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Treatment with mannose oligosaccharides reverses the intestinal injury in the acetylsalicylic acid-treated rat model.
Pol J Vet Sci
June 2024
College of Biological Engineering, Henan University of Technology, Zhengzhou, China.
Mannose oligosaccharide (MOS) has been shown to promote animal growth, maintain intestinal health, and activate the intestinal immune system. However, the question of whether MOS can stimulate the immune system and alleviate acetylsalicylic acid (ASA)-induced gut damage remains unresolved. The purpose of this study was to investigate the impact of MOS pretreatment on the immunological and anti-inflammatory capabilities of rats with ASA-induced intestinal injury.
View Article and Find Full Text PDFThe effects of camel milk in systemic inflammation and oxidative stress of cigarette smoke-induced chronic obstructive pulmonary disease model in rat.
Front Vet Sci
December 2024
Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Background: The effects of camel milk in inflammation and systemic oxidative stress of cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) associated with small airway inflammation in rats were investigated.
Methods: 35 male Wistar rats were randomly divided into five groups: (a) control, (b) CS-exposed rats, c and (d) CS-exposed rats treated with the 4 and 8 mL/kg camel milk, and (e) CS-exposed rats treated with 1 mg/kg dexamethasone.
Results: Total and differential WBC counts, serum level of TNF- and malondialdehyde (MDA) level in serum and homogenized tissues of the heart, kidney, liver, and testicle were significantly increased, but catalase (CAT), superoxide dismutase (SOD) and thiol levels were significantly decreased in CS-exposed rats ( < 0.
Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.
eGastroenterology
October 2024
Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Alcohol-associated liver disease (ALD) is a growing global health concern and its prevalence and severity are increasing steadily. While bacterial endotoxin translocation into the portal circulation is a well-established key factor, recent evidence highlights the critical role of sterile inflammation, triggered by diverse stimuli, in alcohol-induced liver injury. This review provides a comprehensive analysis of the complex interactions within the hepatic microenvironment in ALD.
View Article and Find Full Text PDFChild-Pugh Score and Vitamin D: Exploring a New Frontier in Liver Cirrhosis Assessment.
Cureus
November 2024
Medicine, Shri. B. M. Patil Medical College Hospital and Research Centre, Vijayapura, IND.
This study investigates the relationship between vitamin D levels and liver cirrhosis severity, a leading cause of global morbidity and mortality. Chronic liver diseases, stemming from conditions such as hepatitis, alcohol use, non-alcoholic fatty liver disease, autoimmune diseases, and cryptogenic disorders, disrupt vitamin D metabolism, as the liver converts dietary and skin-derived vitamin D into 25-hydroxyvitamin D (25[OH]D), the primary circulating form. The cross-sectional study conducted at the Department of General Medicine of BLDE (DU) Shri.
View Article and Find Full Text PDFKupffer-Cell-Targeted Carboxylesterase 1f Knockdown Deteriorates Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure Through Regulating Cellular Polarization in Mice.
Can J Gastroenterol Hepatol
December 2024
Department of Infectious Diseases, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aims: Carboxylesterase (Ces)1f is implicated in protection against hepatic inflammation, but it is unclear whether the enzyme has an influence in polarization of Kupffer cells (KCs), the innate immune cells mediating hepatic inflammatory injury including acute liver failure (ALF). In the present study, we aim to explore KC polarization induced by Ces1f in mice with lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced ALF. We adopted a novel delivery system, β-1,3-D-glucan-encapsulated Endoporter-siRNA particles, to specifically target KC Ces1f knockdown via tail vein injection in mice.
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