Metalloporphyrin-Based Metal-Organic Frameworks for the Ultrasensitive Chemiresistive Detection of NO2: Effect of the Central Metal on Tuning the Sensing Performance.

The highly sensitive and selective detection of trace hazardous gases at room temperature is very promising for health protection and environmental safety. Herein, chemiresistive sensors for NO2 were fabricated based on self-assembled films of the four metalloporphyrin (MPor)-based metal-organic frameworks PCN-222-M (M = Cu, Ni, Co, Fe) by the quasi-Langmuir-Shäfer method. It is found that the relative responses of the four PCN-222-M films are linearly related to the NO2 concentration, and the PCN-222-Cu possessed an unprecedented high response to NO2 with a sensitivity of 2209% ppm-1 in the 4-20 ppb range and a low limit of detection (LOD) of 0.93 ppb, achieving the best performance reported so far for NO2 detection at room temperature. Meanwhile, PCN-222-Ni showed the fastest recovery among the four PCN-222-M films, which can be used for the rapid detection of NO2. Excellent reproducibility, stability, selectivity, and moisture resistance are shown for both PCN-222-Cu and PCN-222-Ni. Combining the experimental study and density functional theory (DFT) calculation, the essential roles of MPor units and the MPor/Zr6 cluster hybrid material in tuning the Fermi level and the electron transfer between PCN-222-M and NO2 were further proved. These were less considered topics in previous studies on MOFs. This work explores the application of MPor-based MOFs in gas sensing by selecting appropriate MPor units, thus providing guidance for the development of MOF-based chemiresistive sensors.

Neuroprotective effects and dynamic expressions of MMP9 and TIMP1 associated with atorvastatin pretreatment in ischemia-reperfusion rats.

Atorvastatin has been reported to ameliorate ischemic brain damage after stroke, but the underlying mechanisms are not clear. This study investigated the effect of atorvastatin on dynamic expressions of MMP9 and TIMP1 in rats after cerebral ischemia reperfusion (I/R). Atorvastatin (5 mgkg(-1)d(-1)) or vehicle was administered orally to rats for 21d before middle cerebral artery occlusion (MCAo) for 2h, with perfusion at 3-, 12-, 24-, 48-, or 96-h thereafter. To evaluate functional outcome, a 5-point behavioral rating scale was performed. Ischemic lesion volume was assessed via triphenyl tetrazolium chloride (TTC) staining. mRNA levels of MMP-9 and TIMP-1 were detected by reverse transcription-PCR, and protein levels of MMP-9 and TIMP-1 were measured by immunohistochemical SABC method. At all reperfusion time points, atorvastatin pretreatment was associated with significantly (P<0.05) improved neurological function and reduced brain infarct sizes compared with vehicle treatment, and MMP9 levels were significantly (P<0.05) lower and TIMP1 levels were significantly (P<0.05) higher in both mRNA and protein levels. In conclusion, Oral administration of atorvastatin before stroke may reduce the severity in I/R injury and improve neurological outcome by lowering MMP9 levels and elevating TIMP1 levels.

2,5-hexanedione induced apoptosis in mesenchymal stem cells from rat bone marrow via mitochondria-dependent caspase-3 pathway.

2,5-hexanedione (HD) induces apoptosis of nerve cells. However,the mechanism of HD-induced apoptosis remains unknown. Mesenchymal stem cells (MSCs) are multipotential stem cells with the ability to differentiate into various cell types. This study is designed to investigate the apoptosis induced by HD in rat bone marrow MSCs (BMSCs) and the related underlying mechanisms. The fifth generation of MSCs was treated with 0, 10, 20 and 40 mM HD respectively. The viability of BMSCs was observed by MTT. Apoptosis were estimated by Hoechst 33342 staining and TUNEL assay. The disruption of mitochondrial transmembrane potential (MMP) was examined by JC-1 staining. Moreover, the expression of Bax and Bcl-2, cytochrome c release, and caspase-3 activity were determined by real-time RT-PCR, Western blot and Spectrophotometry. Our results showed that HD induced apoptosis in MSCs in a dose dependent manner. Moreover, HD downregulated the Bcl-2 expression,upregulated the Bax expression and the Bax/Bcl-2 ratio, promoted the disruption of MMP, induced the release of cytochrome c from mitochondria to cytosol, and increased the activity of caspase-3 in MSCs. These results indicate that HD induces apoptosis in MSCs and the activated mitochondria-dependent caspase-3 pathway may be involved in the HD-induced apoptosis.