K16ApoE inhibits the activity of acetylcholinesterase but is not the primary toxicological mechanism in mice

The blood-brain barrier restricts the administration of drugs for neurological diseases. K16ApoE is an effective drug delivery carrier to deliver across barrier, but it contains acute and high toxicity. toxicity mechanism must be revealed clinical uses. Previous studies hypothesized that was acetylcholinesterase inhibition in brain. However, these used improper buffers AChE assay, further leading anomalous results. Meanwhile, previous have not investigated effects on all AChE-containing tissues organs throughout body. dose design also too narrow. Herein, we designed a more comprehensive rational interval K16ApoE, observed recorded mouse responses after receiving collected brain, diaphragm, serum investigate systemic AChE. We incubated purified with vitro. It could reveal direct effect without influence absorption metabolism vivo. vitro results demonstrated inhibits rhAChE activity as increases. vivo does affect tissue female mice. Therefore, confirmed inhibitory contrary our hypothesis, toxicological K16ApoE. mice received which would promote investigation