A copper(ii)-catalyzed annulative formylation of -alkynylanilines with DMF: a single-step strategy for 3-formyl indoles.

In this paper, a copper(ii)-catalyzed reaction of -alkynylanilines with dimethylformamide (DMF) in the presence of oxygen has been developed for synthesizing multisubstituted 3-formyl indole scaffolds. This one-pot reaction proceeds through a cascade 5--dig cyclization followed by formylation to construct 1,2-disubstituted 3-formyl indoles. The key aspects of this synthesis method are the broad substrate scope (with 38 examples), and well tolerating various functional groups.

The role of IL-7 in renal proximal tubule epithelial cells fibrosis.

Background: Hyperglycemia is the most important risk factor in the progression of renal fibrosis in diabetic kidney. Based on previous studies, interleukin-7 (IL-7) may exert antifibrotic activities in pulmonary fibrosis model. However, the role of IL-7 in the pathogenesis of renal tubulointerstitial fibrosis remains unclear.

Potassium-encapsulated arsenic-dithiolato compounds: synthesis, structural calculation, and biological relevance.

This study based on the synthesis, characterization, and structural calculation of small molecular potassium-encapsulated arsenic-dithiolato compounds will provide fundamental knowledge about arsenic metabolism behavior in biological system. Two novel air-stable potassium-encapsulated arsenic-dithiolato compounds, [K@As(2)(L1)(3)](BF(4)) (1) and [K@As(2)(L2)(3)](BF(4)) (2), were prepared using deprotonated 2,6-bis(mercaptomethyl)pyridine (L1H(2)) and 1,3-dimercapto-m-xylene (L2H(2)) to react with AsCl(3) in the presence of potassium cation. Compounds 1 and 2 have been characterized by electrospray ionization-mass spectra, nuclear magnetic resonance spectra, and elemental microanalysis.

BMP-2 suppresses renal interstitial fibrosis by regulating epithelial-mesenchymal transition.

Dysregulation of epithelial-to-mesenchymal transition (EMT) may contribute to renal fibrogenesis. Our previous study indicated that bone morphogenetic protein-2 (BMP-2) significantly reversed transforming growth factor (TGF)-β1-induced renal interstitial fibrosis. In this study, we examined the underlying mechanism and elucidate the regulation of EMT process under BMP-2 treatment.

A non-fluorescent derivative from derivatizing trans, trans-muconic acid with 2-(2-naphthoxy)ethyl-2-(piperidino)ethanesulfonate.

trans, trans-Muconic acid (MA) is a polar metabolite of benzene and used as a biomarker for monitoring human exposure to benzene. Because MA is a trace metabolite, sensitive method is required for its detection. In addition, MA is a highly polar compound with dicarboxyl functions that could incur unfavorable adsorption on silica-based stationary phase usually used for separation.

Bone morphogenetic protein-2 antagonizes renal interstitial fibrosis by promoting catabolism of type I transforming growth factor-beta receptors.

TGF-beta is a therapeutic target for renal fibrosis. Scientists have long sought ways to antagonize TGF-beta to ameliorate diabetic nephropathy. Bone morphogenetic protein (BMP-2) is a member of the TGF-beta superfamily and is highly regulated in the kidney.

Safflower extract: a novel renal fibrosis antagonist that functions by suppressing autocrine TGF-beta.

Progressive renal disease is characterized by the accumulation of extracellular matrix proteins in the renal interstitium. Hence, developing agents that antagonize fibrogenic signals is a critical issue facing researchers. The present study investigated the blood-circulation-promoting Chinese herb, safflower, on fibrosis status in NRK-49F cells, a normal rat kidney interstitial fibroblast, to evaluate the underlying signal transduction mechanism of transforming growth factor-beta (TGF-beta), a potent fibrogenic growth factor.

CD36 is a novel and potential anti-fibrogenic target in albumin-induced renal proximal tubule fibrosis.

Albumin is not only a risk factor for diabetic nephropathy (DN), but also a therapeutic target. Hence, scientists have long sought ways to elucidate the interactions between albumin and diabetic renal tubule fibrosis. CD36, a surface receptor for thrombospondin-1, has been reported to interact with latent transforming growth factor-beta1 (TGF-beta1) and activate its fibrogenic bioactivity.

Albumin induces cellular fibrosis by upregulating transforming growth factor-beta ligand and its receptors in renal distal tubule cells.

Albuminuria is indicative of nephropathy. However, little literature has focused on the role of albumin in renal distal tubule fibrosis. We used a well-defined distal tubule cell, Madin-Darby Canine Kidney (MDCK).

Effect of nitric oxide-cGMP-dependent protein kinase activation on advanced glycation end-product-induced proliferation in renal fibroblasts.

Renal interstitial fibrosis is believed to play a key role in the development of diabetic nephropathy (DN), and advanced glycation end-products (AGE) may contribute importantly to this. Recent reports have shown that nitric oxide (NO) is closely linked to the renal interstitial fibrosis of DN. In this study, the mechanisms by which NO and its downstream signals mediate the AGE-induced proliferative response in normal rat kidney fibroblasts (NRK-49F) are examined.

Thrombospondin-1 mediates distal tubule hypertrophy induced by glycated albumin.

Diabetic nephropathy is characterized by early hypertrophy in both glomerular and tubuloepithelial elements. However, no studies to date have established a direct causal link between hyperglycaemia and renal hypertrophy. Our previous studies have found that high glucose does not induce cellular hypertrophy or expression of TGF-beta1 (transforming growth factor-beta1) in distal renal tubule cells [Yang, Guh, Yang, Lai, Tsai, Hung, Chang and Chuang (1998) J.

Regulation of type II transforming-growth-factor-beta receptors by protein kinase C iota.

TGF-beta (transforming growth factor-beta) is implicated in the pathogenesis of diabetic nephropathy. We previously demonstrated that up-regulation of type II TGF-beta receptor (TbetaRII) induced by high glucose might contribute to distal tubular hypertrophy [Yang, Guh, Yang, Lai, Tsai, Hung, Chang and Chuang (1998) J. Am.