Enhanced photoluminescence of CsPbBr3-xIx nanocrystals via plasmonic Au nanoarrays.

Large scale ordered Au nanoarrays are fabricated by nanosphere lithography technique. The photoluminescence improvement of CsPbBr3-xIx nanocrystals by more than three times is realized in the CsPbBr3-xIx nanocrystal/Au nanoarray/Si structure. Time-resolved photoluminescence decay curves indicate that the lifetime is decreased by introducing the Au nanoarrays, which results in a increasing radiation recombination rate. The reflection spectra with two major valleys (the dip in the curve) located at ∼325 nm and 545 nm of Au nanoarray/Si structure, which illustrates two plasmonic resonance absorption peaks of the Au nanoarrays. The enhancement of photoluminescence is ascribed to a well match between the excitation/emission of CsPbBr3-xIx nanocrystals and localized surface plasmon/gap plasmon resonance absorption of the ordered Au nanoarrays, as also revealed from the finite-difference time-domain simulation analysis. Our work offers an effective strategy to improve the fluorescence of perovskite nanocrystals and provide the potential for further applications.

Shuxuening injection protects against myocardial ischemia-reperfusion injury through reducing oxidative stress, inflammation and thrombosis.

BACKGROUND: Shuxuening injection (SXNI) has a good effect on cardiovascular and cerebrovascular diseases. Here, our study aims to investigate whether SXNI have the protective effect on myocardial ischemia-reperfusion injury (MIRI) and elucidate the mechanism of SXNI's cardiac protection. METHODS: In this experiment, the coronary arteries of Sprague-Dawley (SD) rats were ligated for the induction of a MIRI model. TTC staining and haematoxylin-eosin (HE), as well as troponin I (TnI), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatine kinase (CK) and CK-MB levels, were used to detect the protective effect of SXNI. In rat cardiac tissue, superoxide dismutase, catalase, glutathione and malondialdehyde (MDA) activities and glucose-regulated protein 78 (GRP78), calreticulin (CRT), CCAAT/enhancer binding protein homologous protein (CHOP) and caspase-12 expression levels were detected. In rat serum, the levels of inflammatory factors, including high-sensitivity C-reactive protein, monocyte chemoattractant protein-1, tumour necrosis factor-α, interleukin-6 (IL-6) and IL-1ß, were measured by Elisa. In the rat arterial tissue, Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) expression was measured by western blot. In the rat plasma, ELISA was used to assay the levels of coagulation and plasmin system indicators, including platelet activating factor, endothelin, tissue factor (TF), plasminogen inhibitor, thromboxane B2, plasma fibrinogen. RESULTS: The results showed that SXNI can reduce the infarct size of myocardial tissue, decrease the myocardial enzyme and TnI levels and decrease the degree of myocardial damage compared with the model group. Additionally, SXNI can increase the activity of antioxidant enzymes, reduce the MDA level and decrease the GRP78, CRT, CHOP and caspase-12 expression levels. SXNI also decreased the levels of inflammatory cytokines in rat serum, lowered the level of procoagulant molecules in plasma and reduced the TLR4/NF-κB expression. CONCLUSIONS: SXNI has protective effect on MIRI mainly by inhibiting oxidative stress and endoplasmic reticulum stress (ERS), thereby regulating TLR4/NF-κB pathway to reduce inflammation, and lowing procoagulant-related factors levels to reduce the risk of thrombosis.