Alumina inorganic molecularly imprinted polymer modified multi-walled carbon nanotubes for uric acid detection in sweat.

Alumina inorganic molecularly imprinted polymer (MIP) modified multi-walled carbon nanotubes (MWCNTs) on a glassy carbon electrode (MWCNTs-Al2O3-MIP/GCE) was firstly designed and fabricated by one-step electro deposition technique for the detection of uric acid (UA) in sweat. The UA templates were embedded within the inorganic MIP by co-deposition with Al2O3. Through the evaluation of morphology and structure by Field Emission Scanning Electron Microscope (SEM), Energy Dispersive X-ray Spectroscopy (EDS), X-ray Photoelectron Spectroscopy (XPS) and Transmission Electron Microscopy (TEM), it was verified that the specific recognition sites can be fabricated in the electrodeposited Al2O3 molecular imprinted layer. Due to the high selectivity of molecular imprinting holes, the MWCNTs-Al2O3-MIP/GCE electrode demonstrated an impressive imprinting factor of approximately 2.338 compared to the non-molecularly imprinted glassy carbon electrode (MWCNTs-Al2O3-NIP/GCE) toward uric acid detection. Moreover, it exhibited a remarkable limit of detection (LOD) of 50 nM for UA with wide detection range from 50 nM to 600 µM. The MWCNTs-Al2O3-MIP/GCE electrode also showed strong interference resistance against common substances found in sweat. These results highlight the excellent interference resistance and selectivity of MWCNTs-Al2O3-MIP/GCE sensor, positioning it as a novel sensing platform for non-invasive uric acid detection in human sweat.

[Study on time-toxicity relationship and mechanism of Gardeniae Fructus extract on hepatoxicity in rats based on proteomics].

To study the time-toxicity relationship and mechanism of Gardeniae Fructus extract on the hepatoxicity in rats. Rats were randomly divided into C group(0 day), D5 group(5 days), D12 group(12 days), D19 group(19 days), and D26 group(7 days recovery after 19 days of administration). The rats in normal group received normal saline through intragastric administration, and the rats in other groups received 10 g·kg~(-1 )Gardeniae Fructus extract through intragastric administration. After the final administration, the livers were collected. Hematoxylin-eosin staining was used to observe the histopathological changes in the liver tissue. Total liver proteins were extracted for proteomic analysis, detected by the Nano-ESI liquid-mass spectrometry system and identified by Protein Disco-very software. SIEVE software was used for relative quantitative and qualitative analysis of proteins. The protein-protein interaction network was constructed based on STRING. Cytoscape software was used for cluster analysis of differential proteins. Kyoto encyclopedia of genes and genomes(KEGG) database was used to perform enrichment signal pathway analysis. Pearson correlation analysis was performed for the screened differential protein expression and liver pathology degree score. The results showed that the severity of liver injury in D5, D12 and D19 groups was significantly higher than that in group C. The degree of liver damage in D5 group was slightly higher than that in D12 and D19 groups, with no significant difference between group D26 and group C. Totally 147 key differential proteins have been screened out by proteomics and mainly formed 6 clusters, involving in drug metabolism pathways, retinol metabolism pathways, proteasomes, amino acid biosynthesis pathways, and glycolysis/gluconeogenesis pathways. The results of Pearson correlation analysis indicated that differential protein expressions had a certain temporal relationship with the change of liver pathological degree. The above results indicated that the severity of liver damage caused by Gardeniae Fructus extract did not increase with time and would recover after drug with drawal. The above pathways may be related to the mechanism of liver injury induced by Gardeniae Fructus extract.