Terahertz large-area unidirectional surface magnetoplasmon and its applications.

Unidirectional surface waves in nonreciprocal plasmonic platforms with nonlocal effects have been a topic of significant interest and some controversy. In this study, we present a scheme to achieve unidirectional surface magnetoplasmons (USMPs) with large modal areas at terahertz frequencies. Such large-area USMPs (LUSMPs) exist in a metal-UENZ (uniaxial-[Formula: see text]-near-zero)-Si-InSb structure under external magnetic field, where the effect of nonlocality is included. The field of the LUSMP extends almost uniformly in the UENZ layer with a thickness of wavelength scale, thus its modal size can be represented by the UENZ-layer thickness. Due to the modal energy primarily distributed in the thick UENZ layer, the nonlocality-induced leakage of the LUSMP is significantly reduced by an order of magnitude, compared to previous USMP existing at interface between InSb and opaque isotropic medium. Due to their large modal sizes, such LUSMPs can be efficiently excited by terahertz radiations directly from free space. In addition, LUSMPs offer high degree of freedom for manipulating terahertz waves, such as energy squeezing and trapping. Based on LUSMPs, a terahertz free-space isolator is also developed. Our findings have important implications to the development of innovative plasmonic devices in terahertz regime.

Broadband unidirectional surface plasmon polaritons with low loss.

Unidirectional surface plasmon polaritons (SPPs) have been proven to truly exist at an interface between a magnetized semiconductor and an opaque isotropic material, however, they suffer rather serious leakage loss (with propagation length shorter than two wavelengths) caused by nonlocality. In this work, we investigate an alternative category of unidirectional SPPs existing on a nonreciprocal plasmonic platform with a cladding composed of a dielectric heterostructure transversely terminated by metal. This unidirectional SPP mode exists for small wavenumbers within the entire upper bulk-mode bandgap of the magnetized semiconductor, hence it is robust against nonlocal effects over a broad band. In contrast to previous unidirectional SPPs, the leakage loss of the present unidirectional SPPs is significantly reduced by more than five times, since the portion of modal energy distributed in the cladding is substantially increased. A similar reduction in absorption losses associated with semiconductor dissipation is observed. Though the nonlocality induces a backward-propagating SPP with extremely large wavenumbers, it can be suppressed even at very small level of dissipation. Therefore, our proposed plasmonic waveguide actually exhibits exceptional unidirectional characteristics.

Singly protonated dehydronorcantharidin silver coordination polymer induces apoptosis of lung cancer cells via reactive oxygen species-mediated mitochondrial pathway.

Silver complexes have been shown to possess antimicrobial and anticancer properties. Ag-SP-DNC, a novel silver and singly protonated dehydronorcantharidin complex, was synthesized in our previous study. In this study, we offer evidence that Ag-SP-DNC elicits a reactive oxygen species (ROS)-mediated mitochondrial apoptosis in lung cancer cells. Ag-SP-DNC inhibited the growth of A549 cells by inducing G2/M phase cell cycle arrest and apoptosis. Ag-SP-DNC induced apoptosis was associated with the levels of intracellular ROS. The further study revealed that Ag-SP-DNC disrupted the mitochondrial membrane potential, induced the caspase-3 activation and led to the translocation of apoptosis inducing factor and endonucleaseG to the nucleus. These findings have important implications for the development of silver complexes for anticancer applications.

Tetramethylpyrazine analogue CXC195 protects against cerebral ischemia/reperfusion-induced apoptosis through PI3K/Akt/GSK3ß pathway in rats.

CXC195 showed strongest protective effects among the ligustrazine derivatives in cells and prevented apoptosis induced by H2O2 injury. We recently demonstrated that CXC195 protected against cerebral ischemia/reperfusion (I/R) injury by its antioxidant activity. However, whether the anti-apoptotic action of CXC195 is involved in cerebral I/R injury is unknown. Here, we investigated the role of CXC195 in apoptotic processes induced by cerebral I/R and the possible signaling pathways. Male Wistar rats were submitted to transient middle cerebral artery occlusion for 2h, followed by 24h reperfusion. CXC195 was injected intraperitoneally at 2h and 12h after the onset of ischemia. The number of apoptotic cells was measured by TUNEL assay, apoptosis-related protein cleaved caspase-3, Bcl-2, Bax and the phosphorylation levels of Akt and GSK3ß in ischemic penumbra were assayed by western blot. The results showed that administration of CXC195 at the doses of 3mg/kg and 10mg/kg significantly inhibited the apoptosis by decreasing the number of apoptotic cells, decreasing the level of cleaved caspase-3 and Bax, and increasing the level of Bcl-2 in rats subjected to I/R injury. Simultaneously, CXC195 treatment markedly increased the phosphorylation of Akt and GSK3ß. Blockade of PI3K activity by wortmannin, dramatically abolished its anti-apoptotic effect and lowered both Akt and GSK3ß phosphorylation levels. Our study firstly demonstrated that CXC195 protected against cerebral I/R injury by reducing apoptosis in vivo and PI3K/Akt/GSK3ß pathway involved in the anti-apoptotic effect.

Tetramethylpyrazine analogue CXC195 protects against cerebral ischemia/reperfusion injury in the rat by an antioxidant action via inhibition of NADPH oxidase and iNOS expression.

AIMS: This study was conducted to investigate the protective effects of CXC195, a tetramethylpyrazine analogue, in acute focal cerebral ischemia/reperfusion (I/R) injury in rats and to elucidate the potential mechanism. METHODS: Middle cerebral artery occlusion for 2 h followed by reperfusion for 24 h was conducted in male Wistar rats and different doses of tetramethylpyrazine and CXC195 were intraperitoneally injected at 30 min after reperfusion. RESULTS: Our results demonstrated that CXC195 at the dosage of 3 and 10 mg/kg significantly reduced the neurological deficit score and the infarct volume compared to the vehicle-treated group. In addition, CXC195 exhibited a protective effect against hippocampus neuronal cell death and significantly restored the brain ATP content. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and total antioxidative capability (T-AOC), as well as production of malondialdehyde (MDA) and reactive oxygen species (ROS) were assayed in ipsilateral hemisphere homogenates to evaluate the redox status after I/R injury. Treatment with CXC195 significantly attenuated the decrease of SOD, GPx and T-AOC activities and inhibited the elevation of MDA content and ROS generation. Furthermore, CXC195 prevented the upregulation of the NADPH oxidase (NOX) 2 and NOX4, and reduced inducible nitric oxide synthase (iNOS) induction and production of nitric oxide induced by I/R. CONCLUSION: These results suggest that CXC195 has a neuroprotective effect in transient focal ischemia, which is most likely due to its antioxidant activity by inhibiting NOX and iNOS expression.