Integrative proteomics and metabolomics of Guizhou Miao Sour Soup affecting simple obese rats.

Miao Sour Soup (MSS) is a fermented product from the Qiandongnan region of Guizhou Province, which enrich many beneficial ingredients and is widely consumed in the whole China. Fermented food is beneficial to physical health with the potential positive regulating affection on simple obesity. In this study, we analyzed the mechanism of action of MSS to prevent simple obesity induced by high-fat diet by proteomics and metabolomics. Quantitative proteomics with tandem mass tagging labeling and liquid chromatography-mass spectrometry was used to analyze the changes of liver proteins and metabolites after the MSS intervention. MSS intervention upregulated 33 proteins and 9 metabolites and downregulated 19 proteins and 10 metabolites. Bioinformatics analysis showed that MSS could prevent simple obesity by acting on the PPAR signaling pathway, retinol metabolism, fatty acid ß-oxidation, fatty acid degradation, fatty acid biosynthesis, glycine, serine and threonine metabolism, pyruvate metabolism, citrate cycle (TCA cycle) and other signaling pathways. This study provides new insights into the use of MSS to prevent simple obesity caused by high-fat diets and the search for healthy eating patterns with MSS.

The role of PSMB5 in sodium arsenite-induced oxidative stress in L-02 cells.

Endemic arsenism is widely distributed in the world, which can damage multiple organs, especially in skin and liver. The etiology is clear, but the mechanisms involved remain unknown. Ubiquitin-proteasome pathway (UPP) is the main pathway regulating protein degradation of which proteasome subunit beta type-5(PSMB5) plays a dominant role. This paper aims to study the role and mechanism of PSMB5 in sodium arsenite (NaAsO2)-induced oxidative stress liver injury in L-02 cells. Firstly, L-02 cells were exposed to different concentrations of NaAsO2 to establish a liver injury model of oxidative stress, and then mechanisms of oxidative stress were studied with carbobenzoxyl-leucyl-leucl-leucll-line (MG132) and knockdown PSMB5 (PSMB5-siRNA). The oxidative stress indicators, levels of 20S proteasome, the transcription and protein expression levels of PSMB5, Cu-Zn superoxide dismutase (SOD1), and glutathione peroxidase 1 (GPx1) were detected. The results demonstrated that NaAsO2 could induce oxidative stress-induced liver injury and the activity of 20S proteasome and the protein expression of PSMB5, SOD1, and GPx1 decreased. After MG132 or PSMB5-siRNA pretreatment, the gene expression of PSMB decreased. After MG132 or PSMB5-siRNA pretreatment, and then L-02 cells were treated with NaAsO2, the gene expression of PSMB remarkably decreased; however, the protein expression of SOD1 and GPx1 increased. Overall, NaAsO2 exposure could induce oxidative stress liver injury and low expression of PSMB5 in L-02 cells, and PSMB5 might play an important role in the regulation of oxidative stress by regulating the expression of SOD1 and Gpx1.