HAT regimen attenuates NF-κb-driven megakaryocyte apoptosis and neuronal cell death in sepsis: convergent mechanisms protecting thrombocytopenia and cognitive function.

HAT therapy protects two distinct cell populations-megakaryocytes and hippocampal neurons-from sepsis-induced programmed cell death through convergent, component-specific suppression of NF-κB-driven apoptotic signaling.

These mechanistic findings reframe HAT as a broad-spectrum anti-apoptotic intervention, providing a cellular and molecular rationale consistent with its dual clinical benefit against thrombocytopenia and cognitive dysfunction in sepsis.