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
Featured in 600+ scientific articles
Collaboration with 17 Top Pharmas,
170+ Biotechs and 380+ Academic Institutions
Generated with biopharma partners and in-house
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Models with certified health status from professional breeders in US and Europe
