AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture,...AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Lucigenin assay showed the generation of ROS in cells under incubation with JTE-522. The increased ROS generation might contribute to the induction of AGS cells to apoptosis. EMSA and Western blot revealed that NF-kB activity was almost completely inhibited by preventing the degradation of IkBalpha. Additionally, by using Western blot we confirmed that the level of bcl-2 was decreased, whereas p53 showed a great increase following JTE-522 treatment. Their changes were in a dose-dependent manner. CONCLUSION: These findings suggest that reactive oxygen species, NF-kB, p53, bcl-2 and caspase-3 may play an important role in the induction of apoptosis in AGS cells after treatment with JTE-522.展开更多
AIM: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (D...AIM: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (Deltapsim). METHODS: Cell culture, cell counting, ELISA assay, TUNEL, flow cytometry, Western blot and fluorometric assay were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanism. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Caspases 8 and 9 were activated during apoptosis as judged by the appearance of cleavage products from procaspase and the caspase activities to cleave specific fluorogenic substrates. To elucidate whether the activation of caspases 8 and 9 was required for the apoptosis induction, we examined the effect of caspase-specific inhibitors on apoptosis. The results showed that caspase inhibitors significantly inhibited the apoptosis induced by JTE-522. In addition, the membrane translocation of Bax and cytosolic release of cytochrome C accompanying with the decrease of the uptake of Rhodamin 123, were detected at an early stage of apoptosis. Furthermore, Bax translocation, cytochrome C release, and caspase 9 activation were blocked by Z-VAD.fmk and Z-IETD-CHO. CONCLUSION: The present data indicate a crucial association between activation of caspases 8, 9, cytochrome C release, membrane translocation of Bax, loss of Deltapsim and JTE-522-induced apoptosis in AGS cells.展开更多
Disubstituted oxazoles were prepared conveniently by treatment of aromatic -methyl ketones and nitriles with poly[styrene(iodosodiacetate)] in one-pot process.
The mechanism of nitrocompounds quenching of the fluorescence of 5, 5′ dipheny1 2, 2′ bisoxazole (POOP) and trans 1, 2 bis [2 (5 phenyloxazolyl)] ethene (POEOP) has been studied. It was found that the fluores...The mechanism of nitrocompounds quenching of the fluorescence of 5, 5′ dipheny1 2, 2′ bisoxazole (POOP) and trans 1, 2 bis [2 (5 phenyloxazolyl)] ethene (POEOP) has been studied. It was found that the fluorescence of oxazoles was quenched mainly by the absorption competition and radiationless energy transfer of nitrocompounds. The fluorescence quenching rate constants of nitrobenzene and nitromethane are 3.0×10 10 L·mol -1 ·s -1 and 1.5×10 8 L·mol -1 ·s -1 respectively for POEOP. This remarkable difference was explicated.展开更多
Main observation and conclusion A facile and efficient strategy for the synthesis of 5-aryl-2-(quinolin-2-yl)oxazoles via rhodium-catalyzed formal[3+2]cyclization of 4-aryl-1-tosyl-1H-1,2,3-triazoles with quinoline-2-...Main observation and conclusion A facile and efficient strategy for the synthesis of 5-aryl-2-(quinolin-2-yl)oxazoles via rhodium-catalyzed formal[3+2]cyclization of 4-aryl-1-tosyl-1H-1,2,3-triazoles with quinoline-2-carbaldehydes has been described.The protocol employs mild conditions and offers good yields of diverse 2,5-aryloxazole derivatives with a broad reaction scope.It is amenable to gram-scale synthesis and easily transformation.Moreover,this 5-aryl-2-(quinolin-2-yl)oxazole skeleton is indeed a new fluorophore and its applications in metal ions probes are also investigated and showed fluorescent responses to mercury ion.展开更多
基金National Natural Science Foundation of China,No.39770300,30070873the Overseas Chinese Affairs Office of the State Council Foundation,No.98-33
文摘AIM: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process. METHODS: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Lucigenin assay showed the generation of ROS in cells under incubation with JTE-522. The increased ROS generation might contribute to the induction of AGS cells to apoptosis. EMSA and Western blot revealed that NF-kB activity was almost completely inhibited by preventing the degradation of IkBalpha. Additionally, by using Western blot we confirmed that the level of bcl-2 was decreased, whereas p53 showed a great increase following JTE-522 treatment. Their changes were in a dose-dependent manner. CONCLUSION: These findings suggest that reactive oxygen species, NF-kB, p53, bcl-2 and caspase-3 may play an important role in the induction of apoptosis in AGS cells after treatment with JTE-522.
基金National Natural Science Foundation of China,No.39770300,30070873the Overseas Chinese Affairs Office of the State Council Foundation,No.98-33
文摘AIM: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (Deltapsim). METHODS: Cell culture, cell counting, ELISA assay, TUNEL, flow cytometry, Western blot and fluorometric assay were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanism. RESULTS: JTE-522 inhibited the growth of AGS cells and induced the apoptosis. Caspases 8 and 9 were activated during apoptosis as judged by the appearance of cleavage products from procaspase and the caspase activities to cleave specific fluorogenic substrates. To elucidate whether the activation of caspases 8 and 9 was required for the apoptosis induction, we examined the effect of caspase-specific inhibitors on apoptosis. The results showed that caspase inhibitors significantly inhibited the apoptosis induced by JTE-522. In addition, the membrane translocation of Bax and cytosolic release of cytochrome C accompanying with the decrease of the uptake of Rhodamin 123, were detected at an early stage of apoptosis. Furthermore, Bax translocation, cytochrome C release, and caspase 9 activation were blocked by Z-VAD.fmk and Z-IETD-CHO. CONCLUSION: The present data indicate a crucial association between activation of caspases 8, 9, cytochrome C release, membrane translocation of Bax, loss of Deltapsim and JTE-522-induced apoptosis in AGS cells.
文摘Disubstituted oxazoles were prepared conveniently by treatment of aromatic -methyl ketones and nitriles with poly[styrene(iodosodiacetate)] in one-pot process.
文摘The mechanism of nitrocompounds quenching of the fluorescence of 5, 5′ dipheny1 2, 2′ bisoxazole (POOP) and trans 1, 2 bis [2 (5 phenyloxazolyl)] ethene (POEOP) has been studied. It was found that the fluorescence of oxazoles was quenched mainly by the absorption competition and radiationless energy transfer of nitrocompounds. The fluorescence quenching rate constants of nitrobenzene and nitromethane are 3.0×10 10 L·mol -1 ·s -1 and 1.5×10 8 L·mol -1 ·s -1 respectively for POEOP. This remarkable difference was explicated.
基金the National Natural Sci-ence Foundation of China(No.21772001)the Anhui Provincial Natural Science Foundation(No.1808085MB41)the Cultiva-tion Project for University Outstanding Talents of Anhui Province(2019).
文摘Main observation and conclusion A facile and efficient strategy for the synthesis of 5-aryl-2-(quinolin-2-yl)oxazoles via rhodium-catalyzed formal[3+2]cyclization of 4-aryl-1-tosyl-1H-1,2,3-triazoles with quinoline-2-carbaldehydes has been described.The protocol employs mild conditions and offers good yields of diverse 2,5-aryloxazole derivatives with a broad reaction scope.It is amenable to gram-scale synthesis and easily transformation.Moreover,this 5-aryl-2-(quinolin-2-yl)oxazole skeleton is indeed a new fluorophore and its applications in metal ions probes are also investigated and showed fluorescent responses to mercury ion.
