Recent advances in nanomedicine make it auspicious for cancer diagnosis and treatment. A possible non-invasive photothermal therapy (PTT) for cancer treatment could be constructed by combining the nanomedicine and laser. PTT employs photothermal agents (PTAs) with high photothermal conversion efficacy for converting light into heat to selectively kill cancer cells under the help of lasers. Because of the unique Surface Plasmon Resonance (SPR) phenomenon and the tunable near-infrared (NIR) region absorption, noble metal nanoparticles like gold nanoparticles can be applied as a PTA for PTT. Gold nanoparticles (AuNPs) offer the enhanced absorption and scattering properties, the optical properties tunability, and specific tumor targeting capability, therefore, AuNPs based PTT turns to furthermore promising. However, drawbacks such as long retention time, cytotoxicity, and insufficient cancer cells targeting restrict the application of AuNPs as PTTs. This review overviews a systematic research of the PTT applications of various modified AuNPs in previous publications. With the advancement of chemical synthesis technology, AuNPs of various shapes and sizes can be synthesized with desired properties, which can achieve multimodal cancer treatment with enhanced anti-tumor effect. In this review, we summarized the major features of five principal types of AuNPs: gold nanorods, gold nanoshells, gold nanospheres, gold nanocages, and gold nanostars with different size, discussed their advantages and disadvantages in PTT. We also detailed the surface modification of AuNPs which could be beneficial for the performance of AuNPs based PTT. In addition, depending on properties of AuNPs and lasers, the underlying mechanism of cell death triggered by NIR laser can be different, which also affect the anti-cancer effects and outcomes of PTT. However, controlling cell death through a desired cell death mechanism to achieve desired PTT outcome is still a challenge.

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Uniform dodecahedral Co3O4 hollow architectures can be prepared from ZIF-67 templates, which were synthesized by controlling the reactants mole ratio, shows excellent catalytic performance for CO oxidation.

We have previously shown that interleukin-6 (IL-6)-protected neurons against the suppression of neuronal vitality and overload of intracellular Ca(2+) induced by glutamate or N-methyl-D: -aspartate (NMDA). Herein we provide further evidence for IL-6 neuroprotection against NMDA-induced apoptosis and explore the signal-transduction mechanisms underlying the anti-apoptotic action of IL-6. Cerebellar granule neurons (CGNs) from postnatal 8-day infant rats were chronically exposed to IL-6 (40 or 120 ng/ml) for 8 days, and stimulated with NMDA (100 μM) for 30 min. To observe the signaling pathways, we employed AG490 (5 or 10 μM), an inhibitor of Janus kinases (JAKs), or LY294002 (5 or 10 μM), an inhibitor of phosphatidylinositol 3-kinase (PI3K), to pretreat the CGNS together with IL-6. The levels of phosphorylation for the downstream effectors of JAKs and PI3K, i.e., phosphorylated STAT3 and Akt, were quantified by Western blot assay. In the cultured CGNs with various drug exposures, the expressions of Bcl-2, Bax, and caspase-3 were measured by real-time PCR and Western blot, and the percentage of apoptotic nuclei was tested by Hoechst 33342 staining. After the CGNs were chronically exposed to IL-6, NMDA stimulation led to an increase in the expression of Bcl-2 mRNA and a decrease in the expression of Bax and caspase-3 mRNAs and proteins when compared with those neurons lacking IL-6 exposure. IL-6 pretreatment of the neurons without NMDA stimulation concentration-dependently enhanced the expressions of Bcl-2 mRNA and protein while attenuating the expressions of Bax and caspase-3 mRNAs and proteins in comparison with control lacking any treatment. Furthermore, IL-6 prevented the increase in the percentage of apoptotic neurons induced by NMDA. The combined pretreatment of the CGNs with AG490 and IL-6 or with LY294002 and IL-6 reduced these anti-apoptotic effects of IL-6. Neither AG490 nor LY294002 exposure alone altered the expressions of Bcl-2, Bax, and cleaved caspase-3 proteins. IL-6 up-regulated the levels of phosphorylated STAT3 and Akt, and this was blocked by AG490 and LY294002, respectively. These results suggest that IL-6 protects neurons against NMDA-induced apoptosis, and that the IL-6 neuroprotection is jointly mediated by JAK-STAT3 and PI3K-Akt signaling pathways.

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