This study investigates the protective role of albumin against TNF-α-induced liver injury. Using albumin-deficient mouse models, the researchers demonstrated that the absence of albumin exacerbates liver damage upon TNF-α challenge, leading to increased hepatocellular apoptosis and inflammation. Supplementation with exogenous albumin mitigated these effects, highlighting albumin's critical function in maintaining hepatic immune homeostasis during inflammatory insults.
Albumin deficiency enhances susceptibility to TNF-α-induced liver injury, while albumin supplementation confers protective effects, underscoring its therapeutic potential in inflammatory liver diseases.
Albumin-deficient (Alb⁻/⁻) mouse model, generated by targeted deletion of the Alb gene to study its role in liver immunopathology.
Liver immunopathology, TNF-α, Albumin therapy, Hepatic inflammation
Constitutive Knockout model, Alb gene deletion, TNF-α challenge, Albumin supplementation
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
