Biomedical subjects

C Tang

Publications and source records attributed to C Tang.

At least 73 records · Page 4Linked to original sources

PubMed2000

SU6668 is a potent antiangiogenic and antitumor agent that induces regression of established tumors.

Vascular endothelial growth factor, fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF) and their cognate receptor tyrosine kinases are strongly implicated in angiogenesis associated with solid tumors. Using rational drug design coupled with traditional screening technologies, we have discovered SU6668, a novel inhibitor of these receptors. Biochemical kinetic studies using isolated Flk-1, FGF receptor 1, and PDGF receptor beta kinases revealed that SU6668 has competitive inhibitory properties with respect to ATP. Cocrystallographic studies of SU6668 in the catalytic domain of FGF receptor 1 substantiated the adenine mimetic properties of its oxindole core. Molecular modeling of SU6668 in the ATP binding pockets of the FIk-1/KDR and PDGF receptor kinases provided insight to explain the relative potency and selectivity of SU6668 for these receptors. In cellular systems, SU6668 inhibited receptor tyrosine phosphorylation and mitogenesis after stimulation of cells by appropriate ligands. Oral or i.p. administration of SU6668 in athymic mice resulted in significant growth inhibition of a diverse panel of human tumor xenografts of glioma, melanoma, lung, colon, ovarian, and epidermoid origin. Furthermore, intravital multifluorescence videomicroscopy of C6 glioma xenografts in the dorsal skinfold chamber model revealed that SU6668 treatment suppressed tumor angiogenesis. Finally, SU6668 treatment induced striking regression of large established human tumor xenografts. Investigations of SU6668 activity in cancer patients are ongoing in Phase I clinical trials.

3T3 Cells↗

PubMed2000

Binding of retinol induces changes in rat cellular retinol-binding protein II conformation and backbone dynamics.

The structure and backbone dynamics of rat holo cellular retinol-binding protein II (holo-CRBP II) in solution has been determined by multidimensional NMR. The final structure ensemble was based on 3980 distance and 30 dihedral angle restraints, and was calculated using metric matrix distance geometry with pairwise Gaussian metrization followed by simulated annealing. The average RMS deviation of the backbone atoms for the final 25 structures relative to their mean coordinates is 0.85(+/-0.09) A. Comparison of the solution structure of holo-CRBP II with apo-CRBP II indicates that the protein undergoes conformational changes not previously observed in crystalline CRBP II, affecting residues 28-35 of the helix-turn-helix, residues 37-38 of the subsequent linker, as well as the beta-hairpin C-D, E-F and G-H loops. The bound retinol is completely buried inside the binding cavity and oriented as in the crystal structure. The order parameters derived from the (15)N T(1), T(2) and steady-state NOE parameters show that the backbone dynamics of holo-CRBP II is restricted throughout the polypeptide. The T(2) derived apparent backbone exchange rate and amide (1)H exchange rate both indicate that the microsecond to second timescale conformational exchange occurring in the portal region of the apo form has been suppressed in the holo form.

Amides↗

PubMed2000

Identification of substituted 3-[(4,5,6, 7-tetrahydro-1H-indol-2-yl)methylene]-1,3-dihydroindol-2-ones as growth factor receptor inhibitors for VEGF-R2 (Flk-1/KDR), FGF-R1, and PDGF-Rbeta tyrosine kinases.

A series of new 3-substituted indolin-2-ones containing a tetrahydroindole moiety was developed as specific inhibitors of receptor tyrosine kinases associated with VEGF-R, FGF-R, and PDGF-R growth factor receptors. These compounds were evaluated for their inhibitory properties toward VEGF-R2 (Flk-1/KDR), FGF-R1, PDGF-Rbeta, p60(c)()(-)()(Src)(), and EGF-R tyrosine kinases and their ability to inhibit growth factor-dependent cell proliferation. Structure-activity relationships of this new pharmacophore have been determined at the level of kinase inhibition. Compounds containing a propionic acid moiety at the C-3' position of the tetrahydroindole ring represented the most potent indolin-2-ones to inactivate the VEGF, FGF, and PDGF receptor kinases. The inhibitory activities of 9d against VEGF-R2 (Flk-1), 9h against FGF-R1, and 9b against PDGF-Rbeta were 4, 80, and 4 nM, respectively. However, all of these compounds were inactive when tested against the EGF-R tyrosine kinase. Compounds 9a and 9b represented the most potent inhibitors of these classes to inhibit both biochemical kinase and growth factor-dependent cell proliferation for these three targets. In addition, compound 9a was cocrystallized with the catalytic domain of FGF-R1 providing evidence to explain the structure-activity relationship results. This study has provided evidence to support the potential of these new tyrosine kinase inhibitors for the treatment of angiogenesis and other growth factor-related diseases including human cancers.

Animals↗

PubMed2000

Simultaneous determination of urinary free cortisol and 6beta-hydroxycortisol by liquid chromatography-atmospheric pressure chemical ionization tandem mass spectrometry and its application for estimating hepatic CYP3A induction.

A reversed-phase high-performance liquid chromatography coupled to atmospheric pressure chemical ionization tandem mass spectrometry (HPLC-APCI-MS-MS) assay was developed to simultaneously determine monkey urinary free cortisol (C) and 6beta-hydroxycortisol (6beta-OHC) in 8 min. Urine sample (0.5 ml) containing fludrocortisone acetate (F-C) as the internal standard was extracted with ethyl acetate for 5 min with an extraction efficiency of 90% and 75% for C and 6beta-OHC, respectively. A Perkin-Elmer Sciex API 3000 triple quadruple instrument was used for mass spectrometric detection and the column eluent was directed to a heated nebulizer probe. The assay was linear over the range 0.25-10 microM for each analyte. The intra- and inter-day relative standard deviation (RSD) over the entire concentration range for both analytes was less than 10%. Accuracy determined at three concentrations (0.8, 2.0 and 8.0 microM) ranged between 95.5 and 108%. The method described herein is suitable for the rapid and efficient measurement of 6beta-OHC/C ratio in Rhesus monkey urine following administration of known hepatic CYP3A inducers and can be used to estimate potential CYP3A induction by drug candidates in the process of early drug development.

Animals↗

PubMed2000

[Effect of smoking on the guanylin in the injured lung of rats].

In order to survey the influence of smoking on the level of guanylin in lung tissue in rats, a method of passive smoking was used to set up chronic bronchitis model in rats. The content of guanylin was measured by radioimmunoassay. In the smoking group, remarkable pathological changes in the lung tissue were found. There was no significant difference in the contents of guanylin in the plasma of experimental rats, compared with the control(P < 0.05). But in the lung tissue, the difference was significant(P < 0.01).

Animals↗

PubMed2000

Challenge of investigating biologically relevant functions of virulence factors in bacterial pathogens.

Recent innovations have increased enormously the opportunities for investigating the molecular basis of bacterial pathogenicity, including the availability of whole-genome sequences, techniques for identifying key virulence genes, and the use of microarrays and proteomics. These methods should provide powerful tools for analysing the patterns of gene expression and function required for investigating host-microbe interactions in vivo. But, the challenge is exacting. Pathogenicity is a complex phenotype and the reductionist approach does not adequately address the eclectic and variable outcomes of host-microbe interactions, including evolutionary dynamics and ecological factors. There are difficulties in distinguishing bacterial 'virulence' factors from the many determinants that are permissive for pathogenicity, for example those promoting general fitness. A further practical problem for some of the major bacterial pathogens is that there are no satisfactory animal models or experimental assays that adequately reflect the infection under investigation. In this review, we give a personal perspective on the challenge of characterizing how bacterial pathogens behave in vivo and discuss some of the methods that might be most relevant for understanding the molecular basis of the diseases for which they are responsible. Despite the powerful genomic, molecular, cellular and structural technologies available to us, we are still struggling to come to grips with the question of 'What is a pathogen?'

Animals↗

PubMed2000

Biphasic redistribution of muscarinic receptor and the altered receptor phosphorylation and gene transcription are underlying mechanisms in the rat heart during sepsis.

OBJECTIVE: The purpose of this study was to investigate intracellular redistribution of muscarinic cholinergic receptor (m2AChR) and the roles of receptor phosphorylation and gene transcription as underlying mechanisms in the rat heart during different phases of sepsis. METHODS: Sepsis was induced by cecal ligation and puncture (CLP). The density of m2AChR in the sarcolemmal and light vesicle fractions was studied using [3H]-quinuclidinyl benzilate ([3H]-QNB). Phosphorylation of m2AChR was studied by labeling of the myocardial ATP pool by perfusing isolated hearts with [32P]H3PO4 followed by identification of the phosphorylated m2AChR with SDS-PAGE. The steady-state level of m2AChR mRNA was determined by RT-PCR and Southern blot analysis. RESULTS: Septic rat hearts exhibit an initial hypercardiodynamic (9 h after CLP, early sepsis) and a subsequent hypocardiodynamic (18 h after CLP, late sepsis) state. During early sepsis, the Bmax for [3H]-QNB binding was increased in sarcolemma (+69%) but decreased in light vesicles (-22%), whereas during late sepsis, the Bmax was decreased in sarcolemma (-20%) but increased in light vesicles (+32%). The sum of Bmax for sarcolemmal and light vesicle fractions was increased during early sepsis (+43%) but decreased during late sepsis (-14%). The phosphorylation of m2AChR was decreased during early sepsis (-73%) but increased during late sepsis (+36% to +90%). The m2AChR mRNA abundance was increased during early sepsis (+52%) but decreased during late sepsis (-28%). CONCLUSIONS: The m2AChR in the rat heart was externalized from light vesicles to sarcolemma (overexpression) during early sepsis but internalized from surface membranes to intracellular sites (underexpression) during late sepsis. Furthermore, changes in the receptor phosphorylation and gene transcription are responsible for the biphasic redistribution and the altered expression of m2AChR in the rat heart during the progression of sepsis.

Analysis of Variance↗

PubMed2000

Pacing in right ventricular dysplasia after disconnection surgery.

This report describes a 33-year-old patient with arrhythmogenic right ventricular (RV) dysplasia who had a dual chamber pacemaker implanted at age 23 years for drug-induced bradycardia. Pacing was continued after right ventricular free-wall disconnection (RVFWD) at age 24 years. Her pacemaker was not replaced after battery depletion 7 years later. She presented the following year in severe right-sided heart failure. Her old pacemaker generator was replaced. This was followed by rapid resolution of her clinical failure and return to a full, active, physical lifestyle. This observation suggests the potential benefit of dual chamber pacing in patients with RV dysplasia after RVFWD.

Adult↗

PubMed2000

Heregulin regulates the actin cytoskeleton and promotes invasive properties in breast cancer cell lines.

The metastatic process requires changes in tumor cell adhesion properties, cell motility and remodeling of the extracellular matrix. The erbB2 proto-oncogene is overexpressed in approximately 30% of breast cancers and is a major prognostic parameter when present in invasive disease. A ligand for the erbB2 receptor has not yet been identified but it can be activated by heterodimerization with heregulin (HRG)-stimulated erbB3 and erbB4 receptors. The HRGs are a family of polypeptide growth factors that have been shown to play a role in embryogenesis, tumor formation, growth and differentiation of breast cancer cells. The erbB3 and erbB4 receptors are involved in transregulation of erbB2 signaling. The work presented here suggests biological roles for HRG including regulation of the actin cytoskeleton and induction of motility and invasion in breast cancer cells. HRG-expressing breast cancer cell lines are characterized by low erbB receptor levels and a high invasive and metastatic index, while those which overexpress erbB2 demonstrate minimal invasive potential in vitro and are non-tumorigenic in vivo. Treatment of the highly tumorigenic and metastatic HRG-expressing breast cancer cell line MDA-MB-231 with an HRG-neutralizing antibody significantly inhibited proliferation in culture and motility in the Boyden chamber assay. Addition of exogenous HRG to non-invasive erbB2 overexpressing cells (SKBr-3) at low concentrations induced formation of pseudopodia, enhanced phagocytic activity and increased chemomigration and invasion in the Boyden chamber assay. The specificity of the chemomigration response to HRG is demonstrated by inhibition with the anti-HRG neutralizing antibody. These results suggest that either HRG can act as an autocrine or paracrine ligand to promote the invasive behavior of breast cancer cells in vitro or thus may enhance the metastatic process in vivo.

Actins↗

PubMed2000

Association between delayed cardioprotection of aged rat myocytes and activation of mitogen-activated protein kinase.

OBJECTIVE: To study the cardioprotective effects of hypoxic preconditioning (HPC) on aged rat ventricular myocytes and the cellular mechanism of protection. METHODS: In the model of hypoxia/reoxygenation (H/R) of isolated ventricular myocytes of aged rat, the effects of HPC on aged rat ventricular myocytes against lethal H/R stimulated ischemia/reperfusion (I/R) injury 24 hours later and the changes of mitogen-activated protein kinase (MAPK) system were observed in the present study. RESULTS: HPC attenuated the lactate dehydrogenase (LDH) release and ATP depletion in myocytes and increased the viability of myocytes. It was also found that MAPK and its down-stream kinase--S6 kinase were also activated after HPC. CONCLUSION: There is delayed cardioprotection in cardiac myocytes of aged rat and the cellular mechanism underlying might involve the activation of MAPK system.

Adenosine Triphosphate↗

PubMed2000

Substrate-dependent effect of acetonitrile on human liver microsomal cytochrome P450 2C9 (CYP2C9) activity.

Acetonitrile is an organic solvent commonly used to increase the solubility of lipophilic substrates for in vitro studies. In this study, we examined its effect on four reactions (diclofenac hydroxylation, tolbutamide methyl hydroxylation, phenytoin hydroxylation, and celecoxib methyl hydroxylation) catalyzed by human liver microsomes and by the recombinant CYP2C9. In both cases, the effect of acetonitrile on activity was found to be substrate-dependent. Namely, it increased diclofenac 4'-hydroxylase and tolbutamide methyl hydroxylase activities, but decreased celecoxib methyl hydroxylase activity in a concentration-dependent manner. By comparison, hydroxylation of phenytoin was resistant to its effect. The presence of acetonitrile (3%, v/v) gave rise to a lower K(m) and a higher V(max) for diclofenac hydroxylase in both liver microsomes and recombinant CYP2C9 preparations (87 and 52% increase in V(max)/K(m) ratio, respectively). On the other hand, the inhibitory effect of the solvent (1%, v/v) toward celecoxib hydroxylase was characterized by a decrease in V(max) (human liver microsomes) or a change in both K(m) and V(max) (rCYP2C9), leading to 25 and 46% decrease in V(max)/K(m) for both systems. The results of this study underscore the need for careful evaluation of solvent effects before initiation of inhibition or cytochrome P450 reaction phenotyping studies.

Acetonitriles↗

PubMed2000

Major role of human liver microsomal cytochrome P450 2C9 (CYP2C9) in the oxidative metabolism of celecoxib, a novel cyclooxygenase-II inhibitor.

In vitro studies were conducted to identify the cytochromes P450 (CYP) involved in the oxidative metabolism of celecoxib. The hydroxylation of celecoxib conformed to monophasic Michaelis-Menten kinetics (mean +/- S.D., n = 4 livers, K(m) = 3.8 +/- 0.95 microM, V(max) = 0.70 +/- 0.45 nmol/min/mg protein) in the presence of human liver microsomes, although substrate inhibition was significant at higher celecoxib concentrations. The treatment of a panel of human liver microsomal samples (n = 16 subjects) with antibodies against CYP2C9 and CYP3A4 inhibited the formation of hydroxy celecoxib by 72 to 92% and 0 to 27%, respectively. The presence of both antibodies in the incubation suppressed the activity by 90 to 94%. In addition, the formation of hydroxy celecoxib significantly correlated with CYP2C9-selective tolbutamide methyl hydroxylation (r = 0.92, P <. 001) and CYP3A-selective testosterone 6beta-hydroxylation (r = 0.55, P <.02). In contrast, correlation with activities selective for other forms of CYP was weak (r </= 0.46). Chemical inhibition studies showed that ketoconazole (selective for CYP3A4) and sulfaphenazole (selective for CYP2C9) inhibited the formation of hydroxy celecoxib in a concentration-dependent manner, whereas potent inhibitors selective for other forms of CYP did not show any significant effect over a range of 1 to 10 microM. In agreement, cDNA-expressed CYP2C9 catalyzed the formation of hydroxy celecoxib with an apparent K(m) value (microM) and a V(max) value (pmol/min/pmol recombinant CYP) of 5.9 and 21.7, whereas a higher K(m) value (18.2) and a lower V(max) value (1.42) were obtained with rCYP3A4. It is concluded that methyl hydroxylation of celecoxib is primarily catalyzed by human liver microsomal CYP2C9, although CYP3A4 also plays a role.

Animals↗

PubMed2000

Comparison of imidazole- and 2-methyl imidazole-containing farnesyl-protein transferase inhibitors: interaction with and metabolism by rat hepatic cytochrome P450s.

Methylation at the 2-position of the imidazole ring of IBN (I), a 1, 5-substituted imidazole-containing compound, was carried out to minimize its inhibition of rat cytochrome P450 (CYP)3A activity. The resulting analog 2-MIBN (II) exhibited an inhibitory potency 70-fold weaker (K(i) = 25 microM) than that of I (K(i) = 0.3 microM) toward CYP3A, the major rat liver microsomal P450 isoform(s) for the metabolism of I and II by rat liver microsomes in the presence of NADPH. The structural modification did not switch the major metabolic pathways for I and II, but significantly decreased the affinity of II to the metabolizing enzyme(s) as reflected by the difference in their K(i) values for CYP3A. Enzyme kinetic studies also demonstrated that I had a lower apparent K(m) (0.3 microM) than than II (18 microM), but an apparent V(max) 14 times lower than II. This finding indicates that methylation at the imidazole ring reduced the affinity of the compound to CYP3A, but increased the catalytic capacity, turning I as a substrate of low K(m) value but low capacity into a compound of high K(m) but high capacity for the metabolism. Our results suggest the significance of substrate concentration in comparing the metabolic stability of compounds with different kinetic parameters. Although higher intrinsic clearance is implied for I when the substrate concentration is below or close to its K(m) value, higher metabolic rate was constantly seen with II over micromolar range. The different kinetic parameters of I and II may also explain the observation that no significant difference in pharmacokinetic behavior was seen after an i.v. administration of I and II to the rat.

Alkyl and Aryl Transferases↗

PubMed2000

KAI1 protein is down-regulated during the progression of human breast cancer.

The KAI1 gene was identified as a metastasis suppressor gene for human prostate cancer. Recently, we showed that KAI1 mRNA levels were higher in an immortal, normal-like breast epithelial cell line and nonmetastatic breast cancer cell lines but lower substantially in highly metastatic breast cancer cell lines. In this study, we examined KAI1 protein expression in breast cancer cell lines by Western blot and immunohistochemical study. KAI1 protein levels paralleled KAI1 mRNA levels and were inversely correlated with the metastatic potential of breast cancer cells. Furthermore, we examined KAI1 protein expression immunohistochemically in specimens from 81 patients with breast cancer and then correlated the findings with the clinical and histopathological parameters of the patients. High levels of KAI1 protein expression were found in normal breast tissues and noninvasive breast cancer (ductal carcinoma in situ). In contrast, KAI1 expression was reduced in most of the infiltrating breast tumors. We found that, in general, more malignant tumors demonstrated significantly lower KAI1 expression (P = 0.004). Additionally, among 29 specimens demonstrating multiple stages of malignancy within a single specimen, 23 demonstrated significant differences in KAI1 expression between benign breast tissue, ductal carcinoma in situ, and invasive carcinoma. The higher the incidence for malignancy within a given specimen, the lower the KAI1 expression (P < 0.001). These data suggest that in advanced breast cancer, KAI1 expression is down-regulated. Therefore, KAI1 may be a potentially useful indicator of human breast cancer progression.

Antigens, CD↗

PubMed2000

Alternation of Na(+)-Ca2+ exchange in rat cardiac sarcolemmal membranes during different phases of sepsis.

OBJECTIVE: To study the alteration of Na(+)-Ca2+ exchange in rat cardiac sarcolemmal membrane during phases of septic shock. METHODS: Sepsis was induced by cecal ligation and puncture (CLP). Na(+)-Ca2+ exchange was assayed by radioactive analysis. RESULTS: Na(+)-dependent 45Ca2+ uptake was decreased by 62%-69% in late phase of sepsis, whereas it was not affected in early phase of sepsis. Na(+)-Ca2+ exchange stimulated by 5' guanylyl imidodiphosphate [Gpp (NH) p] was decreased by 65.7% in late phase of sepsis but unaltered in early phase of sepsis. Two agonists (angiotensin II and phenylephrine) coupled to Gq and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA) all inhibited Na(+)-Ca2+ exchange in late phase of sepsis. Na(+)-Ca2+ exchange activities induced by phosphorylation of Na(+)-Ca2+ exchange were decreased in late phase of sepsis, whereas inhibition of Na(+)-Ca2+ exchange by dephosphorylation was increased both in early and late phases of sepsis. CONCLUSION: The alteration of Na(+)-Ca2+ exchange during different phases of sepsis might be related to the activities of Gq, protein kinase C, and phosphorylation/dephosphorylation.

Animals↗

PubMed2000

Vasoactive effects of adrenotensin and its interactions with adrenomedullin.

OBJECTIVE: To investigate the vasoactive effects of adrenotensin and the interactions between adrenotensin and adrenomedullin (ADM). METHODS: Isolated rat aortic tension, rat mean arterial pressure and 3H-TdR incorporation of rat vascular smooth muscle cells were measured. Isolated rat aortas were incubated in K-H solution containing adrenomedullin or adrenotensin. The released adrenotensin or adrenomedullin (in incubation medium) from rat aortas was measured by radioimmunoassay. RESULTS: 1 x 10(-8) and 1 x 10(-7) mol/L adrenotensin augmented rat aortic tension in a dose-dependent manner (P < 0.01). An intravenous bolus injection of adrenotensin (2.5 nmol/kg, i.v.) increased the mean arterial pressure by 28% in anesthetized rats (P < 0.01). 1 x 10(-7) mol/L adrenotensin increased 3H-TdR incorporation in cultured rat vascular smooth muscle cells by 55% (P < 0.01). Adrenomedullin inhibited these activities of adrenotensin to different extents. 1 x 10(-9), 1 x 10(-8) and 1 x 10(-7) mol/L adrenotensin decreased adrenomedullin release rates by 19%, 35% and 46%, respectively (P < 0.05 or P < 0.01) and 1 x 10(-8) mol/L adrenomedullin also inhibited adrenotensin release by 45% from rat aorta (P < 0.01). CONCLUSION: Adrenotensin is a novel peptide that elicits the activities of vasoconstriction, pressor effects and induces the proliferation of vascular smooth muscle cells. There is antagonism in vascular activities and reciprocal inhibition in the release between adrenotensin and adrenomedullin. These interactions are manifestations of intramolecular regulation of proadrenomedullin (Pro-ADM).

Adrenomedullin↗

PubMed2000

[The inhibition of prourokinase gene transfer on deposition of platelets on rabbit carotid artery intima].

OBJECTIVE: To observe the expression of pro-urokinase (proUK) gene in rabbit carotid artery transfected with replication-deficient adenovirus vector containing proUK gene (Ad/prouk) and the deposition of platelet on the same injured vessel. METHODS: Ad/proUK (Ad/proUK, 3 x 10(10) pfu/ml) was injected into the right carotid artery locally. Wild type adenovirus (Ad) was locally injected into the left carotid artery as self-control. The expression of proUK gene was investigated by immunohistochemistry assay. After injury of the gene-transfected vessel by electric stimulation, the deposition of (111) In-labeled platelet was quantitatively observed. The thrombosis was observed with HE-stained vessel section. RESULTS: There were lots of proUK granules in the endothelium of Ad/proUK gene-transfected vessel. The differences in (111) In-platelets deposition per gram dry weight vessel segment were significant between Ad/proUK and Ad transfected control vessels [(4.60 +/- 0.93) x 10(7)/g vs control (27.95 +/- 4.93) x 10(7)/g, P < 0.01)]. The HE-stained vessel section showed that there were only small thrombi in proUK gene-transfected vessel but massive thrombi almost blocked up the whole vessel in control vessel. CONCLUSION: The proUK gene-transfected vessel can obviously inhibit (111) In-labeled platelet deposition on injured vessel and thus thrombosis.

Adenoviridae↗

PubMed2000

[Effect of qiongyugao on the action of DDP in inhibiting the division of GLC-82 cell strain in vitro].

OBJECTIVE: To observe the effect of Qiongyugao (QYG) on the action of DDP in inhibiting the division of GLC-82 cell strain in vitro. METHODS: The method of serum pharmacology was used in observing the morphological change of the cancer cells. By accounting the number of the live cells of each day during 6 days respectively, the growth curve was drawn up. The effects of the three groups on the cancer cells apoptosis of GLC-82 cell strain were analysed by FACS. RESULLTS: The growth of the cancer cells in control group (normal saline) was much better than the other two groups; in chemical therapy group (DDP), the number of the live cells almost kept steady; the number of the live cells in combined group(DDP plus QYG) became even lower. QYG could enhance the action of DDP in inducing the apoptosis of GLC-82 cells strain remarkably. CONCLUSION: QYG can enhance the effects of chemotherapy in inhibiting cancer cells division and inducing their apoptosis.

Adenocarcinoma↗