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A new micellar electrokinetic chromatography (MEKC) method using beta-cyclodextrins (β-CDs) and 1-butyl-3-methylimidazolium hexafluorophosphates (ionic liquids) as additives was successfully developed for determination of para-, meta-, and ortho-phenylenediamines isomers (p-P, m-P, and o-P) in hair dyes. To improve the sensitivity of the MEKC-UV, a simple and cheap flow injection (FI) technique using a micro-column packed with coal cinders (the by-products from combustion in a boiler) as solid-phase extractant was also investigated. In the presence of 20 mmol L(-1) phosphates at pH 5.5, addition of 12 mmol L(-1) ionic liquids and 8 mmol L(-1) β-CDs greatly improved the separation efficiency. The three analytes could be quantitatively adsorbed by coal cinders, and desorbed readily with 0.15 mL of 0.01 mol L(-1) NaOH. Under the optimum conditions, an enrichment factor (EF) of 33.3 was obtained, and determination limits of p-P, m-P, and o-P were 1.97 × 10(-7), 0.99 × 10(-7), and 0.61 × 10(-7) mol L(-1), respectively. The adsorption capacities of the coal cinders micro-column for p-P, m-P, and o-P were all 1.20 mg g(-1). The presented procedure was successfully applied to the determination of p-P, m-P, and o-P in hair dyes with satisfactory results.

Gestational diabetes mellitus (GDM) causes oxidative stress in mothers and infants and causes vascular endothelial dysfunction, which is a key factor for maternal and fetal cardiovascular diseases in the later stage of GDM, seriously threatening the life and health of mothers and infants. Nowadays, metformin (MET) has been discovered to improve endothelial function, but studies regarding the mechanism of MET improving endothelial cell function and alleviating endothelial function under hyperglycemia are still extremely limited. We aimed to investigate whether MET exerts its protective role against hyperglycemia-induced endothelial dysfunction through p65 and Nrf2. In our studies, applying cell migration assay and tube formation assay, we observed an obvious improvement of endothelial function under MET-treated, as characterized by that MET accelerated GDM-attenuated migration and angiogenesis of HUVECs. And ELISA assay results uncovered that Nrf2 expression level was decreased in GDM placenta, HVUECs and maternal serum comparing with normal group, however activation Nrf2 largely ameliorated tube formation under hyperglycemic condition. Furthermore, MET elevated the Nrf2 expression level and the level of nuclear Nrf2 accumulation in hyperglycemic HUVECs. Besides, preliminary evidence predicted that Nrf2 expression was modulated by transcription factor p65, which was increased in GDM peripheral blood, placenta and HUVECs, and suppression of p65 could recover GDM-induced suppression of angiogenesis. In addition, we also confirmed MET restores the GDM-induced angiogenesis impairment may via downregulation of p65 and upregulation of Nrf2. Taken together, the endothelial protective effect of MET under GDM (HG) conditions could be partly attributed to its role in downregulating p65 and upregulating Nrf2.