ABSTRACT
Modulating the structure and morphology is essential in fabricating high-performance electromagnetic absorbing materials. Herein, we obtained porous Fe3O4/carbon hollow microspheres and porous Fe4N/carbon hollow microspheres derived from Fe-glycerol hollow microspheres. Through structure and morphology analysis, we proved the existence of porous and hollow features. By comparison, it can be found that the porous Fe4N/carbon hollow microspheres have electromagnetic wave absorption performance superior to that of porous Fe3O4/carbon hollow microspheres. The reflection loss value of porous Fe4N/carbon hollow microspheres reaches -42.2 dB at a matching thickness of merely 1.4 mm, and its effective absorbing bandwidth approaches 4.5 GHz, whereas the reflection loss of porous Fe3O4/carbon hollow microspheres in the 2-18 GHz range is over -10 dB. Reasons for the better electromagnetic wave absorption performance are revealed to be that the magnetic Fe4N has higher complex permittivity and complex permeability, and the porous hollow microspherical structure increases the multiple scattering and reflection of electromagnetic waves. Meanwhile, the impedance matching and attenuation constant are optimized together through the synergy of dielectric and magnetic loss. This research can provide instructive findings for thin-thickness electromagnetic wave absorbing materials based on Fe4N with an appropriate microstructure.
ABSTRACT
We previously demonstrated the antioxidant activity of Coeloglossum viride var. bracteatum extract (CE) in rat cortical neurons and in mice with chemically induced cognitive impairment. In this work, we established a staurosporine (STS)-induced toxicity model to decipher the neuroprotective mechanisms of CE. We found that CE protected cell viability and neurite integrity in STS-induced toxicity by restoring the levels of FGF2 and its associated PI3K/Akt signaling axis. LY294002, a pan-inhibitor of PI3K, antagonized the activity of CE, although its-mediated restoration of FGF2 was unaffected. In addition, CE restored levels of Bcl-2/Caspase-3, PKCα/CaM pathway, and Dnmt3a and Dnmt3b, two methyltransferases that contribute to de novo DNA methylation. The Dnmts inhibitor 5-azacytidine impaired CE-mediated restoration of Dnmt3 or CaM, as well as the transition of DNA methylation status on the Dnmt3 promoter. These results reveal potential mechanisms that could facilitate the study and application of CE as a neuroprotective agent.
ABSTRACT
Ginsenoside Rg1 is the main active ingredient of Panax ginseng with the activity of neuroprotective, antioxidant and strengthening the immune system. Therefore, we hypothesized that Rg1 may afford anti-aging effects although the mechanism remains to be elucidated. In this study, chemically induced aging mice were established by consecutive administration of D-galactose and AlCl3. We found that Rg1 effectively ameliorates spatial learning and memory deficits in aging mice demonstrated by their improved performance in step down avoidance tests and Morris water maze experiments. Rg1 restored aging-induced decline of FGF2 and BDNF, reactivated TrkB/Akt signaling pathways in the hippocampus and prefrontal cortex to inhibit apoptosis, for the expression of anti-apoptotic protein Bcl-2 and apoptosis promoting enzyme cleaved-Caspase3 were antagonistically restored. Therefore, these results established the anti-aging effects of Rg1, and FGF2, BDNF and associated signaling pathways might be promising targets. Our data may provide a new avenue to the pharmacological research and diet therapeutic role of ethnic products such as Rg1 in anti-aging and aging associated diseases.
Subject(s)
Antioxidants/pharmacology , Cognitive Dysfunction/drug therapy , Ginsenosides/pharmacology , Signal Transduction/drug effects , Aging/drug effects , Aging/physiology , Aluminum Chloride/administration & dosage , Aluminum Chloride/toxicity , Animals , Antioxidants/therapeutic use , Apoptosis/drug effects , Behavior Observation Techniques , Behavior, Animal/drug effects , Brain-Derived Neurotrophic Factor/metabolism , Cognition/drug effects , Cognitive Dysfunction/chemically induced , Cognitive Dysfunction/diagnosis , Cognitive Dysfunction/physiopathology , Disease Models, Animal , Fibroblast Growth Factor 2/metabolism , Galactose/administration & dosage , Galactose/toxicity , Ginsenosides/therapeutic use , Hippocampus/drug effects , Hippocampus/pathology , Humans , Male , Membrane Glycoproteins/metabolism , Mice , Panax/chemistry , Protein-Tyrosine Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction/physiologyABSTRACT
To investigate the anti-tumor activities of WZ35 and its possible molecular mechanism, bioinformatics analysis and the hematoxylin-eosin (HE) staining were applied to evaluate the Yes-associated-protein (YAP) level in gastric cancer. Cell counting kit-8 (CCK-8) was used to examine cell viability. Apoptosis was determined by flow cytometry analysis. Seahorse bioenergetics analyzer was used to investigate the alteration of oxygen consumption and aerobic glycolysis rate. SiRNA transfection was applied to silence endogenous YAP. Western blot was performed to detect indicated proteins. We found that treatment of gastric cancer cells with WZ35 exerted stronger anti-tumor activities than curcumin. Mechanistically, our research showed that WZ35 inhibited glycolysis, and induced reactive oxygen species (ROS) generation, resulting in Jun N-terminal Kinase (JNK) activation through downregulation of YAP in gastric cancer cells. ROS mediated YAP downregulation and JNK activation was regulated by glycolysis. Abrogation of ROS production markedly attenuated WZ35 induced anti-tumor activities as well as YAP downregulation and JNK activation. Similarly, the JNK inhibitor significantly reversed WZ35 induced anti-tumor activities in gastric cancer cells. Our study reveals a novel anti-gastric cancer mechanism of WZ35 by inhibiting glycolysis through the ROS-YAP-JNK pathway. WZ35 might be a potential therapeutics for the treatment of gastric cancer.