In this report, we demonstrate a rapid, simple, and green method for synthesizing silver-gold (Ag-Au) bimetallic nanoparticles (BNPs). We used a novel modification to the galvanic replacement reaction by suspending maltose coated silver nanoparticles (NPs) in ≈ 2% aqueous solution of EO100PO65EO100 (Pluronic F127) prior to HAuCl4 addition. The Pluronic F127 stabilizes the BNPs, imparts biocompatibility, and mitigates the toxicity issues associated with other surfactant stabilizers. BNPs with higher Au:Ag ratios and, subsequently, different morphologies were successfully synthesized by increasing the concentration of gold salt added to the Ag NP seeds. These BNPs have enhanced catalytic activities than typically reported for monometallic Au or Ag NPs (∼ 2–10 fold) of comparable sizes in the sodium borohydride reduction of 4-nitrophenol. The 4-nitrophenol reduction rates were highest for partially hollow BNP morphologies.

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Glutamate-induced excitotoxicity is a wellrecognized cause of neuronal cell death. Nutritional supplementation with Coenzyme Q10 (CoQ10) has been previously demonstrated to serve neuro-protective effects against glutamate-induced excitotoxicity. The aim of the present study was to determine whether the protective effect of CoQ10 against glutamate toxicity could be attributed to stimulating mitochondrial biogenesis. Mouse hippocampal neuronal HT22 cells were incubated with glutamate with or without ubisol Q10. The results revealed that glutamate significantly decreased levels of mitochondrial biogenesis related proteins, including peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α and nuclear respiratory factor (NRF)2. Additionally, glutamate reduced mitochondrial biogenesis, as determined using a mitochondrial biogenesis kit. Pretreatment with CoQ10 prevented decreases in phosphorylated (p)-Akt, p-cAMP response element-binding protein, PGC-1α, NRF2 and mitochondrial transcription factor A, increasing mitochondrial biogenesis. Taken together, the results described a novel mechanism of CoQ10-induced neuroprotection and indicated a central role for mitochondrial biogenesis in protecting against glutamate-induced excitotoxicity.

Background: Glutamate-induced excitotoxicity is a well-recognized cause of neuronal cell death and nutritional supplementation with Coenzyme Q10 (CoQ10) has previously been shown to have neuro-protective actions against it. The objective of this study was to determine whether the protective effect of CoQ10 against glutamate could be attributed to stimulating mitochondrial biogenesis. Results: The mouse hippocampal neuronal HT22 cells were incubated with glutamate with or without ubisol Q10 treatment. Significant deterioration of cells after glutamate exposure was observed under a light microscope and cell viability assay, along with a significant drop in clonogenic ability. Glutamate significantly decreased the mitochondrial biogenesis related protein levels of Akt, CREB, PGC-1α, and NRF2, and reduced mitochondrial biogenesis assessed by a mitochondrial biogenesis kit. Pretreatment with CoQ10 prevented the decreases of Akt, CREB, PGC-1α, and NRF2 and increased mitochondrial biogenesis. Conclusions: Taken together, these results describe a new mechanism of CoQ10-conveyed neuro-protection and indicate a central role for mitochondrial biogenesis in protecting against glutamate-induced excitotoxicity.