Inhibition of H₂O₂-induced apoptosis of GC2-spg cells by functionalized selenium nanoparticles with lentinan through ROS-mediated ERK/p53 signaling pathways

A H₂O₂-induced oxidative stress injury cell model was established to investigate the antioxidant effect of nano-selenium on mouse spermatocyte lines and the regulation mechanism of the expression level and activity of selenium-containing antioxidant enzymes induced by oxidative stress. A safe and effective nano-drug system of functionalized selenium-containing nanoparticles (SeNPs) was developed with lentinan (LNT) (SeNPs@LNT). Mice spermatocyte line GC2-spg cells were treated with SeNPs@LNT (1, 2, 4, 8, 16, 32 μM) for 24–72 h to evaluate the cytotoxicity of selenium. GC2-spg cells were randomly divided into the following groups: control, hydrogen peroxide (H₂O₂), SeNPs@LNT, and H₂O₂+SeNPs@LNT groups. H₂O₂+SeNPs@LNT group was pretreated with SeNPs@LNT 4 μM for 12 h, followed by H₂O₂ 600 μM for 8 h. The cell viability decreased in the H₂O₂ group and increased significantly in the SeNPs@LNT group. Compared with the H₂O₂ group, the SeNPs@LNT+H₂O₂ group exhibited obvious red fluorescence, indicating a higher level of mitochondrial membrane potential. The content of intracellular reactive oxygen species (ROS) in the SeNPs@LNT group reduced significantly, and the intensity of green fluorescence in the SeNPs@LNT+H₂O₂ group decreased significantly compared with the H₂O₂ group, indicating the inhibitory effect of SeNPs@LNT on the generation of ROS-induced oxidative stress. The activity of GPx and SOD increased significantly in the SeNPs@LNT group. The expression of p53 decreased significantly under the intervention of nano-selenium, and GPx1 expression increased. In the oxidative stress group, the expressions of DNA damage-related proteins and apoptosis-related proteins were higher than those in other groups. Thus, SeNPs@LNT can promote GC2-spg cell proliferation, improve GPx and SOD activities, remove intracellular ROS, and reduce mitochondrial damage and functional abnormalities caused by oxidative stress by regulating the ERK and p53 protein levels. SeNPs@LNT has good biological activity and antioxidant effect, which can be used to protect the male reproductive system from oxidative stress.     

Synergistically toughening effect of SiC whiskers and nanoparticles in Al<Subscript>2</Subscript>O<Subscript>3</Subscript>-based composite ceramic cutting tool material

In recent decades, many additives with different characteristics have been applied to strengthen and toughen Al₂O₃-based ceramic cutting tool materials. Among them, SiC whiskers and SiC nanoparticles showed excellent performance in improving the material properties. While no attempts have been made to add SiC whiskers and SiC nanoparticles together into the ceramic matrix and the synergistically toughening effects of them have not been studied. An Al₂O₃-SiC_w-SiC_np advanced ceramic cutting tool material is fabricated by adding both one-dimensional SiC whiskers and zero-dimensional SiC nanoparticles into the Al₂O₃ matrix with an effective dispersing and mixing process. The composites with 25 vol% SiC whiskers and 25 vol% SiC nanoparticles alone are also investegated for comparison purposes. Results show that the Al₂O₃-SiC_w-SiC_np composite with both 20 vol% SiC whiskers and 5 vol% SiC nanoparticles additives have much improved mechanical properties. The flexural strength of Al₂O₃-SiC_w-SiC_np is 730±95 MPa and fracture toughness is 5.6±0.6 MPa·m^1/2. The toughening and strengthening mechanisms of SiC whiskers and nanoparticles are studied when they are added either individually or in combination. It is indicated that when SiC whiskers and nanoparticles are added together, the grains are further refined and homogenized, so that the microstructure and fracture mode ratio is modified. The SiC nanoparticles are found helpful to enhance the toughening effects of the SiC whiskers. The proposed research helps to enrich the types of ceramic cutting tool and is benefit to expand the application range of ceramic cutting tool.