581 – Establishment of Folfox-Induced Sinusoidal Obstruction Syndrome Model in Microminipig

rIGF1 to restore the dampened IGF1 signaling attenuated the neurological and neuromuscular deficits, as well as the neuroinflammation observed in AOM-treated mice.Conclusion: Elevated cortical Let-7f expression contributes to the pathogenesis of HE in AOM-treated mice via mechanisms involving the suppression of IGF1 expression.These deleterious effects of Let-7f during HE can be reversed by inhibiting Let-7f expression or by increasing IGF1 concentration in the brain.