To explore the effect of spacer structure on the adsorption capability of organo-vermiculites (organo-Vts), a series of aza-containing gemini surfactants (5N, 7N and 8N) are applied to modify Na-vermiculite (Na-Vt). Large interlayer spacing, strong binding strength and high modifier availability are observed in organo-Vts, which endow them with superiority for the adsorption of 2-naphthol (2-NP) and bromophenol blue (BPB). The maximum adsorption capacities of 5N-Vt, 7N-Vt and 8N-Vt toward 2-NP/BPB are 142.
View Article and Find Full Text PDFBackground: The migration, proliferation and apoptosis of vascular smooth muscle cells (VSMCs) are critical for plaque stability. WNT-inducible signalling pathway protein-1 (WISP1), a member of the CCN family of extracellular matrix proteins, can expedite the migration and proliferation of VSMCs. However, its underlying mechanism and relationship with atherosclerosis remain elusive.
View Article and Find Full Text PDFAS is an important pathological basis of cardiovascular disease. miRNAs are involved in almost all steps of AS, including the injury and dysfunction of endothelial cells and vascular smooth muscle cells. This work elucidated the biological functions of miR-512-3p in AS and probed into the underlying molecular mechanism.
View Article and Find Full Text PDFThe present review aims at reviewing the role of metformin in the treatment of endometrial cancer (EC). According to the literature, excessive estrogen levels and insulin resistance are established risk factors of EC. As a traditional insulin sensitizer and newly discovered anticancer agent, metformin directly and indirectly inhibits the development of EC.
View Article and Find Full Text PDFLipid deposition in macrophages plays an important role in atherosclerosis. The WNT1-inducible signalling pathway protein 1(WISP1) can promote proliferation and migration of smooth muscle cells. Its expression is up-regulated in obesity, which is associated with atherosclerosis, but the effect of WISP1 on atherosclerosis remains unclear.
View Article and Find Full Text PDFIn myocardial ischemia‑reperfusion injury (MIRI), increased activity of the c‑Jun N‑terminal kinase (JNK) pathway and the activation of platelets that leads to the formation of platelet‑leukocyte aggregates (PLAs) have been observed. It was hypothesized that ischemic postconditioning in MIRI exerts cardioprotective effects by altering JNK activity, which in turn leads to reduced PLA levels. A total of 60 rats were randomly divided into 6 groups (n=10 for each group): i) Control; ii) ischemia‑reperfusion injury alone; iii) ischemia‑reperfusion with postconditioning (PostC group), iv) treatment with the JNK inhibitor‑SP600125; v) postC and treatment with anisomycin; and vi) treatment with the JNK activator‑anisomycin.
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