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The aim of the study was to analyze the differences in the activity of beta-glucuronidase and beta-glucosidase in stool specimens of children with Inflammatory Bowel Diseases (IBD) and healthy subjects. The disease activity was determined according to the PCDAI scale (Crohn disease) and
Activation of protein kinase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces ceramide formation through the salvage pathway involving, in part, acid beta-glucosidase 1 (GBA1), which cleaves glucosylceramide to ceramide. Here, we examine the role of the GBA1-ceramide pathway,
Current anti-inflammatory strategies for the treatment of pulmonary disease in cystic fibrosis (CF) are limited; thus, there is continued interest in identifying additional molecular targets for therapeutic intervention. Given the emerging role of sphingolipids (SLs) in various respiratory
Increases in the risk of infections and malignancy due to immune suppressive therapies of inflammatory bowel diseases (IBDs) have led the researchers to focus on more nontoxic and acceptable natural products like curcumin. Here we investigate whether prophylactic and therapeutic application of the
The iridoid compound genipin (GNP) is a geniposide hydrolysate of β-glucosidase. GNP has many pharmacological effects, including antioxidant, anti-apoptotic, and anti-inflammation effects. However, its exact target and mechanism of action remain poorly understood. In this study, the binding of GNP
We have recently identified a novel gene, termed klotho, that is involved in the suppression of several aging phenotypes. The gene encodes a membrane protein that shares sequence similarity with the beta-glucosidases of bacteria and plants. In this study, we isolated rat klotho cDNA and examined its
The ginsenoside Rg2(S), which is one of the pharmaceutical components of ginseng, is known to have neuroprotective, anti-inflammation, and anti-diabetic effects. However, the usage of ginsenoside Rg2(S) is restricted owing to the small amounts found in white and red ginseng. To enhance the
OBJECTIVE
The non-lysosomal glucosylceramidase, β-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer). Cer is a potent second-messenger lipid that plays an important role in signaling cascades involved in apoptosis. The aim of this study was to investigate whether Gba2
Human gallbladder epithelium was homogenized with a view to maintaining the integrity of subcellular components. In such homogenates, N-acetyl-beta-glucosaminidase, beta-glucuronidase, beta-galactosidase, beta-glucosidase, beta-fucosidase, beta-xylosidase, and acid phosphatase were demonstrated
BACKGROUND
Carnosic acid (CA) and rosemary extracts (RE) show body-weight, energy metabolism and inflammation regulatory properties in animal models but the mechanisms are not yet understood. Gut microbiota plays an important role in the host metabolism and inflammatory status and is modulated by
Saposins A, B, C and D are derived from a common precursor, prosaposin (psap). The few patients with saposin C deficiency develop a Gaucher disease-like central nervous system (CNS) phenotype attributed to diminished glucosylceramide (GC) cleavage activity by acid beta-glucosidase (GCase). The in
Enzyme inhibitory activities of 14 iridoids previously obtained from two Malaysian medicinal plants, Saprosma scortechinii and Rothmannia macrophylla, were evaluated in vitro using soybean lipoxygenase and bovine testis hyaluronidase. Most of the iridoids, including asperulosidic acid, paederosidic
Liver fibrosis was produced in rats by subcutaneous injections of carbon tetrachloride. The effect of anti-inflammatory steroids (hydrocortisone, prednisone, dexamethasone) on the activity of serum lysosomal hydrolases (beta-N-acetylglucosaminidase, beta-glucosidase and alpha-mannosidase) was
OBJECTIVE
Gaucher's disease type 1 (GD1) pathophysiology includes an imbalance on brain-derived neurotrophic factor (BDNF) levels and in the inflammatory system. However, the pathways involved remain poorly understood. The hypothesis of this study is that epigenetic mechanisms might be involved, at
High mobility group box protein 1 (HMGB1) plays an important role in the pathogenesis of rheumatoid arthritis (RA), but the pathogenic mechanisms of HMGB1 in RA and the involvement of the lysosomal enzyme acid β-glucosidase 1 (GBA1) are not fully elucidated. The aim of the present study was to use