Effect of Reticulate Unit Spacing on Microstructure and Properties of Biomimetic 7075 Aluminum Alloy by Laser Cladding.

In the context of energy conservation and emission reduction, more and more attention has been paid to the development of lightweight metal materials with both high strength and high toughness. Inspired by the non-smooth surface of natural organisms, a biomimetic surface with various spacing reticulate units of 7075 aluminum alloys was modified by laser cladding. The microstructure, microhardness and tensile properties of the various spacing units with CeO2-SiC-Ni60 were studied. The finer microstructure and the higher microhardness of various spacing units in comparison with that of 7075 aluminum alloys were obtained, no matter the strip-like treated region or the cross-junction region. Moreover, the best combination of strength and toughness of the biomimetic sample with 2.5 mm spacing reticulate unit was discussed. Finally, by combining the microstructure, XRD phase change, thermal gradient effect, thermal expansion coefficient difference and hard phase strengthening mechanism, it was concluded that the 2.5 mm spacing reticulate unit had the best ability to inhibit crack propagation, and the dispersive hard phases of Al3Ni2 and SiC played a major role in stress release of the matrix.

Icaritin alleviates docetaxel-induced skin injury by suppressing reactive oxygen species via estrogen receptors.

BACKGROUND: Docetaxel (DTX) exhibits antitumor effects against breast cancer by stabilizing microtubules and increasing the accumulation of reactive oxygen species (ROS). DTX extravasation during infusion often causes skin injury. The present study aimed to investigate the effects and mechanisms of icaritin (ICT) on DTX-induced skin injury. METHODS: The effects of ICT on the viability and apoptosis of HaCaT cells were measured by SRB assay and flow cytometry, respectively. Endogenous LC3 puncta and microtubules were determined by immunofluorescence. The number of mitochondria was measured by MitoTracker orange staining. ROS were determined by dihydroethidium staining. The expression of markers of ROS and autophagy were measured by western blotting. Chloroquine, compound D, and tamoxifen were employed as the inhibitor for autophagy and AMPK, estrogen receptors (ERs) modulator, respectively. RESULTS: DTX inhibited the viability and decreased apoptosis of HaCaT cells, which can be rescued by ICT. ICT decreased microtubule bundles, increased the number of mitochondria, and attenuated ROS of HaCaT cells induced by DTX. ICT blocks autophagy and the autophagic flux. Compound C or tamoxifen diminished the protection effects of ICT on DTX-treated HaCaT cells. CONCLUSION: ICT alleviates DTX-induced skin injury by suppressing ROS, reducing microtubule bundles, and blocking autophagy via ERs. Our study indicated that ICT may be a potential candidate for DTX-induced skin injury.

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats.

BACKGROUND/AIMS: To explore the effects of sulforaphane (SFN) on neuronal apoptosis in hippocampus and memory impairment in diabetic rats. METHODS: Thirty male rats were randomly divided into normal control, diabetic model and SFN treatment groups (N = 10 in each group). Streptozotocin (STZ) was applied to establish diabetic model. Water Morris maze task was applied to test learning and memory. Tunel assaying was used to detect apoptosis in hippocampus. The expressions of Caspase-3 and myeloid cell leukemia 1(MCL-1) were detected by western blotting. Neurotrophic factor levels and AKT/GSK3ß pathway were also detected. RESULTS: Compared with normal control, learning and memory were apparently impaired, with up-regulation of Caspase-3 and down-regulation of MCL-1 in diabetic rats. Apoptotic neurons were also found in CA1 region after diabetic modeling. By contrast, SFN treatment prevented the memory impairment, decreased the apoptosis of hippocampal neurons. SFN also attenuated the abnormal expression of Caspase-3 and MCL-1 in diabetic model. Mechanically, SFN treatment reversed diabetic modeling-induced decrease of p-Akt, p-GSK3ß, NGF and BDNF expressions. CONCLUSION: SFN could prevent the memory impairment and apoptosis of hippocampal neurons in diabetic rat. The possible mechanism was related to the regulation of neurotropic factors and Akt/GSK3ß pathway.