Metal–organic frameworks (MOFs) have been extensively studied in recent years due to their tunable porosity, huge specific area, and controllable structure. The rich metal centers and large specific area have endowed MOFs with excellent electrochemical activity due to the multiple valence states, but the poor electronic conductivity of MOFs seriously impedes their electrocatalytic performance. Here, a polyhedral Co-based zeolite imidazole frame [Co­(mim)2] n (denoted as ZIF-67, mim = 2-methylimidazole) is in situ loaded on the two sides of physically exfoliated graphene nanosheets (GSs) at room temperature, and sandwich-like GS@ZIF-67 hybrids with an ordered nanostructure are easily obtained. Compared with each individual component, the as-synthesized GS@ZIF-67 hybrids exhibit higher electrochemical activity toward glucose oxidation. Besides, the hierarchical nanocomposites also show better electrocatalytic performance compared with the same ratio of a physical mixture of GSs and ZIF-67, further demonstrating the synergistic effect between ZIF-67 and GSs. Thus, a highly sensitive nonenzymatic glucose electrochemical sensor is proposed with a linear range of 1–805.5 μM, sensitivity of 1521.1 μA Mm–1 cm–2, detection limit of 0.36 μM (S/N = 3), and excellent stability and selectivity. More importantly, the newly fabricated sensor is also successfully applied for glucose determination in human serums with satisfactory results, suggesting its promising potential toward glucose detection in real samples.

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disease. NLRP3 inflammasome activation has been widely studied in the pathogenesis of NAFLD. Cathepsin B (CTSB) is a ubiquitous cysteine cathepsin, and the role of CTSB in the progression and development of NAFLD has received extensive concern. However, the exact roles of CTSB in the NAFLD development and NLRP3 inflammasome activation are yet to be evaluated. In the present study, we used methionine choline-deficient (MCD) diet to establish mice NASH model. CTSB inhibitor (CA-074) was used to suppress the expression of CSTB. Expressions of CTSB and caspase-1 were evaluated by immunohistochemical staining. Serum IL-1β and IL-18 levels were also determined. Palmitic acid was used to stimulate Kupffer cells (KCs), and protein expressions of CTSB, NLRP3, ASC (apoptosis-associated speck-like protein containing CARD), and caspase-1 in KCs were detected. The levels of IL-1β and IL-18 in the supernatant of KCs were evaluated by enzyme-linked immunosorbent assay (ELISA). Our results showed that CTSB inhibition improved the liver function and reduced hepatic inflammation and ballooning, and the levels of pro-inflammatory cytokines IL-1β and IL-18 were decreased. The expressions of CTSB and caspase-1 in liver tissues were increased in the NASH group. In in vitro experiments, PA stimulation could increase the expressions of CTSB and NLRP3 inflammasome in KCs, and CTSB inhibition downregulated the expression of NLRP3 inflammasome in KCs, when challenged by PA. Moreover, CTSB inhibition effectively suppressed the expression and activity of caspase-1 and subsequently secretions of IL-1β and IL-18. Collectively, these results suggest that CTSB inhibition limits NLRP3 inflammasome-dependent NASH formation through regulating the expression and activity of caspase-1, thus providing a novel anti-inflammatory signal pathway for the therapy of NAFLD.

Purpose: To investigate the effects of atorvastatin and rosuvastatin on blood lipids, platelet aggregation rate (PAR) and inflammatory factors in patients with cerebral infarction.Methods: Patients (n = 120) with cerebral infarction treated in Feng Hua People's Hospital, Jiang Feng Hua, China from January 2014 to October 2016 were randomly divided into control group (clopidogrel combined with atorvastatin, 60 cases) and observation group (clopidogrel combined with rosuvastatin, 60 cases). Blood lipids, PAR, inflammatory factors and carotid atherosclerotic plaque were recorded and compared.Results: Following treatment, total cholesterol (TC), triglycerides (TG) and low  density lipoprotein cholesterol (LDL-C) in the observation group were significantly lower (p < 0.05) than in the control group, while high density lipoprotein cholesterol (HDL-C) was significantly higher (p < 0.05). C-reactive protein (CRP), tumor necrosis factor-α (IL-6) and interleukin-6 (IL-6) were significantly decreased in the two groups after treatment (p < 0.05). Plaque area, intima-media thickness (IMT) and number of plaques in the two groups were significantly lower after treatment than before treatment (p < 0.05). Plaque area, IMT and number of plaques in the observation group were significantly lower than those in the control group (p < 0.05).Conclusion: Atorvastatin and rosuvastatin have no significant effect on the  antiplatelet function of clopidogrel, but rosuvastatin shows better control of blood lipids, carotid atherosclerosis and inflammatory factors.Keywords: Atorvastatin, Rosuvastatin, Cerebral infarction, Blood lipids, Platelet aggregation rate, Inflammatory factors