Gestational diabetes mellitus (GDM) refers to the first sign or onset of diabetes mellitus during pregnancy rather than progestation. In recent decades, more and more research has focused on the etiology and pathogenesis of GDM in order to further understand GDM progress and recovery. Using an advanced metabolomics platform based on ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF-MS), we explored the changes in serum metabolites between women with GDM and healthy controls during and after pregnancy. Some significant differences were discovered using multivariate analysis including partial least-squares discriminant analysis (PLS-DA) and orthogonal PLS-DA (OPLS-DA). The dysregulated metabolites were further compared and verified in several databases to understand how these compounds might function as potential biomarkers. Analyses of the metabolic pathways associated with these potential biomarkers were subsequently explored. A total of 35 metabolites were identified, contributing to GDM progress to some extent. The identified biomarkers were involved in some important metabolic pathways including glycine, serine, and threonine metabolism; steroid hormone biosynthesis; tyrosine metabolism; glycerophospholipid metabolism; and fatty acid metabolism. The above mentioned metabolic pathways mainly participate in three major metabolic cycles in humans, including lipid metabolism, carbohydrate metabolism, and amino acid metabolism. In this pilot study, the valuable comprehensive analysis gave us further insight into the etiology and pathophysiology of GDM, which might benefit the feasibility of a rapid, accurate diagnosis and reasonable treatment as soon as possible but also prevent GDM and its related short- and long-term complications.
Animal studies have demonstrated that scutellarin (SCU) limits damage after myocardial ischemia injury. However, the underlying molecular mechanisms of SCU protecting against myocardial injury induced by ischemia reperfusion (IR) are not well known. This study examined whether SCU protects against myocardial IR injury in rats is mediated by the Janus kinase and signal transducer and activator of transcription (JAK/STAT) pathway. Protein expression of JAK2/STAT3 and phosphorylative products were assessed by Western blot and immunohistochemistry methods in myocardial tissue from myocardial IR rats pretreated with SCU (45 and 90 mg/kg, iv). Western blot and immunohistochemistry assays showed that myocardial IR injury caused significant increases of phosphorylated JAK2 (p‐JAK2) and phosphorylated STAT3 (p‐STATS) levels in the rat myocardial IR model. SCU (45 and 90 mg/kg, iv) significantly reduced ischemic size, and decreased histological p‐JAK2 and p‐STATS expression. SCU attenuates myocardial IR injury which involved in JAK/STAT signaling pathway.
Grant Funding Source: Supported by grants from the National Natural Science Foundation of China (Nos. 30960450 and 81173110) and Yunnan Provincial Science and Technology Department (Nos. 2011FA022, 2012BC012, 2008CD054, and 2008ZC111M).
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