Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.6.5.2 (
NQO1
)
6,196
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
C-Glucosides, in which sugars are attached to the aglycone by carbon-carbon bonds, are generally resistant to acid and enzyme hydrolysis. The C-glucosyl bond of mangiferin, a xanthone C-glucoside, was cleaved by anaerobic incubation with a human intestinal bacterium, Bacteroides sp. MANG, to give norathyriol. A cell-free extract obtained by sonication of B. sp. MANG demonstrated cleaving activity for mangiferin to norathyriol by adding NADH,
diaphorase
, and dithiothreitol. Both high molecular weight (>10 k) and low molecular weight (<10 k) fractions obtained from the cell-free extract were required for the activity. MnCl2 was necessary for the activity, but other metal ions were not. By purification of the high molecular weight fraction using DEAE-cellulose and Phenyl Sepharose column chromatography, two fractions, designated as proteins A and B, were separated and required for the activity. Neither protein A nor
protein B
alone showed any activity. This is the first report describing a C-glucosyl-cleaving enzyme from human intestinal bacterium that seems to involve a novel enzyme mechanism.
...
PMID:Two proteins, Mn2+, and low molecular cofactor are required for C-glucosyl-cleavage of mangiferin. 1627 85
The epidermal growth factor (EGF) has been widely used for protection of stress-induced intestinal mucosa dysfunction. However, whether EGF would alleviate oxidative injury and reduce apoptosis in porcine intestine is not yet known. Therefore, the aim of this study was to investigate the effect of EGF on lipopolysaccharides (LPS)-induced induction of oxidative stress and ensuing apoptosis in the porcine intestinal epithelial cell line, IPEC-J2. The present study showed that EGF significantly increased cell viability and decreased the LPS-induced induction of apoptosis, dehydrogenase (LDH) release and malonaldehyde (MDA) production. EGF also (i) decreased expression of the pro-apoptotic genes
Fas
,
Bax
,
Cascase-3
,
Cascase-8
,
Cascase-9
, and proteins such as P53, Fas, Bax, Caspase3; (ii) increased antiapoptotic
protein B
-cell lymphoma 2 (Bcl2) expression; (iii) increased mRNA levels of the nuclear factor erythroid 2-related factor 2 (
Nrf2
) related genes Nrf2, manganese superoxide dismutase (
SOD2
), catalase (
CAT
), glutathione peroxidase (
GSH-Px
), heme oxygenase (
HO-1
) and quinone oxidoreductase (
NQO1
); (iv) protein level of Nrf2-realeted proteins Nrf2, HO-1,
NQO1
; and (v) total antioxidant capacity (T-AOC), CAT, SOD, GSH-Px concentrations. Collectively, our results indicated that EGF enhanced Nrf2 protein expression, and upregulated the expression of phase II metabolizing enzymes (such as HO-1 and
NQO1
) and antioxidative enzymes (SOD, CAT and GSH-Px) to alleviate oxidative injury, and then protect IPEC-J2 cells from apoptosis induced by LPS.
...
PMID:Epidermal Growth Factor, through Alleviating Oxidative Stress, Protect IPEC-J2 Cells from Lipopolysaccharides-Induced Apoptosis. 2953 5