ABSTRACT
Lanthanide metal-organic framework (Ln-MOF) based phosphors for light-emitting diodes (LEDs) play an important role in the fields of solid-state lighting and display. The rational design of organic antennae to address the drawback of low extinction coefficients of the lanthanide ions is highly desired. In this work, we provide a new design strategy to achieve an energy transfer molecule with a through-space conjugated folded structure, which can strengthen the skeleton rigidity and facilitate triplet state energy transfer. Consequently, one U-type π-conjugated molecule 2,6-bis(3,5-dicarboxylphenoxy) pyridine (H4L) was selected as a light gatherer to sensitize lanthanide ions for the construction of Ln-MOFs [Ln(HL)(H2O)3]n (Eu-MOF and Tb-MOF), which exhibit a long-lived luminescence lifetime (0.88 ms for Eu-MOF and 1.31 ms for Tb-MOF) and high quantum yields (50.87% for Eu-MOF and 85.64% for Tb-MOF). Furthermore, a white LED device with a colour rendering index (89) was fabricated using the mixture of Ln-MOFs with a commercial blue phosphor.
ABSTRACT
OBJECTIVE: To study the effects of dopamin receptors-2 (DR2) on myocardial ischemic postconditioning and explore its underlying mechanisms. METHODS: The myocardial ischemic postconditioning (PC) model was established in cultured primary rat neonatal cardiomyocytes which were then randomly assigned in the following groups: Nomial control group, Isehemia/reperfusion (L'R) group, PC (ischemic postconditioning) group, PC + Bro (Bromocriptine, a DB2 antagonist) group, PC + Hal (Haloperidol, a DB2 repressor) and PC + Hal + Bro groups. The lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell medium were analyzed by colorunetry. The cell ultrastructure changes were observed by transmission electron microscope. The cell apoptosis was analyzed using flowcytometiy. The protein expression level of D112 and activity of p-p38 and p-JNK were detected by Western blot. RESULTS: Compared with the nonnal control group, hR increased the protein expression level of DB2, enhanced LDH activity and MDA content, promoted cell injury and apoptosis, decreased SOD activity, up-regulated the activity of p-p38 and p-JNK. Compared with the hR group, although PC further increased the expression of DR2 protein, it decreased LDH activity and MDA content, cell injury and apoptosis, increased SOD activity, down-regulated activity of p-p38 and p-JNK. Bromocriptine treatment further enhanced PC-induced canlioprotective effect, yet Hal addition attenuated this enhancing effect exerted by bromocriptine. CONCLUSION: The activation of DB2 is involved in the protective effect of ischemic postconditioning on myocardial ischemia/reperfusion injury through down-regulating the activity of p-p38 and p-JNK.
