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Nanoparticle-emitted light attenuates amyloid-?-induced superoxide and inflammation in astrocytes.

ABSTRACT: Alzheimer's disease (AD) is the sixth leading cause of age-related death with no effective intervention yet available. Our previous studies have demonstrated the potential efficacy of Low Level Laser Therapy (LLLT) in AD cell models by mitigating amyloid-? peptide (A?)-induced oxidative stress and inflammation. However, the penetration depth of light is still the major challenge for implementing LLLT in animal models and in the clinical settings. In this study, we present the potential of applying Bioluminescence Resonance Energy Transfer to Quantum Dots (BRET-Qdots) as an alternative near infrared (NIR) light source for LLLT. Our results show that BRET-Qdot-emitted NIR suppresses A?-induced oxidative stress and inflammatory responses in primary rat astrocytes. These data provide a proof of concept for a nanomedicine platform for LLLT.Low Level Laser Therapy has already been demonstrated to mitigate amyloid-? peptide induced oxidative stress and inflammation, a key driver of Alzheimer's disease. The major issue in moving this forward from cell cultures to live animals and potentially to human subjects is light penetration depth. In this novel study, BRET-Qdots were used as an alternative near infrared light source with good efficacy, paving the way to the development of a nanomedicine platform.

SUBMITTER: Bungart BL

PROVIDER: S-EPMC3895489 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Nanoparticle-emitted light attenuates amyloid-β-induced superoxide and inflammation in astrocytes.

Bungart Brittani L BL Dong Li L Sobek Daniel D Sun Grace Y GY Yao Gang G Lee James C-M JC

Nanomedicine : nanotechnology, biology, and medicine 20131104 1

Alzheimer's disease (AD) is the sixth leading cause of age-related death with no effective intervention yet available. Our previous studies have demonstrated the potential efficacy of Low Level Laser Therapy (LLLT) in AD cell models by mitigating amyloid-β peptide (Aβ)-induced oxidative stress and inflammation. However, the penetration depth of light is still the major challenge for implementing LLLT in animal models and in the clinical settings. In this study, we present the potential of applyi ...[more]

PMID: 24200521

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Project description:AimsThe accumulation and deposition of β-amyloid (Aβ) has always been considered a major pathological feature of Alzheimer's disease (AD). The latest and mainstream amyloid cascade hypothesis indicates that all the main pathological changes in AD are attributed to the accumulation of soluble Aβ. However, the exploration of therapeutic drugs for Aβ toxicity has progressed slowly. This study aims to investigate the protective effects of Icaritin on the Aβ-induced Drosophila AD model and its possible mechanism.MethodsTo identify the effects of Icaritin on AD, we constructed an excellent Drosophila AD model named Aβarc (arctic mutant Aβ42) Drosophila. Climbing ability, flight ability, and longevity were used to evaluate the effects of Icaritin on AD phenotypes. Aβarc was determined by immunostaining and ELISA. To identify the effects of Icaritin on oxidative stress, we performed the detection of ROS, hydrogen peroxide, MDA, SOD, catalase, GST, and Caspase-3. To identify the effects of Icaritin on energy metabolism, we performed the detection of ATP and lactate. Transcriptome analysis and qRT-PCR verifications were used to detect the genes directly involved in oxidative stress and energy metabolism. Mitochondrial structure and function were detected by an electron microscopy assay, a mitochondrial membrane potential assay, and a mitochondrial respiration assay.ResultsWe discovered that Icaritin almost completely rescues the climbing ability, flight ability, and longevity of Aβarc Drosophila. Aβarc was dramatically reduced by Icaritin treatment. We also found that Icaritin significantly reduces oxidative stress and greatly improves impaired energy metabolism. Importantly, transcriptome analysis and qRT-PCR verifications showed that many key genes, directly involved in oxidative stress and energy metabolism, are restored by Icaritin. Next, we found that Icaritin perfectly restores the integrity of mitochondrial structure and function damaged by Aβarc toxicity.ConclusionThis study suggested that Icaritin is a potential drug to deal with the toxicity of Aβarc, at least partially realized by restoring the mitochondria/oxidative stress/energy metabolism axis, and holds potential for translation to human AD.

Dataset Information

Nanoparticle-emitted light attenuates amyloid-?-induced superoxide and inflammation in astrocytes.

Publications

Nanoparticle-emitted light attenuates amyloid-β-induced superoxide and inflammation in astrocytes.

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