HEPPS exhibits inhibitory activity against the amyloid-beta precursor protein, reducing Aβ aggregation burden and improving neuronal autophagy flux, thereby alleviating neuronal apoptosis and traumatic brain injury (TBI) in mice. It can be used for research into Alzheimer's disease and neurological disorders.

Methods:
A mouse model of traumatic brain injury (TBI) was established using controlled cortical impact (CCI). HEPPS was administered orally at a dose of 120 mg/kg immediately after injury and then once daily for 3 or 7 days. Aβ accumulation, autophagy, apoptosis, and neurological function were evaluated through histological and molecular analyses. A chloroquine-treated group was included to assess whether the effects of HEPPS were mediated through autophagy.
Results:
HEPPS significantly reduced Aβ accumulation and axonal injury in the brain after TBI, improved synaptic function and autophagic flux, decreased neuronal apoptosis, prevented brain tissue loss, and enhanced motor and cognitive functions. These protective effects were partially reversed by chloroquine treatment, suggesting that the neuroprotective effect of HEPPS is associated with enhanced autophagy [1].