Biomedical subjects

X W Zhang

Publications and source records attributed to X W Zhang.

At least 19 recordsLinked to original sources

PubMed2005

Effects of music on target-controlled infusion of propofol requirements during combined spinal-epidural anaesthesia.

The sedative effects of music were evaluated using the bispectral index (BIS) during target-controlled infusion (TCI) propofol. A total of 110 women undergoing hysterectomy were randomly allocated to receive either music or no music. Propofol was administered using target-controlled infusion and the concentration adjusted gradually to achieve an observer's assessment of alertness/sedation (OAA/S) score of 3 intra-operatively. The haemodynamic and bispectral index values during the sedation phase were recorded. Interleukin-6 was evaluated before, immediately after and 1 h following intervention. The music group had a significant reduction in mean (SD) induction time of sedation: 12 (12) min vs. 18 (12) min, p < 0.01; propofol target concentration: 1.6 (0.3) microg.ml(-1) vs. 2.4 (0.4) microg.ml(-1), p < 0.0001; intra-operative amount of propofol: 171 (98) mg vs. 251 (92) mg, p < 0.0001; and significantly higher levels of satisfaction with their peri-operative care: 9.6 (0.6) compared to the control group: 8.1 (1.0), p < 0.0001. No other differences were found. The results show the influence of music on the induction time of sedation, concentration and level of propofol during surgery, and suggest sedative benefits of music.

Adult↗

PubMed2005

New genotype of avian influenza H5N1 viruses isolated from tree sparrows in China.

The 2004 outbreaks of highly pathogenic avian influenza H5N1 disease in China led to a great poultry loss and society attention. A survey of avian influenza viruses was conducted on tree sparrows (Passer montanus) collected in China in 2004. Four viruses were isolated from free-living tree sparrows. The results of the whole-genome analysis indicated that an H5N1 virus with a new genotype is circulating among tree sparrows. The hemagglutinin and neuraminidase genes of the new genotype were derived from Gs/Gd/96-like viruses and the nuclear protein gene descended from the 2001 genotype A H5N1 viruses, while the other inner genes originated from an unknown influenza virus. In experimental infection, all four viruses were highly pathogenic to chickens but not pathogenic to ducks or mice. The four tree sparrow viruses were different from the 2003 tree sparrow strain (genotype Z) in Hong Kong. The results suggested that H5N1 viruses might be distributed widely in tree sparrows.

Animals↗

PubMed2004

Testing the hypothesis of a recombinant origin of the SARS-associated coronavirus.

The origin of severe acute respiratory syndrome-associated corona-virus (SARS-CoV) is still a matter of speculation, although more than one year has passed since the onset of the SARS outbreak. In this study, we implemented a 3-step strategy to test the intriguing hypothesis that SARS-CoV might have been derived from a recombinant virus. First, we blasted the whole SARS-CoV genome against a virus database to search viruses of interest. Second, we employed 7 recombination detection techniques well documented in successfully detecting recombination events to explore the presence of recombination in SARS-CoV genome. Finally, we conducted phylogenetic analyses to further explore whether recombination has indeed occurred in the course of coronaviruses history predating the emergence of SARS-CoV. Surprisingly, we found that 7 putative recombination regions, located in Replicase 1ab and Spike protein, exist between SARS-CoV and other 6 coronaviruses: porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV), bovine coronavirus (BCoV), human coronavirus 229E (HCoV), murine hepatitis virus (MHV), and avian infectious bronchitis virus (IBV). Thus, our analyses substantiate the presence of recombination events in history that led to the SARS-CoV genome. Like the other coronaviruses used in the analysis, SARS-CoV is also a mosaic structure.

Computational Biology↗

PubMed2003

Roquinimex inhibits dextran sodium sulfate-induced murine colitis.

OBJECTIVE: Roquinimex is a modulator of the immune system and has been shown to attenuate induction of several inflammatory and autoimmune diseases. The objective of the present study was to determine the efficacy of roquinimex in a model of murine colitis. MATERIALS AND METHODS: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for five to six days. Roquinimex (300 mg kg(-1) day(-1)) was administered by subcutaneous (s.c.) injection 3 days prior to and throughout the treatment period with DSS. In separate experiments, 300 mg kg(-1) day(-1) of roquinimex was given therapeutically after initiation of DSS challenge. RESULTS: DSS provoked clinical signs of colitis, reduced crypt height (CH) and increased mucosal damage score (MDS) as analyzed by histology. In addition, challenge with DSS increased the colonic content of myeloperoxidase (MPO). Prophylactic administration of DSS-treated mice with roquinimex significantly reduced clinical signs of colitis, MDS and the CH-reduction. Moreover, in roquinimex treated animals, the MPO activity was significantly reduced by more than 50% compared to DSS control mice. Notably, therapeutic administration of roquinimex in DSS-treated mice also significantly inhibited the MDS, CH-reduction and MPO activity. CONCLUSIONS: These findings suggest that roquinimex strongly inhibits murine colitis and may provide a novel pharmacological approach to treat inflammatory bowel disease.

Adjuvants, Immunologic↗

PubMed2003

Epitaxy of cubic boron nitride on (001)-oriented diamond.

Cubic boron nitride (c-BN), although offering a number of highly attractive properties comparable to diamond, like hardness, chemical inertness and a large electronic bandgap, up to now has not found the attention it deserves. This mostly has to do with preparational problems, with easy chemical routes not available and, instead, the necessity to apply ion-bombardment-assisted methods. Hence, most of the c-BN samples prepared as thin films have been nanocrystalline, making the prospect of using this material for high-temperature electronic applications an illusion. Although heteroepitaxial nucleation of c-BN on diamond substrates has been demonstrated using the high-pressure-high-temperature technique, none of the low-pressure methods ever succeeded in the epitaxial growth of c-BN on any substrate. Here, we demonstrate that heteroepitaxial c-BN films can be prepared at 900 degrees C on highly (001)-oriented diamond films, formed by chemical vapour deposition, using ion-beam-assisted deposition as a low-pressure technique. The orientation relationship was found to be c-BN(001)[100]||diamond(001)[100]. High-resolution transmission electron microscopy additionally proved that epitaxy can be achieved without an intermediate hexagonal BN layer that is commonly observed on various substrates.

Journal Article↗

PubMed2002

Acoustic characteristics of twin jets.

Experiments were conducted to investigate the acoustic characteristics of underexpanded supersonic twin jets in different azimuthal measurement planes. Compared with two independent jets, the twin jets produced additional noise due to the enhanced mixing and entrainment. The larger pressure ratio for switching from the axisymmetric mode to the helical mode led to lower noise levels at 90 degrees than for two independent jets. For pressure ratios greater than 5.00, the noise reduction was due to cessation of screeching of the twin jets while screeching of a single jet was still detected. The apparent shielding phenomenon was measured for the screech helical mode. The screech tone intensities were attenuated largely due to the shielding effects. The noise reductions due to shielding were obtained over a wide range of pressure ratios relative to the sum of two independent jets.

Acoustics↗

PubMed2001

Redundant function of macrophage inflammatory protein-2 and KC in tumor necrosis factor-alpha-induced extravasation of neutrophils in vivo.

Tumor necrosis factor-alpha (TNF-alpha) stimulates the expression CXC chemokines, i.e. macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC), and neutrophil extravasation. However, the individual role of MIP-2 and KC in the recruitment process of neutrophils in vivo remains elusive. By use of intravital microscopy in the mouse cremaster muscle, we analyzed the effect of specific inhibition of CXC chemokines, alone and together, on TNF-alpha-induced leukocyte rolling, firm adhesion and recruitment. After stimulation with TNF-alpha, the mRNA levels of both MIP-2 and KC were increased. Notably, separate administration of antibodies directed against MIP-2 and KC had no effect on TNF-alpha-induced neutrophil extravasation. In contrast, combined injection of anti-MIP-2 and anti-KC antibodies markedly inhibited extravascular migration of neutrophils. Moreover, MIP-2 and KC dose-dependently increased neutrophil recruitment, however, no synergistic effect of combined stimulation with MIP-2 and KC on the neutrophil response was found. Taken together, these data suggest that MIP-2 and KC are functionally redundant in TNF-alpha-induced neutrophil accumulation and that neutralization of both MIP-2 and KC may be necessary in order to reduce accumulation of neutrophils in cytokine-activated tissues.

Animals↗

PubMed2001

Low molecular weight heparin inhibits tumor necrosis factor alpha-induced leukocyte rolling.

OBJECTIVE: Heparins may exert several anti-inflammatory actions. This study investigated the impact of low molecular weight heparin (LMWH) on tumor necrosis factor (TNF)-alpha-provoked leukocyte rolling, adhesion and extravascular accumulation. MATERIALS AND METHODS: Leukocyte-endothelium interactions and tissue accumulation of leukocytes were induced by TNF-alpha in Balb/c mice and analyzed by the use of intravital microscopy in the mouse cremaster muscle microcirculation. RESULTS: We observed that administration of 5000 units/kg of LMWH, but not 50 and 500 units/kg, markedly reduced TNF-alpha-induced leukocyte rolling, adhesion and tissue infiltration. Notably, when LMWH was given after TNF-alpha only leukocyte rolling was reduced and no effect was observed on firm adhesion of leukocytes. CONCLUSIONS: Taken together, these findings indicate that LMWH inhibits TNF-alpha-induced leukocyte accumulation by inhibiting the rolling adhesive interaction which may help explain the anti-inflammatory effects of LMWH.

Animals↗

PubMed2001

Neurotransmitter action in osteoblasts: expression of a functional system for serotonin receptor activation and reuptake.

Neurotransmitter regulation of bone metabolism has been the subject of increasing interest and investigation. Because serotonin (5-HT) plays a role as a regulator of craniofacial morphogenesis, we investigated the expression and function of 5-HT receptors and the 5-HT transporter (5-HTT) in bone. Primary cultures of rat osteoblasts (rOB) and a variety of clonal osteoblastic cell lines, including ROS 17/2.8, UMR 106-H5, and Py1a, showed mRNA expression for 5-HTT as well as the 5-HT(1A), 5-HT(1D), 5-HT(2A), and 5-HT(2B) receptors by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Protein expression of the 5-HT(1A), 5-HT(2A), and 5-HT(2B) receptors was confirmed by immunoblot. 5-HTT binding sites were assessed in ROS 17/2.8 and UMR 106-H5 cells by binding of the stable cocaine analog [125I]RTI-55, which showed a relatively high density of nanomolar affinity binding sites. Imipramine and fluoxetine, antagonists with specificity for 5-HTT, showed the highest potency to antagonize [125I]RTI-55 binding in ROS and UMR cells. GBR-12935, a relatively selective dopamine transporter antagonist, had a much lower potency, as did desipramine, a selective norepinephrine transporter antagonist. The maximal [3H]5-HT uptake rate in ROS cells was 110 pmol/10 min per well, with a K(m) value of 1.13 micromol/L. Imipramine and fluoxetine inhibited specific [3H]5-HT uptake with IC(50) values in the nanomolar range. In normal differentiating rOB cultures, 5-HTT functional activity was observed initially at day 25, and activity increased almost eightfold by day 31. In mature rOB cultures, the estimated density of [125I]RTI-55 binding sites was 600 fmol/mg protein. Functional downregulation of transporter activity was assessed after PMA treatment, which caused a significant 40% reduction in the maximal uptake rate of [3H]5-HT, an effect that was prevented by pretreatment with staurosporine. The affinity of 5-HT for the transporter was significantly increased following PMA treatment. We assessed the functional significance of expression of the 5-HT receptors by investigating the interaction between 5-HT and parathyroid hormone (PTH) signaling. 5-HT potentiates the PTH-induced increase in AP-1 activity in UMR cells. These results demonstrate that osteoblastic cells express a functional serotonin system, with mechanisms for responding to and regulating uptake of 5-HT.

Animals↗

PubMed2001

CXC chemokines, MIP-2 and KC, induce P-selectin-dependent neutrophil rolling and extravascular migration in vivo.

The purpose of this study was to examine the impact of CXC chemokines, i.e. macrophage inflammatory protein-2 (MIP-2) and KC, on leukocyte-endothelium interactions in detail and to evaluate the role of P-selectin by use of intravital microscopy in the mouse cremaster muscle. Administration of MIP-2 and KC provoked a dose (5 - 500 ng)- and time (0 - 4 h)-dependent increase in leukocyte rolling, adhesion and tissue recruitment. Neutrophils comprised more than 92% of the leukocyte response. Pretreatment with an antibody directed against P-selectin (RB40.34) significantly inhibited MIP-2- and KC-induced leukocyte rolling by more than 96%. This marked decrease in rolling abolished firm adhesion and extravascular accumulation of neutrophils (>89% reduction), suggesting that CXC chemokines induce P-selectin-dependent rolling, which in turn apparently is a precondition for the subsequent stationary adhesion and extravasation of neutrophils. Moreover, the extravascular recruitment of leukocytes was evaluated in whole-mounts of the cremaster muscle without preceding intravital microscopy. Using this approach, it was again observed that MIP-2- and KC-induced neutrophil accumulation was completely dependent onP-selectin function. In contrast to the CXC chemokines, administration of the classical chemoattractant formyl-methionyl leucyl phenylalanine (fMLP) did not provoke extravascular tissue accumulation of neutrophils. We could not detect gene expression of CXCR2 in murine endothelial cells, whereas neutrophils were positive, indicating that the stimulatory effect of CXC chemokines on leukocyte-endothelium interactions is not a direct effect on the endothelium but rather an indirect effect via activation of an intermediary tissue cell. However, challenge with MIP-2 and KC did not increase the number of degranulated mast cells. In conclusion, our data demonstrate that CXC chemokines induce all steps in the extravasation process of leukocytes, including rolling, adhesion and transmigration in vivo. Moreover, these results show that P-selectin plays a critical role in MIP-2 and KC provoked neutrophil recruitment as a critical mediator of initial leukocyte rolling. Additionally, our study suggest that a restricted action of MIP-2 and KC on neutrophils is far too simplistic to explain the complex mechanisms of action of CXC chemokines on neutrophil infiltration in vivo.

Animals↗

PubMed2001

Cell cycle distribution of primitive haematopoietic cells stimulated in vitro and in vivo.

A novel approach is used to study the proliferating behaviour of primitive haematopoietic cell populations in response to different stimuli. A mathematical model based on the average proportion of apoptotic, dividing and quiescent cells in primitive haematopoietic cell populations is developed to describe the mitotic history of 5- (and 6-) carboxyfluorescein diacetate succinimidyl ester-labelled cells. The cell cycle distributions in different cytokine-supplemented cultures of primitive human and mouse bone marrow cells are determined and compared with those found in vivo. The results indicate that a combination of flt-3 ligand, Steel factor and interleukin-11 or hyper-interleukin-6 provide a level of mitogenic stimulation similar to that existing in vivo after a myeloablative radiation dose. The comparison of the cell cycle distribution obtained for different cultures of human bone marrow CD34(+)(45RA/71)(-) cells demonstrates that the addition of flt-3 ligand in these cultures decreases apoptosis significantly but does not reduce quiescence. In addition, in vivo and in vitro, it was found that more than 3 days of stimulation are required to recruit a maximum number of quiescent cells into active cell cycle. These kinetics of cell cycle activation are found to be similar to those identified for the haematopoietic stem cells compartment in the same cultures. This mathematical analysis provides a useful tool for the development of haematopoietic stem cell culture processes for clinical applications.

Animals↗

PubMed2001

Inhibition of selectin function and leukocyte rolling protects against dextran sodium sulfate-induced murine colitis.

BACKGROUND: The selectin family of adhesion molecules (P-, E- and L-selectin) plays an important role in inflammatory reactions by mediating interactions between leukocytes and activated endothelial cells. However, a recent study using gene-targeted mice has suggested that adhesion molecules (P- and E-selectin and ICAM-1) may not be relevant targets in intestinal inflammation. The objective of the present study was to re-evaluate the potential role of selectins in experimental colitis in wild-type mice using the polysaccharide fucoidan, which inhibits the function of P- and L-selectin. METHODS: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for 5 days with and without daily administration of fucoidan (25 mg/kg, i.v.). In separate experiments, the effect of fucoidan on leukocyte-endothelium interactions was examined by use of intravital microscopy. RESULTS: It was found that pretreatment with fucoidan (25 mg/kg/day) reduced mucosal damage and crypt destruction in the colon of DSS-treated mice. Moreover, this fucoidan treatment markedly reduced the colonic MPO activity in mice exposed to DSS. In vivo microscopy revealed that the dose of fucoidan used in the present study abolished TNF-alpha-induced venular leukocyte rolling and extravascular recruitment. CONCLUSIONS: These results suggest that selectins mediate leukocyte infiltration and tissue damage in experimental colitis. Moreover, our data support the concept that functional interference with adhesion molecules of the selectin family may have a beneficial effect in the treatment of inflammatory bowel disease.

Animals↗

PubMed2001

[Repairing deformity of the head and face with tissue flap pedicled with the superficial temporal artery in children].

OBJECTIVE: To evaluate the effect of tissue flap pedicled with the superficial temporal artery in repairing deformity of the head and face in children. METHODS: From October 1986 to December 1996, 13 children with deformity of the head and face were repaired by this tissue flap. Among them, there were congenital deformity in 9 cases, burned scar in 3 cases and infection scar in 1 case. Among the flaps, 1 was temporal skin flap, 3 were temporal flap with hairbearing scalp, 1 was frontal skin flap, and 8 were posterio-uricular superficial fascia flap and skin flap. The area of tissue flap was ranged from 5.0 cm x 1.2 cm to 10.0 cm x 5.0 cm. The length of the pedicle was 5-8 cm. RESULTS: All tissue flaps healed with first intention. Followed up for 6 months to 12 years, the appearance and function of tissue flaps were satisfactory. CONCLUSION: The tissue flap pedicled with the superficial temporal artery is suitable to repair many kinds of deformities of the head and face in children. It has the advantages of good blood supply, closely acceptor area, easy operation and satisfactory appearance.

Adolescent↗

PubMed2000

Inhibitory actions of ropivacaine on tumor necrosis factor-alpha-induced leukocyte adhesion and tissue accumulation in vivo.

We have examined the effect of ropivacaine, a local anesthetic, on leukocyte-endothelium interactions induced by tumor necrosis factor-alpha (TNF-alpha) in vivo by the use of intravital microscopy in the mouse cremaster microcirculation. It was found that ropivacaine markedly reduced venular leukocyte adhesion and tissue recruitment in response to TNF-alpha challenge, whereas leukocyte rolling was unchanged. Thus, treatment with ropivacaine may be a useful pharmacological tool to control acute inflammation.

Amides↗

PubMed2000

Dexamethasone inhibits arteriolar leukocyte rolling and adhesion induced by tumor necrosis factor-alpha in vivo.

OBJECTIVE: Glucocorticoids are widely used in vasculitis syndromes, however, the protective mechanisms remain to be elucidated. In this study, we wanted to examine the effect of dexamethasone on leukocyte rolling and adhesion in arterioles in vivo. MATERIALS AND METHODS: NMRI mice were treated intrascrotally with tumor necrosis factor-alpha (TNF-alpha) for 3-4 h: Intravital microscopy was used to study leukocyte-endothelium interactions in arterioles in the cremaster muscle. RESULTS: It was found that TNF-alpha markedly increased the number of rolling and adherent leukocytes in the arterioles. Pretreatment (2 h) with dexamethasone significantly reduced TNF-alpha-induced leukocyte rolling and adhesion. In fact, 1 mg/kg of dexamethasone decreased leukocyte rolling and adhesion by 76% and 87%, respectively. CONCLUSIONS: These findings suggest that the beneficial effect of dexamethasone in vasculitis disorders may in part be attributable to an inhibitory impact on cytokine-induced leukocyte rolling and adhesion in arterioles.

Animals↗

PubMed2000

Important role of CD18 in TNF-alpha-induced leukocyte adhesion in muscle and skin venules in vivo.

OBJECTIVE: To examine the role of CD 18 in tumor necrosis factor-alpha (TNF-alpha)-induced leukocyte adhesion and extravasation in vivo. MATERIAL: Male wild-type (WT) and mutated mice with hypomorphic expression of CD 18. METHODS: Intravital microscopy was used to quantitate leukocyte-endothelium interactions provoked by TNF-alpha (0.5 microg) in the cremaster muscle and dorsal skin microcirculation. Tissue recruitment of leukocytes was evaluated in wholemounts of the cremaster muscle and in air pouches in the dorsal skin after TNF-alpha stimulation. RESULTS: TNF-alpha markedly increased venular leukocyte adhesion and recruitment in the cremaster muscle and skin in WT. Notably, in CD 18-targeted animals, leukocyte adhesion triggered by TNF-alpha challenge was significantly reduced by 58% and 72% in venules of the cremaster muscle and skin, respectively. Moreover, in CD18-mutants, tissue accumulation of polymorphonuclear leukocytes (PMNLs) provoked by TNF-alpha in the muscle and skin was decreased by 84% and 70%, respectively. Interestingly, the observed level of reduction in TNF-alpha-induced neutrophil adhesion and recruitment in CD18 gene-targeted animals corresponded well with the decrease in CD 18 expression on neutrophils from these mice, i.e. the surface density of CD18 was reduced by 77% in mutants compared to WT. Differential analysis revealed that the extravascular leukocytes comprised more than 90% PMNLs, indicating that neutrophils were the main inflammatory cell responding to TNF-alpha activation. Notably, the expression of CD18 increased by more than two-fold on extravasated neutrophils compared to circulating neutrophils in the peripheral blood both in WT and mutant animals. CONCLUSIONS: These findings suggest that CD18 is a dominant mediator of firm neutrophil adhesion to venular endothelial cells in the muscle and skin stimulated by TNF-alpha in vivo. In addition, this decreased adhesion in CD18-mutants attenuates leukocyte extravasation in response to TNF-alpha activation. Thus, inhibition of CD 18-function may provide an important strategy to inhibit leukocyte recruitment in cytokine-dependent diseases.

Animals↗

PubMed2000

Critical role of P-selectin-dependent rolling in tumor necrosis factor-alpha-induced leukocyte adhesion and extravascular recruitment in vivo.

Leukocyte-endothelium interactions are dependent on a coordinated expression and function of specific adhesion molecules. The objective of the present study was to examine the role of selectin function and leukocyte rolling in tumor necrosis factor-alpha (TNF-alpha)-induced leukocyte adhesion and extravasation in venules in vivo. For this purpose, we used intravital microscopy in the mouse cremaster muscle stimulated for 2-3 h with TNF-alpha intrascrotally. Pretreatment with fucoidan, which inhibits P- and L-selectin, and a P-selectin monoclonal antibody (RB40.34) abolished TNF-alpha-stimulated leukocyte rolling. This great reduction in rolling caused a marked attenuation of firm adhesion and extravascular accumulation of leukocytes. When fucoidan and RB40.34 were administrated after stimulation with TNF-alpha, it was found that leukocyte rolling was greatly reduced whereas the number of firmly adherent leukocytes was completely unchanged, suggesting that the inhibitory effect of blocking P-selectin function on firm leukocyte adhesion and recruitment was due to the reduction in leukocyte rolling along the endothelium. Moreover, pretreatment with a monoclonal antibody against intercellular adhesion molecule-1 (ICAM-1) and a platelet-activating factor (PAF)-receptor antagonist had no effect of TNF-alpha-induced leukocyte rolling and adhesion, indicating that molecules other than ICAM-1 and PAF mediate firm adhesion and recruitment of leukocytes in TNF-alpha-activated tissues. Taken together, our data demonstrate that P-selectin function plays an important role in TNF-alpha-induced inflammatory cell recruitment by mediating leukocyte rolling as a precondition for cytokine-provoked firm adhesion and transmigration in vivo. These findings, thus, suggest that inhibition of P-selectin may be a central target for pharmacological intervention in inflammatory diseases.

Adhesiveness↗

PubMed2000

Differential regulation of P53, c-Myc, Bcl-2, Bax and AFP protein expression, and caspase activity during 10-hydroxycamptothecin-induced apoptosis in Hep G2 cells.

10-Hydroxycamptothecin (HCPT), a DNA topoisomerase I (Topo I) inhibitor, exhibited a remarkable apoptosis-inducing effect on human hepatoma Hep G2 cells. We studied the effect of HCPT upon the expression of P53, c-Myc, Bcl-2, Bax and alpha-fetoprotein (AFP) proteins, and caspase (caspase-1 and caspase-3) activity of Hep G2 cells. It showed that HCPT at a dose of 0.1 microg/ml increased the expression of P53, c-Myc and Bax protein, and decreased the expression of Bcl-2 and AFP. The increase of P53, which was remarkable after only 3 h incubation with HCPT, occurred much earlier than the changes of other proteins, suggesting that the increase of P53 expression may be the upstream event in the apoptosis of Hep G2 cells induced by HCPT. Both caspase-1 and caspase-3 were activated in Hep G2 cells by HCPT treatment, suggesting that caspase-1 and caspase-3 are involved in the process of apoptosis in Hep G2 cells, and may be the main effectors of the apoptosis.

Antineoplastic Agents, Phytogenic↗