The present study was designed to determine the chemical constituents of the stem tuber of Pinellia pedatisecta. The chemical constituents were isolated and purified by various chromatographic techniques, and their st...The present study was designed to determine the chemical constituents of the stem tuber of Pinellia pedatisecta. The chemical constituents were isolated and purified by various chromatographic techniques, and their structures were elucidated on the basis of physicochemical properties and spectral data. Three new alkaloids(compounds 1, 2, and 3) were obtained and identified as 9-((5-methoxypyridin-2-yl)methyl)-9 H-purin-6-amine(1), 4-(2-(2, 5-dioxopyrrolidin-1-yl)ethyl)phenyl acetate(2), and N-(9-((5-methoxypyridin-2-yl)methyl)-9 H-purin-6-yl)acetamide(3). These compounds were evaluated for their cytotoxicity against human cervical cancer He La cells. Compounds 1 and 3 significantly inhibited the proliferation of He La cells with IC_(50) values being 3.02 ± 0.54 and 7.16 ± 0.62 μmol·L^(-1), respectively.展开更多
Background Epithelial-mesenchymal transition is a cellular process characterized by the loss of cell adhesion, inhibition of E-cadherin expression, and increased cell mobility. Cells without Napsin A are susceptible t...Background Epithelial-mesenchymal transition is a cellular process characterized by the loss of cell adhesion, inhibition of E-cadherin expression, and increased cell mobility. Cells without Napsin A are susceptible to transition. Further studies are required to investigate whether this transition can be reversed by restoration of Napsin A. Methods A Napsin A expression vector PLJM1-Napsin A plasmid was constructed and then transfected into the epithelial cell line A549 by lentivirus transfection to obtain A549-PLJM1-Napsin A cell line. Cell proliferation was assayed by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide and cell cycle was measured by flow cytometry. The E-cadherin, type I collagen, and focal adhesion kinase mRNA level was detected by reverse transcription-polymerase chain reaction. The Napsin A, E-cadherin, type I collagen, and focal adhesion kinase protein level in A549 cells was detected by Western blotting. Results Transforming growth factor-β1 induced epithelial-mesenchymal transition in A549 cells, as demonstrated by significant reduction of E-cadherin mRNA and protein levels （P 〈0.01） as well as up-regulation of type I collagen （P 〈0.01）. Transfection of Napsin A in A549 cells can partially block the transforming growth factor-β1-regulated expression of E-cadherin and type I collagen （P 〈0.01）. In addition, transforming growth factor-β1-induced cell proliferation was inhibited by Napsin A （P 〈0.01）. Further study demonstrated that Napsin A caused G0/G1 arrest and inhibited the expression of focal adhesion kinase （P 〈0.01）, a key protein in the integrin signaling pathway, in the in vitro epithelial-mesenchymal transition model. Conclusions Sustained Napsin A expression in A549 cells can inhibit the transforming growth factor-β1-induced epithelial-mesenchymal transition. This may be due to the Napsin A-mediated inhibition of focal adhesion kinase expression and integrin signaling pathway.展开更多
基金supported by the grants from National Science&Technology Major Project"Key New Drug Creation and Manufacturing Program",China(Nos.2009ZX09308-005,2009ZX09311-001,2009ZX09502-020,2009ZX09304-002)Major Projects of Knowledge InnovationProgram of the Chinese Academy of Sciences(No.KSCX2-YW-R-166)~~
基金supported by the National Natural Science Foundation of China(No.81373964)Introduction Program of Scientific Researcher of Sichuan University of Science&Engineering(Nos.2016RCL07 and 2017RCL61)+2 种基金the Opening Project of Key Laboratory of Green Chemistry of Sichuan Institutes of Higher Education(No.LYJ1302)the Scientific Research Fund of the Sichuan Provincial Education Department(No.13ZB0133)the Science and Technology Program Project of Sichuan(No.2015JY0024)
文摘The present study was designed to determine the chemical constituents of the stem tuber of Pinellia pedatisecta. The chemical constituents were isolated and purified by various chromatographic techniques, and their structures were elucidated on the basis of physicochemical properties and spectral data. Three new alkaloids(compounds 1, 2, and 3) were obtained and identified as 9-((5-methoxypyridin-2-yl)methyl)-9 H-purin-6-amine(1), 4-(2-(2, 5-dioxopyrrolidin-1-yl)ethyl)phenyl acetate(2), and N-(9-((5-methoxypyridin-2-yl)methyl)-9 H-purin-6-yl)acetamide(3). These compounds were evaluated for their cytotoxicity against human cervical cancer He La cells. Compounds 1 and 3 significantly inhibited the proliferation of He La cells with IC_(50) values being 3.02 ± 0.54 and 7.16 ± 0.62 μmol·L^(-1), respectively.
文摘Background Epithelial-mesenchymal transition is a cellular process characterized by the loss of cell adhesion, inhibition of E-cadherin expression, and increased cell mobility. Cells without Napsin A are susceptible to transition. Further studies are required to investigate whether this transition can be reversed by restoration of Napsin A. Methods A Napsin A expression vector PLJM1-Napsin A plasmid was constructed and then transfected into the epithelial cell line A549 by lentivirus transfection to obtain A549-PLJM1-Napsin A cell line. Cell proliferation was assayed by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide and cell cycle was measured by flow cytometry. The E-cadherin, type I collagen, and focal adhesion kinase mRNA level was detected by reverse transcription-polymerase chain reaction. The Napsin A, E-cadherin, type I collagen, and focal adhesion kinase protein level in A549 cells was detected by Western blotting. Results Transforming growth factor-β1 induced epithelial-mesenchymal transition in A549 cells, as demonstrated by significant reduction of E-cadherin mRNA and protein levels （P 〈0.01） as well as up-regulation of type I collagen （P 〈0.01）. Transfection of Napsin A in A549 cells can partially block the transforming growth factor-β1-regulated expression of E-cadherin and type I collagen （P 〈0.01）. In addition, transforming growth factor-β1-induced cell proliferation was inhibited by Napsin A （P 〈0.01）. Further study demonstrated that Napsin A caused G0/G1 arrest and inhibited the expression of focal adhesion kinase （P 〈0.01）, a key protein in the integrin signaling pathway, in the in vitro epithelial-mesenchymal transition model. Conclusions Sustained Napsin A expression in A549 cells can inhibit the transforming growth factor-β1-induced epithelial-mesenchymal transition. This may be due to the Napsin A-mediated inhibition of focal adhesion kinase expression and integrin signaling pathway.
