydroxylase in man or other compounds are responsible for it. In cross-over studies, doses of 10 mg coumarin, together with combinations of grapefruit juice, water and naringin, were given orally to one healthy male volunteer, We investigated increasing amounts of grapefruit juice, keeping the volume of liquid constant at 1 L; increasing doses of naringin given in water; increasing amounts of juice, keeping the dose of naringin constant; or increasing doses of naringin, keeping the amount of juice constant. Urine samples were collected up to 24 h after dosing and 7-hydroxycoumarin was quantified fluorimetrically in urine hydrolysates after HPLC separation to determine the excretion rates. While increasing amounts of grapefruit juice delay the excretion of 7-hydroxycoumarin by 2 h, increasing doses of naringin in water up to twofold (i.e. naringin content of 2 L grapefruit juice) do not cause any alteration in the time course of excretion. Experiments with increasing amounts of juice, keeping the dose of naringin constant, indicate that the inhibitory potency of small amounts of grapefruit juice can be amplified by naringin. The same is true when the ratio between juice constituents and naringin is enhanced up to threefold by adding naringin. As naringin alone is ineffective, the inhibitory effect of grapefruit juice on the metabolism of coumarin is caused by at least one compound other than naringin. The persistency of the primary inhibitor not identified yet can obviously be modulated by the naring(en)in-system.