Topical treatment with anti-oxidants and Au nanoparticles promote healing of diabetic wound through receptor for advance glycation end-products.

Impairment in diabetic wound healing constitutes an enormous biomedical burden. The receptor for advanced glycation end-products (RAGE) expression in the diabetic cutaneous wound may play a key role. However, the relationship between RAGE expression and topical application of anti-oxidant agents with gold nanoparticles (AuNP) in cutaneous diabetic wounds remains unclear. We tested the 3-5 nm AuNP, epigallocatechin gallate (EGCG), and α-lipoic acid (ALA) could change the RAGE expression and be helpful in diabetic wound. The mixture of AuNP+EGCG+ALA (AuEA) significantly attenuated the AGE-induced RAGE protein expression in fibroblasts (Hs68). Topical EGCG+ALA (EA) and AuEA application accelerated wound healing on diabetic mouse skin and decreased the RAGE expression. Vascular endothelial growth factor but not angiopoietin-1 significantly increased after EA or AuEA treatment for 7 days. Angiopoietin-2 significantly decreased at day 7 in AuEA group. Furthermore, immunoblotting of diabetic wound tissue showed significant decrease of CD68 expression from day 3 to day 7. The results suggest that combination of AuNP, EGCG, and ALA significantly accelerated diabetic cutaneous wound healing through angiogenesis regulation and anti-inflammatory effects. Blockade of RAGE by anti-oxidant agents and nanoparticles may restore effective wound healing in diabetic ulcer.

Magnetization reversal of Co/Pd multilayers on nanoporous templates.

By making use of an e-beam deposition system, the [Co(2 Å)/Pd(10 Å)]15 multilayers were prepared on a Si(100) substrate and anodized aluminum oxide [AAO] templates with average pore diameters of around 185, 95, and 40 nm. The mechanism of magnetization reversal of the Co/Pd multilayers was investigated. Wall motion was observed on the Co/Pd multilayers grown on the Si substrate. A combination of wall motion and domain rotation was found in the sample grown on the AAO template with a 185-nm pore diameter. For the samples grown on the AAO templates with pore diameters of around 95 and 40 nm, the reversal mechanism was dominated by domain rotation. The rotational reversal was mainly contributed from the underlying nanoporous AAO templates that provided an additional pinning effect.PACS: 75.30.Gw, magnetic anisotropy; 78.67.Rb, nanoporous materials; 75.60.Jk, magnetization reversal mechanisms.

The effects of gold nanoparticles in wound healing with antioxidant epigallocatechin gallate and α-lipoic acid.

Topical applications of antioxidant agents in cutaneous wounds have attracted much attention. Gold nanoparticles (AuNPs), epigallocatechin gallate (EGCG), and α-lipoic acid (ALA) were shown to have antioxidative effects and could be helpful in wound healing. Their effects in Hs68 and HaCaT cell proliferation and in mouse cutaneous wound healing were studied. Both the mixture of EGCG + ALA (EA) and AuNPs + EGCG + ALA (AuEA) significantly increased Hs68 and HaCaT proliferation and migration. Topical AuEA application accelerated wound healing on mouse skin. Immunoblotting of wound tissue showed significant increase of vascular endothelial cell growth factor and angiopoietin-1 protein expression, but no change of angiopoietin-2 or CD31 after 7 days. After AuEA treatment, CD68 protein expression decreased and Cu/Zn superoxide dismutase increased significantly in the wound area. In conclusion, AuEA significantly accelerated mouse cutaneous wound healing through anti-inflammatory and antioxidation effects. This study may support future studies using other antioxidant agents in the treatment of cutaneous wounds. FROM THE CLINICAL EDITOR: In this study, topically applied gold nanoparticles with epigallocatechin gallate and alpha-lipoic acid were studied regarding their effects in wound healing in cell cultures. Significant acceleration was demonstrated in wound healing in a murine model.

Identification of the nanogold particle-induced endoplasmic reticulum stress by omic techniques and systems biology analysis.

Growth inhibition and apoptotic/necrotic phenotype was observed in nanogold particle (AuNP)-treated human chronic myelogenous leukemia cells. To elucidate the underlying cellular mechanisms, proteomic techniques including two-dimensional electrophoresis/mass spectrometry and protein microarrays were utilized to study the differentially expressed proteome and phosphoproteome, respectively. Systems biology analysis of the proteomic data revealed that unfolded protein-associated endoplasmic reticulum (ER) stress response was the predominant event. Concomitant with transcriptomic analysis using mRNA expression, microarrays show ER stress response in the AuNP-treated cells. The ER stress protein markers' expression assay unveiled AuNPs as an efficient cellular ER stress elicitor. Upon ER stress, cellular responses, including reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondria damage, chronologically occurred in the AuNP-treated cells. Conclusively, this study demonstrates that AuNPs cause cell death through induction of unmanageable ER stress.