Rh(II)-catalyzed multicomponent reaction achieved to give α-amino-β-indole ketones by trapping α-amino enols with vinylimine ions.

The classic transformations of N-sulfonyl-1,2,3-triazoles were processed via nitrogen anion (hydrolysis, etc.) and carbene intermediates, and no efficient examples via radical intermediates were developed. Here, we reported a catalyst-free radical chain transformation of N-sulfonyl-1,2,3-triazoles to access an intermolecular oxidative C(sp 3 )−H coupling to yield N 2selective products in air without any catalysts.

No abstract

An α-alkyldiazoacetate-involved three-component reaction has been developed via the suppression of intramolecular α-H shift and 1,2-proton transfer by Rh(i) complexes.

Previously the potential therapeutic action of ferulic acid, ligustrazine and tetrahydropalmatine (FLT) are discovered with unclear mechanism in rat autograft endometriosis. However, the effect of FLT on endometrial cells and allograft endometriosis is still unclear. This study is designed to elucidate the influence of FLT on epithelial-mesenchymal transformation in allograft endometriosis and endometrium cells. In vivo, fluorescent xenogeneic endometriosis model was established. In vitro, invasion and metastasis were analyzed after treating FLT. Epithelial-mesenchymal transformation and Wnt/β-catenin pathway were inspected in vitro and in vivo. Activator or inhibitor of Wnt/β-catenin signaling was performed to inspect mechanism of epithelial-mesenchymal transformation. In vivo, FLT not only decreased fluorescent intensity and volume of ectopic lesion, but also ameliorated pathological morphology. E2 and PROG levels in serum were reduced by FLT. In endometrial cells, FLT significantly inhibited the invasion and metastasis. Meantime, epithelial-mesenchymal transformation was reversed, accompanied by suppression of Wnt/β-catenin pathway. In-depth study, activation of Wnt/β-catenin pathway lead to promotion of epithelial-mesenchymal transformation, which was reversed by FLT. FLT prevented fluorescent allograft endometriosis and endometrium cells, which was related to suppress epithelial-mesenchymal transformation through inactivating Wnt/β-catenin pathway. The findings disclose molecular mechanism of epithelial-mesenchymal transformation in endometriosis by FLT, and contribute to further application.