Moxifloxacin Inhibited beta-Amyloid Bio-communication with HSP60 Memristive Devices For Promoting Normal Reversible Membrane Potential

E.T. Chen, J.T. Thornton, S-H. Duh
Advanced Biomimetic Sensors, Inc.,
United States

Keywords: native HSP60 memristive sensor, MMP2/HSP60 network memristor, reversible membrane potential, antibiotics, inhibition of beta-amyloid refolding, ratio of action potential/resting potential, dosage kinectics

Summary:

Preventing beta-Amyloid’s fibrillation is important for human health, especially for Alzheimer’s disease (AD) patients. Chaperones, like human Heat Shock Protein (HSP60) played an important role in protein folding. HSP60 memristor devices were developed by cross-linking native HSP60 with conductive polymers forming a nanostructured membrane on gold chips, named as Sensor 1, compared with Sensor 2, made by HSP60 cross-linked polymers on the top of a native Matrix Metalloproteinase-2 (MMP-2) membrane. Moxifloxacin (MOX) is an antibiotic. The goal is to evaluate moxifloxacin’s inhibition for beta Amyloid’s bio-communication with HSP60 memristors for a normal reversible membrane potential (RMP). Experimental methods conducted were a Cyclic Voltammetry (CV) method, a Double Step Chronopotentiometry (DSCPO) (the voltage) method and an Open Circuit Potential (OPO) method under conditions of antibody-free, labeling-free and reagent-less. Results showed the peak intensity of 250 ng/mL beta Amyloid was eliminated by the various concentration of MOX by the two devices using the CV method against the signal of the 250 ng/mL beta-Amyloid alone. Without the MOX help, beta-Amyloid alone refolded and showed the open circuit potential results at the lowest energy for 2, 6, 12 minutes monitoring, respectively by Sensor 1. Sensor 1 shows the MOX promoted the RMP to a normal level for keeping the Action Potential/Resting Potential (AP/RP) ratio in the safe zoon with MOX concentration from10 to 20 mg/mL with 250 ng/mL beta-Amyloid. Beta- Amyloid alone did not show energy downward in sensor 2 compared with sensor 1. The MMP2/HSP60 Sensor 2 has 25% slower inhibition rate of beta-Amyloid refolding than Sensor 1. The new accomplishments are:1) developed two types of memristors using native HSP60 cross-linked with polymers showed the capability to induce beta- Amyloid biocommunication; 2). Showed compound MOX have the ability to inhibit the beta-Amyloid bio-communication with HSP60 used multiple methods with different dosages in kinetics with the energy change results as the key evaluation factors; 3). Demonstrated beta Amyloid refolded in fibrillated with HSP60 without MOX. 4). A potential working model developed for evaluation new medicines with time saving, burden-less protocols.