ABSTRACT
A lithium-sulfur (Li-S) battery is regarded as the most promising candidate for next generation energy storage systems, because of its high theoretical specific capacity (1675 mA h g-1) and specific energy (2500 W h kg-1), as well as the abundance, low cost and environmental benignity of sulfur. However, the soluble polysulfides Li2Sx (4 ≤ x ≤ 8) produced during the discharge process can cause the so-called "shuttle effect" and lead to low coulombic efficiency and rapid capacity fading of the batteries, which seriously restrict their practical application. Using porous materials as hosts to immobilize the polysulfides is proved to be an effective strategy. In this article, a dual functional cage-like metal-organic framework (Cu-MOF), Cu-TDPAT, combining the Lewis basic sites from the nitrogen atoms of the ligand H6TDPAT with the Lewis acidic sites from Cu(ii) open metal sites (OMSs), was employed as the sulfur host in a Li-S battery for lithium ions and polysulfide anions (Sx2-). In addition, the size of nano-Cu-TDPAT was also optimized by microwave synthesis to reduce the internal resistance of the batteries. The electrochemical test results showed that the optimized Cu-TDPAT material can efficiently confine the polysulfides within the MOF, and the resultant porous S@Cu-TDPAT composite cathode material with the size of 100 nm shows good cycling performance with a reversible capacity of about 745 mA h g-1 at 1C (1C = 1675 mA g-1) after 500 cycles, to the best of our knowledge, which is higher than those of all reported S@MOF cathode materials. The DFT calculation and XPS data indicate that the good cycling performance mainly results from the dual functional binding sites (that is, Lewis acid and base sites) in nanoporous Cu-TDPAT, providing the comprehensive and robust interaction with the polysulfides to overcome their dissolution and diffusion into the electrolyte. Clearly, our work provides a good example of designing MOFs with suitable interaction sites for the polysulfides to achieve S@MOF cathode materials with excellent cycling performance by multiple synergistic effects between nanoporous host MOFs and the polysulfides.
ABSTRACT
OBJECTIVE: To explore the mechanism of apoptosis for resvertrol-mediated reversing the drug-resistance of AML HL-60/ADR cells. METHODS: The HL-60/ADR cells were divided into 4 groups: control group, adriamycin (ADR)-treated group, resveratrol(Res)-treated group and ADR+Res-treated group. The inhibitory rate of cell proliferation was analyzed by CCK-8 method. The auto-fluorescence intensity of intracellular ADR and the apoptotic rate of HL-60/ADR cells were detected by flow cytometry. The mRNA expression levels of multidrug-resistance associated protein-1(MRP1), anti-apoptotic gene BCL-2 and pro-apoptotic gene BAX were analyzed by real-time fluorescence quantitative RT-PCR. The protein expression levels of MRP1, BCL-2 and BAX were detected by Western blot. RESULTS: The maximal inhibition rates of cell proliferation were 44%, 61%, 76% and 81%, respectively in different concentration of Res (25, 50, 100, 200 µmol/L) and with concentration-dependent manner(r=0.876, P<0.05). Compared with ADR group (IC50: 8.534±1.111 µmol/L), the half inhibitory concentration (IC50) of HL-60/ADR cells [(1.591±0.373) µmol/L] decreased significantly in ADR+Res group(P<0.05). The auto-fluorescence intensity of ADR in HL-60/ADR cells of ADR+Res group increased significantly (P<0.05). The apoptotic rate of HL-60/ADR cells in Res or ADR+Res group increased significantly (P<0.05). The mRNA expression levels of MRP1 and Bcl-2 in Res or ADR+Res groups decreased and BAX increased significantly (P<0.05). The protein expression levels of MRP1 and BCL-2 were decreased, BAX increased significantly in Res or ADR+Res group (P<0.05). CONCLUSION: Resveratrol shows the effect of reversing the drug resisitance of HL-60/ADR cells in acute myeloid leukemia, possibly via promoting the apoptosis of HL-60/ADR cells and inhibiting the expression of MRP1, which may be related with the inhibition of BCL-2 expression and the promotion of BAX expression.
