This paper demonstrated a hybrid composite of tin oxide–reduced graphene oxide (rGO) for ppm-level detection of ethanol vapour. A facile and low-cost method of hydrothermal synthesis was used to construct the SnO₂–rGO hybrid film on a PCB substrate with coil-like interdigital microelectrodes. The presence of small-sized SnO₂ nanocrystals on rGO sheets was characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), an X-ray diffractometer (XRD) and Brunauer–Emmett–Teller (BET) measurements. The sensing properties of the SnO₂–rGO hybrid film sensor, including the sensitivity, response–recovery times and repeatability, were investigated by exposing it to various concentrations of ethanol gas varying from 1 ppm to 100 ppm at room temperature. As a result, the presented sensor exhibited a low detection limit of 1 ppm at room temperature, as well as a fast response–recovery time and good repeatability, which outstripped that of pure rGO film sensors. Finally, the possible mechanism of ethanol gas-sensing for the above presented sensor was discussed in detail.

Objectives: Chlorogenic acid (CGA) is one of the most widely consumed polyphenols in diets and is recognized to be a natural hepatoprotective agent. Here, we evaluated the protective effect and the potential mechanism of CGA against ɑ-naphthylisothiocyanate (ANIT)-induced cholestasis and liver injury. Methods: Twenty-five male 129/Sv mice were administered with CGA, and ANIT challenge was performed at 75 mg/kg on the 4th day. Blood was collected and subjected to biochemical analysis; the liver tissues were examined using histopathological analysis and signalling pathways. Key findings: Chlorogenic acid almost totally attenuated the ANIT-induced liver damage and cholestasis, compared with the ANIT group. Dose of 50 mg/kg of CGA significantly prevented ANIT-induced changes in serum levels of alanine aminotransferase, alkaline phosphatases, total bile acid, direct bilirubin, indirect bilirubin (5.3-, 6.3-, 18.8-, 158-, 41.4-fold, P<0.001) and aspartate aminotransferase (4.6-fold, P<0.01). Expressions of the altered bile acid metabolism and transport-related genes were normalized by cotreatment with CGA. The expressions of interleukin 6, tumour necrosis factor-α and suppressor of cytokine signalling 3 were found to be significantly decreased (1.2-fold, ns; 11.0-fold, P<0.01; 4.4-fold, P<0.05) in the CGA/ANIT group. Western blot revealed that CGA inhibited the activation and expression of signal transducer and activator of transcription 3 and NFκB. Conclusions: These data suggest that CGA inhibits both ANIT-induced intrahepatic cholestasis and the liver injury. This protective effect involves down-regulation of STAT3 and NFκB signalling.