Detection and monitoring of the neuroprotective behavior of curcumin micelles based on an AIEgen probe

Abstract

In recent years, the role of mitochondrial injury in the pathogenesis of Alzheimer's disease (AD) has attracted extensive attention. Studies have shown that curcumin (Cur) can protect nerve cells from beta-amyloid (Aβ)-induced mitochondrial damage. However, natural Cur encounters limited application due to its poor biocompatibility and bioavailability. To improve the solubility and biocompatibility of natural Cur, we prepared water-soluble curcumin micelles (CurM). Furthermore, the mitochondria-specific aggregation-induced emission (AIE) probe (TPE-Ph-In) was employed to observe the protective effect of CurM on the damage of mitochondrial morphology, distribution, and membrane potential caused by Aβ. Results showed that CurM had higher solubility, stronger stability and retention effect, and better cellular uptake than that of natural Cur. Furthermore, the inhibitory effects of CurM on mitochondrial morphology, distribution, and membrane potential damage induced by Aβ_25–35 were observed utilizing TPE-Ph-In as an indicator of mitochondrial morphology and membrane potential. Thus, this method provides a useful strategy for experimental research and clinical treatment of AD with mitochondrial damage as the pathogenic mechanism.