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Pagina 1 a partire dal 119 risultati
Disaccharidase activity in children with inflammatory bowel disease.
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OBJECTIVE
The etiopathogenesis of inflammatory bowel disease (IBD) is multifactorial and not well explained. Environmental, genetic, and dietary factors play an important role. The aim of the study was the evaluation of lactase, saccharase, and maltase activity in patients with IBD.
METHODS
The
Granulomatous inflammatory response to recombinant filarial proteins of Brugia species.
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The lymphatic inflammatory response in Brugia-infected jirds peaks early during primary infections and then decreases in severity as judged by the numbers of lymph thrombi present within these vessels. Antigen-specific hypersensitivity reactions in these animals was measured by a pulmonary
Modulation of Intestinal Barrier and Bacterial Endotoxin Production Contributes to the Beneficial Effect of Nicotinic Acid on Alcohol-Induced Endotoxemia and Hepatic Inflammation in Rats.
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Alcohol consumption causes nicotinic acid deficiency. The present study was undertaken to determine whether dietary nicotinic acid supplementation provides beneficial effects on alcohol-induced endotoxin signaling and the possible mechanisms at the gut-liver axis. Male Sprague-Dawley rats were
Differentiation of Myositis-Induced Models of Bacterial Infection and Inflammation with T2-Weighted, CEST, and DCE-MRI.
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We used T2 relaxation, chemical exchange saturation transfer (CEST), and dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI) to assess whether bacterial infection can be differentiated from inflammation in a myositis-induced mouse model. We measured the T2
C-C chemokine receptor type 5 deficiency exacerbates alcoholic fatty liver disease through pro-inflammatory cytokines and chemokines-induced hepatic inflammation.
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OBJECTIVE
Chemokines and chemokine receptors implicated with alcoholic liver disease. Studies have shown that inflammation and oxidative stress induce fat molecules aggregation in liver. We evaluated the relationship between alcoholic fatty liver disease and C-C chemokine receptor 5 (CCR5) and
Anti-oxidant and anti-inflammatory effects of hydrogen-rich water alleviate ethanol-induced fatty liver in mice.
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OBJECTIVE
To investigate the effects of hydrogen-rich water (HRW) treatment on prevention of ethanol (EtOH)-induced early fatty liver in mice.
METHODS
In vitro reduction of hydrogen peroxide by HRW was determined with a chemiluminescence system. Female mice were randomly divided into five groups:
In Vitro Antioxidant, Anti-Inflammatory and Skin Permeation of Myrsine africana and Its Isolated Compound Myrsinoside B.
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Dermal aging is characterized by states of oxidative stress, chronic inflammation, and abnormal proteolytic degradation due to the action of hydrogen peroxide, superoxide, 5-lipoxygenase, and elastase, respectively. Noteworthy elastase inhibition has previously been reported, and so this study aimed
Enzymatic Synthesis of a Novel Kaempferol-3-O-β-d-glucopyranosyl-(1→4)-O-α-d-glucopyranoside Using Cyclodextrin Glucanotransferase and Its Inhibitory Effects on Aldose Reductase, Inflammation, and Oxidative Stress.
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Kaempferol-3-O-β-d-glucopyranoside (astragalin, AS), a major flavonoid that exists in various plants, exerts antioxidant, antitumor, anti-human immunodeficiency virus (HIV), and anti-inflammatory effects. However, the low water solubility of AS limits its use. In this study, we used cyclodextrin
Identification of Constituents Affecting the Secretion of Pro-Inflammatory Cytokines in LPS-Induced U937 Cells by UHPLC-HRMS-Based Metabolic Profiling of the Traditional Chinese Medicine Formulation Huangqi Jianzhong Tang.
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Within non-communicable diseases, chronic inflammatory conditions represent one of the biggest challenges for modern medicine. Traditional Chinese Medicine (TCM) has been practiced over centuries and has accumulated tremendous empirical knowledge on the treatment of such diseases. Huangqi Jianzhong
Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice.
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BACKGROUND
Alcoholic liver disease (ALD) represents a chronic wide-spectrum of liver injury caused by consistently excessive alcohol intake. Few satisfactory advances have been made in management of ALD. Thus, novel and more practical treatment options are urgently needed. Flaxseed oil (FO) is rich
Alpha amylase enzyme inhibitory and anti-inflammatory effect of Lawsonia inermis.
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Previously it was reported elsewhere that Lawsonia inermis have anti-inflammatory and analgesic effect in experimental animals. The in vitro porcine alpha amylase inhibitory effect was investigated of this plant methanolic extracts and consequently hypoglycemic effect by quantitatively determining
Hepatic Peroxisome Proliferator-Activated Receptor Gamma Signaling Contributes to Alcohol-Induced Hepatic Steatosis and Inflammation in Mice.
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Peroxisome proliferator-activated receptor gamma (PPARγ) signaling has been shown to regulate lipogenesis and lipid accumulation. Previous studies have shown that hepatic PPARγ is up-regulated in steatotic liver of both animal and human. However, the effects of hepatic PPARγ signaling on alcoholic
Lipocalin 2 drives neutrophilic inflammation in alcoholic liver disease.
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OBJECTIVE
Alcoholic steatohepatitis (ASH) is characterised by neutrophil infiltration that contributes to hepatic injury and disease. Lipocalin-2 (LCN2) was originally identified as siderophore binding peptide in neutrophils, which exerted tissue protective effects in several disease models. Here we
Metabolic Profiling by UPLC-Orbitrap-MS/MS of Liver from C57BL/6 Mice with DSS-Induced Inflammatory Bowel Disease
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Liver disorder often occurs in patients with inflammatory bowel disease (IBD); however, the changes in IBD-induced liver disorder at the intrinsic molecular level (chiefly metabolites) and therapeutic targets are still poorly characterized. First, a refined and translationally relevant model of DSS
Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage.
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BACKGROUND
Subarachnoid hemorrhage (SAH) frequently results in several complications, including cerebral vasospasm, associated with high mortality. Although cerebral vasospasm is a major cause of brain damages after SAH, other factors such as inflammatory responses and oxidative stress also
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