Biomedical subjects

Hong-Liang Li

Publications and source records attributed to Hong-Liang Li.

5 recordsLinked to original sources

PubMed2002

Sonochemical preparation of GaSb nanoparticles.

A room temperature sonochemical method for the preparation of GaSb nanoparticles using less hazardous Ga and antimony chloride (SbCl(3)) as the precursors has been described. The formation of GaSb has been confirmed by means of XRD, EDAX, and XPS characterization. TEM and SAED results show that the as-prepared solid consists of nanosized GaSb crystals with sizes in the range 20-30 nm. The photoacoustic spectrum result reveals that the GaSb nanoparticles have a direct band gap of about 1.21 eV. On the basis of the control experiments and the extreme conditions produced by ultrasound, an ultrasound-assisted in-situ reduction/combination mechanism has been proposed to explain the reaction.

Journal Article↗

PubMed2002

JTE-522-induced apoptosis in human gastric adenocarcinoma [correction of adenocarcinoma] cell line AGS cells by caspase activation accompanying cytochrome C release, membrane translocation of Bax and loss of mitochondrial membrane potential.

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.

Adenocarcinoma↗

PubMed2002

Changes of NF-kB, p53, Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells: role of reactive oxygen species.

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.

Adenocarcinoma↗

PubMed2002

JTE-522, a selective COX-2 inhibitor, inhibits cell proliferation and induces apoptosis in RL95-2 cells.

AIM: To investigate whether JTE-522 [4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide], a selective COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human endometrial cancer cell line RL95-2 cells and to explore the molecular mechanisms. METHODS: [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), DNA ladder, enzyme-linked immunosorbent assay (ELISA), flow cytometry, RT-PCR, and Western blot analysis were employed to investigate effect of JTE-522 on human endometrial cancer cell line RL95-2 cells and the related molecular mechanisms. RESULTS: JTE-522 inhibited the growth of RL95-2 cells and induced the apoptosis. Furthermore, it arrested G0/G1 phase and inhibited S phase in RL95-2 cells. JTE-522 inhibited the expressions of COX-2 mRNA, phosphorylated Rb, and CDK4 proteins, while increased the levels of p53, p21, cyclin D1 proteins, and the activity of caspase-3 in RL95-2 cells. CONCLUSION: JTE-522 inhibits cell proliferation and induces apoptosis in RL95-2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA, phosphorylated Rb, and CDK4 proteins, and up-regulation of the expressions of p53, p21, and cyclin D1 proteins.

Apoptosis↗

PubMedDate not supplied

Predictive functional control (PFC) and its application in chlorinated polyethylene process.

The main principle and the characteristic of Predictive Functional Control (PFC) strategy are presented in this paper and the corresponding control system aid design software APC-PFC is also introduced. For a chlorinated polyethylene (CPE) process, a design scheme of cascade predictive functional control system is described and the control performance is improved obviously.

Algorithms↗