Role of Gold Nanoparticles in Inhibiting Amyloid Formation and Reducing Vascular Dementia Risk
نویسندگان
1 M. Auezov South Kazakhstan university, Shymkent, Kazakhstan
2 Department of Pharmaceutics, College of Pharmacy, University of Al-Ameed, Karbala, Iraq
3 Department of Pharmacy, Mazaya university college, Iraq
4 College of Medical Technology, Medical Lab techniques, National University of Science and Technology, Dhi Qar, Iraq
5 Tashkent State University of Economics, Uzbekistan
6 Tashkent State Technical University, Tashkent, Uzbekistan
7 Department of Pharmacy, Al-Noor University College, Nineveh, Iraq
8 Department of Medical Instrumentation Engineering Techniques, Imam Ja’afar Al-Sadiq University, Iraq
9 Department of Optical Techniques, Al-Hadi University College, Baghdad, 10011, Iraq
10 Department of Medical Laboratories Technology, AL-Nisour University College, Baghdad, Iraq
11 Tashkent State Technical University, Tashkent, Uzbekistan
doi
10.22052/JNS.2023.03.011چکیده
Lysozyme amyloid aggregation is associated with vascular dementia and other disorders. However, conventional therapies are limited by the blood-brain barrier. Gold nanoparticles (AuNPs) could modulate amyloid aggregation and provide a novel therapeutic approach. We investigated the effect of AuNPs on lysozyme amyloid formation of Hen Egg White Lysozyme (HEWL). We incubated lysozyme (3 mg/ml) in 60 mM glycine buffer (pH 2.8) at 61oC with gentle shaking to induce amyloid formation. We used various techniques to assess the impact of AuNPs (5-50 µg/ml) on lysozyme amyloid accumulation. We performed independent t-test and SPSS 23.0 software for data analysis. AuNPs inhibited lysozyme amyloid aggregation in a concentration-dependent manner. The lowest concentration (5 µg/ml) was the most effective, as it significantly increased the lag phase and decreased the growth phase of amyloid formation, and also reduced the cytotoxicity of amyloid aggregates on cell viability. Our results suggest that AuNPs act as nano-chaperones and prevent lysozyme amyloid fibril formation, and thus they may have therapeutic potential for vascular dementia treatment.
