3D Electron-Rich ZIF-67 Coordination Compounds Based on 2-Methylimidazole: Synthesis, Characterization and Effect on Thermal Decomposition of RDX, HMX, CL-20, DAP-4 and AP.

ZIF-67 is a three-dimensional zeolite imidazole ester framework material with a porous rhombic dodecahedral structure, a large specific surface area and excellent thermal stability. In this paper, the catalytic effect of ZIF-67 on five kinds of energetic materials, including RDX, HMX, CL-20, AP and the new heat-resistant energetic compound DAP-4, was investigated. It was found that when the mass fraction of ZIF-67 was 2%, it showed excellent performance in catalyzing the said compounds. Specifically, ZIF-67 reduced the thermal decomposition peak temperatures of RDX, HMX, CL-20 and DAP-4 by 22.3 °C, 18.8 °C, 4.7 °C and 10.5 °C, respectively. In addition, ZIF-67 lowered the low-temperature and high-temperature thermal decomposition peak temperatures of AP by 27.1 °C and 82.3 °C, respectively. Excitingly, after the addition of ZIF-67, the thermal decomposition temperature of the new heat-resistant high explosive DAP-4 declined by approximately 10.5 °C. In addition, the kinetic parameters of the RDX+ZIF-67, HMX+ZIF-67, CL-20+ZIF-67 and DAP-4+ZIF-67 compounds were analyzed. After the addition of the ZIF-67 catalyst, the activation energy of the four energetic materials decreased, especially HMX+ZIF-67, whose activation energy was approximately 190 kJ·mol-1 lower than that reported previously for HMX. Finally, the catalytic mechanism of ZIF-67 was summarized. ZIF-67 is a potential lead-free, green, insensitive and universal EMOFs-based energetic burning rate catalyst with a bright prospect for application in solid propellants in the future.

MicroRNA-497-5p downregulation inhibits cell viability, reduces extracellular matrix deposition and induces apoptosis in human hyperplastic scar fibroblasts by regulating Smad7.

Hypertrophic scars (HSs) are characterized by excessive extracellular matrix deposition and excessive growth of dense fibrous tissues. MicroRNAs (miRNAs/miRs) serve key roles in HS formation. The present study investigated the expression, role and mechanism underlying the effects of miR-497-5p in HS formation. miR-497-5p expression was detected via reverse transcription-quantitative PCR. The association between miR-497-5p and Smad7 was analyzed using TargetScan and luciferase reporter assays. Protein expression levels of extracellular matrix markers were measured via western blotting. Cell viability and apoptosis were determined using the Cell Counting Kit-8 assay and flow cytometry, respectively. The results suggested that miR-497-5p expression was upregulated in HS tissues and human HS fibroblasts (hHSFs) compared with healthy control skin tissues and CCC-ESF-1 cells, respectively. Smad7 was directly targeted by miR-497-5p, and was downregulated in HS tissues and hHSFs compared with healthy control skin tissues and CCC-ESF-1 cells, respectively. Moreover, Smad7 upregulation significantly inhibited cell viability, decreased extracellular matrix deposition and induced apoptosis in hHSFs compared with the control-plasmid group. Moreover, the results indicated that, compared with the inhibitor control group, miR-497-5p inhibitor inhibited cell viability, decreased extracellular matrix deposition and induced apoptosis in hHSFs, which were significantly reversed by Smad7 knockdown. In conclusion, the results indicated that miR-497-5p downregulation repressed HS formation by inhibiting extracellular matrix deposition and hHSF proliferation at least partly by targeting Smad7.