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PRECLINICAL PUBLICATION · 2019

Hepatospecific ablation of p38alpha MAPK governs liver regeneration through modulation of inflammatory response to CCl4-induced acute injury.

Mouse / Chemical/toxin

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 31601995 ↗2019Reported benefit

Hepatospecific ablation of p38alpha MAPK governs liver regeneration through modulation of inflammatory response to CCl4-induced acute injury.

MouseChemical/toxinMalen = 3 to 10 animals per genotypeIntraperitoneal for carbon tetrachloride, antibodies and BrdU; tamoxifen given in the dietCarbon tetrachloride 0.56 g/kg; tamoxifen diet 1000 mg/kg;…Genetic ablation induced weeks before injury; antibody cocktail given 5 hours b…

Model: Acute liver injury by a single intraperitoneal injection of carbon tetrachloride in sunflower oil (1:9)

Hepatocyte-specific p38alpha deletion protected against carbon tetrachloride-induced acute liver injury by limiting reactive oxygen species and shaping a Ccl2/Ccl5-dependent inflammatory response, and antibody blockade of Ccl2 and Ccl5 abrogated this protection.

Extraction: extract · Supplied extraction confidence: 0.8. Machine-extracted fields require source verification.