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Xiao-nan Gao,1 Xu-yang Nie,1 Jing-lin Gao,1 Tian-fang Heng,2 Yu-qi Zhang,2 Li Hua,1 Ya-qi Sun,1 Zhang-ying Feng,1 Ming-xia Wang,1 Li Jia2 1Department of Clinical Pharmacology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of China; 2Department of Anesthesiology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of ChinaCorrespondence: Ming-xia Wang, Department of Clinical Pharmacology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, People’s Republic of China, Tel +86 311-66696233, Email mxia_wang@163.com Li Jia, Department of Anesthesiology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, People’s Republic of China, Email 281575038@qq.comPurpose: This study aimed to characterize the pharmacokinetics of nalbuphine in patients undergoing general anesthesia with varying degrees of liver dysfunction.Patients and Methods: Twenty-four patients were enrolled and divided into three cohorts based on liver function: normal liver function (n = 13), mild liver dysfunction (n = 5), and moderate/severe liver dysfunction (n = 6). During the induction of anesthesia, they received 15 mg of nalbuphine intravenously. Venous blood samples were collected from each patient. The plasma concentration of nalbuphine was determined using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The pharmacokinetic parameters of nalbuphine were calculated by non-compartmental analysis (NCA) using Phoenix WinNonlin software.Results: Compared with the normal liver function group, the plasma elimination half-life (T1/2) of nalbuphine was increased by approximately 33% in the moderate/severe liver dysfunction group (2.66 h vs 3.54 h, P< 0.05), and the volume of distribution (Vd) increased by approximately 85% (100.08 L vs 184.95 L, P< 0.05). Multivariate analysis revealed that weight and platelet were associated with clearance (CL); total bilirubin as an independent factor was associated with T1/2, and weight associated with area under the curve (AUC(0→∞)) independently.Conclusion: The T1/2, mean residence time, and Vd of nalbuphine in patients with moderate/severe liver dysfunction were prolonged or increased significantly compared with those in the normal liver function group. These data suggest that it may need to be used with caution when nalbuphine is administered to patients with moderate or severe liver dysfunction.Keywords: nalbuphine, intravenous, liver dysfunction, UPLC-MS/MS, pharmacokinetics

Stent implantation has been increasingly applied for the treatment of obstructive coronary artery disease, which, albeit effective, often harasses patients by in-stent restenosis (ISR).The present study was to explore the role of compound Chinese medicine Cardiotonic Pills® (CP) in attenuating ISR-evoked myocardial injury and fibrosis.Chinese miniature pigs were used to establish ISR model by implanting obsolete degradable stents into coronary arteries. Quantitative coronary angiography (QCA) was performed to confirm the success of the model.CP was given at 0.2 g/kg daily for 30 days after ISR. On day 30 and 60 after stent implantation, the myocardial infarct and myocardial blood flow (MBF) were assessed. Myocardial histology was evaluated by hematoxylin-eosin and Masson's trichrome staining. The content of ATP, MPO, and the activity of mitochondrial respiratory chain complex Ⅳ were determined by ELISA. Western blot was performed to assess the expression of ATP5D and related signaling proteins, and the mediators of myocardial fibrosis.Treatment with CP diminished myocardial infarct size, retained myocardium structure, attenuated myocardial fibrosis, and restored MBF. CP ameliorated energy metabolism disorder, attenuated TGFβ1 up-regulation and reversed its downstream gene expression, such as Smad6 and Smad7, and inhibited the increased expression of MCP-1, PR S19, MMP-2 and MMP-9.CP effectively protects myocardial structure and function from ISR challenge, possibly by regulating energy metabolism via inactivation of RhoA/ROCK signaling pathway and inhibition of monocyte chemotaxis and TGF β1/Smads signaling pathway.

Anaerobic digestion is used to treat diverse waste classes, and polycyclic aromatic hydrocarbons (PAHs) are a class of refractory compounds that common in wastes treated using anaerobic digestion. In this study, a microbial consortium with the ability to degrade phenanthrene under methanogenesis was enriched from paddy soil to investigate the cometabolic effect of glucose on methane (CH4) production and phenanthrene (a representative PAH) degradation under methanogenic conditions. The addition of glucose enhanced the CH4 production rate (from 0.37 to 2.25mg⋅L−1⋅d−1) but had no influence on the degradation rate of phenanthrene. Moreover, glucose addition significantly decreased the microbial α-diversity (from 2.59 to 1.30) of the enriched consortium but showed no significant effect on the microbial community (R2=0.39, p=0.10), archaeal community (R2=0.48, p=0.10), or functional profile (R2=0.48, p=0.10). The relative abundance of genes involved in the degradation of aromatic compounds showed a decreasing tendency with the addition of glucose, whereas that of genes related to CH4 synthesis was not affected. Additionally, the abundance of genes related to the acetate pathway was the highest among the four types of CH4 synthesis pathways detected in the enriched consortium, which averagely accounted for 48.24% of the total CH4 synthesis pathway, indicating that the acetate pathway is dominant in this phenanthrene-degrading system during methanogenesis. Our results reveal that achieving an ideal effect is diffcult via co-metabolism in a single-stage digestion system of PAH under methanogenesis; thus, other anaerobic systems with higher PAH removal efficiency should be combined with methanogenic digestion, assembling a multistage pattern to enhance the PAH removal rate and CH4 production in anaerobic digestion.

Soil autotrophic bacteria are important for sequestrating atmospheric CO2 and thus contribute to the global carbon cycle. However, information is limited on how chemical fertilization can alter the composition of soil autotrophic bacteria. In this study, the cbbL gene (a key gene in the Calvin-Benson-Bassham cycle that encodes the large subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase, RubisCO) was used to study the abundance and composition of autotrophic bacteria in an entisol with 26 years of continuous fertilization. In this process, five chemical fertilization regimes were examined: without fertilization control (CT), nitrogen and phosphorus fertilization (NP), N and potassium fertilization (NK), PK fertilization (PK), and NPK fertilization (NPK). The results showed that after the 26-year (1991–2017) period, the CT with a neutral pH (7.55) had a higher RubisCO activity than did the chemical fertilizer treatments, but the cbbL abundance was the lowest under CT. Soil RubisCO activity positively correlated with soil pH (R2 = 0.67, P

The development of a vaccine based on human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (Env) that elicits potent protective antibodies against infection has been challenging. Recently, we compared the antibody production patterns of HIV-1 Env gp120 and hepatitis B virus surface antigen (HBsAg) to provide insights into how we may improve the protective efficacy of Env-based immunogens. Our previous study showed that HIV Env and HBsAg display different mechanisms of antibody elicitation and that T cells facilitate the responses to repeated immunizations. Here, to elucidate the detailed roles of primary immunization in immune memory response formation and antibody production, we immunized C57BL/6 mice with each antigen and evaluated the development of T follicular helper (Tfh) cells, germinal centers, and the memory responses involved in prime and boost immunizations. We found that after prime immunization, compared with HBsAg, gp120 induced higher frequencies of Tfh cells and programmed death (PD)-1+ T cells, greater major histocompatibility complex II expression on B cells, comparable activated B cells, but weaker germinal center (GC) reactions and memory B cell responses in the draining lymph nodes, accompanied by slower antibody recall responses and poor immune memory responses. The above results suggested that more PD-1+ T cells arising in primary immunization may serve as major contributors to the slow antibody recall response elicited by HIV-1 Env. Electronic supplementary material The online version of this article (10.1007/s12250-018-0074-6) contains supplementary material, which is available to authorized users.

Soil pH has been suggested as one of the most important factors affecting the ecological characteristics of soil ammonia-oxidizers (AO), which mediate the conversion of ammonia to nitrate via nitrite and contribute significantly to the leaching of nitrate to groundwater and the production of atmospheric nitrous oxide (N2O). However, the dynamics of the AO community in acidic purple soils, which are widely distributed in Southwest China, remain largely unknown. In this study, two typical purple soils with different pH values (acidic: ACI; alkaline: ALK) were collected and studied. The abundance of amoA (gene encoding ammonia monooxygenase) of ammonia-oxidizing bacteria (AOB) and archaea (AOA) and that of the cbbL gene (encoding ribulose-1,5-biphosphate carboxylase/oxygenase) were determined by real-time PCR, and the community structures of AOB and AOA were investigated by cloning and sequencing. The results revealed that abundances of AOB and AOA were significantly lower in the ACI purple soil sample than in the ALK sample, but a higher ratio of AOA to AOB was found in the ACI purple soil sample. No significant difference in the abundance of cbbL was found between the two soils, but the ratio of AOB and AOA amoA to cbbL genes in the ACI soil samples was higher than that in the ALK sample. Moreover, the ALK and ACI soils harbored contrasting community compositions of AO. AOB in the ALK were dominated by cluster 3a (87 %), while the percentage of cluster 3a decreased and clusters 9 and 10 accounted for almost 77 % of the AOB community in the ACI soil. Nitrososphaera and Nitrosotalea were the major AOA phylotypes in the ALK and ACI soils, respectively. In conclusion, our results revealed the potential relations among pH, AO, and total chemoautotrophic bacteria in soil and that pH might have an essential impact on the adaptation and selection of AO in purple soils.

Fibroblast-like synoviocytes (FLSs) contribute to synovial hyperplasia in rheumatoid arthritis (RA). Smoothened (Smo) is a key component of sonic hedgehog (Shh) signaling and contributes to tumor cell proliferation. The objective of this study was to investigate the role of Smo in RA synoviocyte proliferation. FLSs were isolated from RA synovium. Shh signaling was studied using a Smo antagonist (GDC-0449) and small interfering RNA (siRNA) targeting the Smo gene in FLSs. Cell proliferation was quantified by using kit-8 assay and cell cycle distribution and apoptosis were evaluated by flow cytometry. Cell cycle-related genes and proteins were detected by real-time PCR and western blot. FLSs treated with GDC-0449 or Smo-siRNA showed significantly decreased proliferation compared to controls (P < 0.05). Incubation with GDC-0449 or transfection with Smo-siRNA resulted in a significant increase of G1 phase cells compared to controls (P < 0.05). Cell cycle arrest was validated by the significant increase in cyclin D1 and E1 mRNA expression, decrease in cyclin-dependent kinase p21 mRNA expression in Smo-siRNA transfected cells (P < 0.05). Protein expression of cyclin D1 was also downregulated after Smo gene knockdown (P < 0.05). The results suggest that Shh signaling plays an important role in RA-FLSs proliferation in a Smo-dependent manner and may contribute to synovial hyperplasia. Targeting Shh signaling may help control joint damage in patients with RA.

Through a 60-day microcosm incubation, the effect of 3, 4-dimethylpyrazole phosphate (DMPP) on the activities and abundances of ammonia-oxidizers and denitrifiers in phenanthrene-polluted soil was investigated. Five treatments were conducted for clean soil (CK), phenanthrene added (P), phenanthrene and DMPP added (PD), phenanthrene and urea added (PU), and phenanthrene, urea, and DMPP added (PUD) soils. The results indicate that the potential nitrification rate (PNR) in the P treatment was significantly higher than that in the PD treatment only on day 7, whereas the PNR in the PU treatment was significantly higher than that in the PUD treatment on each sampling day. The abundance of soil ammonia-oxidizing bacteria (AOB) in the PU treatment was significantly higher than that in the PUD treatment on each sampling day. Moreover, the abundance of AOB but rather than the ammonia-oxidizing archaea (AOA) had significantly positive correlation with soil PNR (P 0.05). DMPP showed no obvious effect on the soil denitrification enzyme activity (DEA), which could have inhibited the abundances of denitrification-related narG, nirS, and nirK genes. The results of this study should provide a deeper understanding of the interaction between soil polycyclic aromatic hydrocarbons (PAH) contamination, ammonia oxidization, and denitrification, and offer valuable information for assessing the potential contribution of denitrification for soil PAH elimination.

Mycelial pellets prepared using a marine-derived Penicillium janthinellum sp. strain (P1) were applied as biosorbents to remove dyes from aqueous solutions. Nine different dyes were studied and the effects of pH and salt concentration on the decolorization processes were investigated. The results showed that the mycelial pellet was effective in removing dyes from their water solutions. Moreover, it was found that pH was an important factor of the decolorization process and the best dye removal performance was achieved when pH = 5.0. The adsorption process of the live mycelial pellets was not affected by high salt concentrations. In addition, the mycelial pellets retained 91.3% of the original decolorization activity after five reusing cycles without any desorption treatments. The adsorption isotherms indicated that the biosorption process agreed well with the Langmuir isotherm model with a maximum biosorption capacity of 344.83 mg g(dry)−1 and the kinetic adsorption results showed that the biosorption process followed a pseudo-second-order kinetic model.

Carrier transport in AlGaN-based deep ultraviolet (DUV) light emitting diodes (LEDs) with the wavelength of 273 nm has been investigated by introducing polarization modulated electron blocking layer (EBL) that adopts an Al composition and thickness graded multiple quantum barriers (MQB) structure. The experimental result shows that the maximum light output power and external quantum efficiency for the proposed structure at the current of 250 mA are 9.6 mW and 1.03% respectively, severally increasing by 405% and 249% compared to traditional one, meanwhile, the efficiency droop at 250 mA is also dramatically reduced from 42.2% to 16.6%. Further simulation analysis indicates that this graded MQB-EBL enhances the potential barrier height for electrons and meanwhile reduces that for holes, hence effectively suppresses the electron leakage, and at the same time significantly improves the hole injection efficiency. As a result, the whole performance of the LED with the proposed MQB-EBL is dramatically improved.

Dysfunction of energy metabolism is involved in inflammatory bowel disease (IBD). This study was designed to investigate the potential of astragaloside IV (ASIV), an active ingredient of Radix Astragalus, to ameliorate colonic mucosal injury, with focusing on the implication of energy restoration in the underlying mechanism. Experimental colitis model was established in rats by injecting 2,4,6-trinitrobenzene sulfonic acid (TNBS) through anus. After 24 hours, ASIV was administrated once daily by gavage for 6 days. On day 1 and day 7, colon tissue was collected for macroscopic and histological examination, ELISA, Western blot and immunohistochemical analysis. TNBS impaired colonic mucosa with an injured epithelial architecture, increased inflammatory cell infiltration, and decreased colonic blood flow. Lgr5 positive cell number in crypt and β-catenin nuclear translocation were down-regulated by TNBS treatment. TNBS induced epithelial F-actin disruption and junctional protein degradation. Furthermore, adenosine triphosphate (ATP) content and ATP synthase subunit β expression in the colon tissue were significantly decreased after TNBS stimulation. All of the aforementioned alterations were relieved by ASIV post-treatment. The present study revealed that ASIV promoted mucosal healing process in TNBS-induced colitis, which was most likely attributed to regulating energy metabolism.

Multipartite quantum entanglement is a key resource for ensuring security in quantum network. We show that by using a unified parameter in terms of reduced noise variances one can determine different types of tripartite entanglement of a given state generated in a hybrid optomechanical system, where an atomic ensemble is located inside a single-mode cavity with a movable mirror, with different thresholds for each type. In particular, the special quantum states which allow both entanglement and steering genuinely shared among atom-light-mirror modes can be observed, even though there is no direct interaction between the mirror and the atomic ensemble. We further show the robustness against mechanical thermal noise and damping, the relaxation time of atomic ensemble, as well as the effect of gain factors involved in the criteria. Our analysis provides an experimentally achievable method to determine the type of tripartite quantum correlation in a way.

A practical scheme for the demonstration of perfect one-sided device-independent quantum secret sharing is proposed. The scheme involves a three-mode optomechanical system in which a pair of independent cavity modes is driven by short laser pulses and interact with a movable mirror. We demonstrate that by tuning the laser frequency to the blue (anti-Stokes) sideband of the average frequency of the cavity modes, the modes become mutually coherent and then may collectively steer the mirror mode to a perfect Einstein-Podolsky-Rosen state. The scheme is shown to be experimentally feasible, it is robust against the frequency difference between the modes, mechanical thermal noise and damping, and coupling strengths of the cavity modes to the mirror., Comment: 9 pages, 4 figures

Growth inhibitory effect and apoptosis induced by extracellular ATP and adenosine on human gastric carcinoma cells: involvement of intracellular uptake of adenosine

This study was to explore the protective effects of Deepure tea against insulin resistance and hepatic steatosis and elucidate the potential underlying molecular mechanisms. C57BL/6 mice were fed with a high fat diet (HFD) for 8 weeks to induce the metabolic syndrome. In the Deepure tea group, HFD mice were administrated with Deepure tea at 160 mg/kg/day by gavage for 14 days. The mice in HFD group received water in the same way over the same period. The age-matched C57BL/6 mice fed with standard chow were used as normal control. Compared to the mice in HFD group, mice that received Deepure tea showed significantly reduced plasma insulin and improved insulin sensitivity. Deepure tea increased the expression of insulin receptor substrate 2 (IRS-2), which plays an important role in hepatic insulin signaling pathway. Deepure tea also led to a decrease in hepatic fatty acid synthesis and lipid accumulation, which were mediated by the downregulation of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthesis (FAS), and acetyl-CoA carboxylase (ACC) proteins that are involved in liver lipogenesis. These results suggest that Deepure tea may be effective for protecting against insulin resistance and hepatic steatosis via modulating IRS-2 and downstream signaling SREBP-1c, FAS, and ACC.

Intestinal ischemia and reperfusion (I/R) is a clinical problem occurred for diverse causes with high mortality. The present study was to explore the role of Notoginsenoside R1 (R1), a major component form Panax. Notoginseng, in management of intestinal I/R injury. Intestinal I/R was induced in male Sprague-Dawley rats by clamping the superior mesenteric artery for 90 min followed by reperfusion for 60 min or 3 days. R1 (10 mg/kg/h) was administered either 20 min before ischemia or 20 min after reperfusion. Intestinal microcirculation was evaluated by intravital microscopy over 60 min reperfusion. Sixty min or 3 days after reperfusion, rats were killed for histological examination of the jejunum tissue and immunohistochemical localization of myeloperoxidase and CD68. ATP, ADP and AMP content in jejunum tissue was assessed by ELISA. Activation of NF-κB, expression of ATP5D and tight junction proteins were determined by Western blotting. The results demonstrated that R1 is capable of attenuating intestinal ...

Intestinal ischemia and reperfusion (I/R) is a clinical problem occurred for diverse causes with high mortality. Prophylaxis and treatment of intestinal I/R remains a challenge for clinicians. The purpose of the present study was to explore the role of Notoginsenoside R1 (R1), a major component form of Panax notoginseng, in management of intestinal I/R injury. Intestinal I/R was induced in male Sprague-Dawley rats by clamping the superior mesenteric artery for 90 min followed by reperfusion for 60 min or 3 days. R1 (10 mg·kg−1·h−1) was administered either 20 min before ischemia or 20 min after reperfusion. Intestinal microcirculation was evaluated by intravital microscopy over 60 min reperfusion. Sixty minutes or 3 days after reperfusion, rats were killed for histological examination of the jejunum tissue and immunohistochemical localization of myeloperoxidase and CD68. ATP, ADP, and AMP content in jejunum tissue was assessed by ELISA. Activation of nuclear factor-κB (NF-κB) and expression of ATP5D and tight junction proteins were determined by Western blotting. The results demonstrated that R1 is capable of attenuating intestinal I/R-induced microvascular hyperpermeability, inflammatory cytokine production, NF-κB activation, and loss of tight junction proteins, as well as improving energy metabolism during I/R. The results of the present study suggest R1 as an option in protecting against intestinal I/R injury.

Cochinchina momordica seeds (CMS) have been widely used due to antitumor activity by Mongolian tribes of China. However, the details of the underlying mechanisms remain unknown. In the present study, we found that an EtOAc (ethyl ester) extract of CMS (CMSEE) induced differentiation and caused growth inhibition of melanoma B16 F1 cells. CMSEE at the concentration of 5-200 μg/ml exhibited strongest anti-proliferative effects on B16 F1 cells among other CMS fractions (water or petroleum ether). Moreover, CMSEE induced melanoma B16 F1 cell differentiation, characterized by dendrite-like outgrowth, increasing melanogenesis production, as well as enhancing tyrosinase activity. Western blot analysis showed that sustained phosphorylation of p38 MAP accompanied by decrease in ERK1/2 and JNK dephosphorylation were involved in CMSEE-induced B16 F1 cell differentiation. Notably, 6 compounds that were isolated and identified may be responsible for inducing differentiation of CMSEE. These results indicated that CMSEE contributes to the differentiation of B16 F1 cells through modulating MAPKs activity, which may throw some light on the development of potentially therapeutic strategies for melanoma treatment.

Cancer of the colon and rectum is the third most commonly diagnosed cancer and accounts for approximately 10% of all cancer-related deaths. Although surgical resection or radiotherapy are potentially curative for localized disease, advanced colon cancer is currently associated with poor prognosis. Therefore, the development of a new and effective chemotherapeutic agent is required to target critical pathways to induce responsiveness of colon cancer cells to death signals. Dysregulation of the beta-catenin/TCF pathway plays a central role in early activities of colorectal carcinogenesis. In this study, human colon cancer SW480 cells were used to investigate the effect of CPP (periplocin from Cortex periplocae) on the modulation of the beta-catenin/TCF signaling pathway. Our research results showed that CPP caused a dose- and time-dependent inhibition of cell growth as assessed by MTT assay and an induction in apoptosis as measured by flow cytometry and transmission electron microscopy. Furthermore, the CPP- treated cells were characterized by a decreased expression of beta-catenin protein in the total cell lysates and cytosolic and nuclear extracts. This expression alleviates the binding activity of T-cell factor (Tcf) complexes to its specific DNA-binding sites. Thus, the protein expression of the downstream elements survivin and c-myc was down-regulated. To determine the precise inhibitory mechanisms involved, further in-depth in vivo studies of CPP are warranted. In conclusion, our data suggest that CPP wields a multi-prong strategy to target the beta-catenin/Tcf signaling pathway, leading to the induction of apoptosis and inhibition of growth of colon cancer cells in vitro and in vivo. Therefore, CPP may become a potential agent against colon cancer.

To investigate the effect of total salvianolic acid (TSA) on ischemia-reperfusion (I/R)-induced rat mesenteric microcirculatory dysfunctions.Male Wistar rats were randomly distributed into 5 groups (n = 6 each): Sham group and I/R group (infused with saline), TSA group, TSA + I/R group and I/R + TSA group (infused with TSA, 5 mg/kg per hour). Mesenteric I/R were conducted by a ligation of the mesenteric artery and vein (10 min) and subsequent release of the occlusion. TSA was continuously infused either starting from 10 min before the ischemia or 10 min after reperfusion. Changes in mesenteric microcirculatory variables, including diameter of venule, velocity of red blood cells in venule, leukocyte adhesion, free radicals released from venule, albumin leakage and mast cell degranulation, were observed through an inverted intravital microscope. Meanwhile, the expression of adhesion molecules CD11b/CD18 on neutrophils was evaluated by flow cytometry. Ultrastructural evidence of mesenteric venules damage was assessed after microcirculation observation.I/R led to multiple responses in mesenteric post-capillary venules, including a significant increase in the adhesion of leukocytes, production of oxygen radicals in the venular wall, albumin efflux and enhanced mast cell degranulation in vivo. All the I/R-induced manifestations were significantly reduced by pre- or post-treatment with TSA, with the exception that the I/R-induced increase in mast cell degranulation was inhibited only by pre-treatment with TSA. Moreover, pre- or post-treatment with TSA significantly attenuated the expression of CD11b/CD18 on neutrophils, reducing the increase in the number of caveolae in the endothelial cells of mesentery post-capillary venules induced by I/R.The results demonstrated that TSA protects from and ameliorates the microcirculation disturbance induced by I/R, which was associated with TSA inhibiting the production of oxygen-free radicals in the venular wall and the expression of CD11b/CD18 on neutrophils.

To study the growth inhibitory effects of ATP on TE-13 human squamous esophageal carcinoma cells in vitro.MTT assay was used to determine the inhibition of proliferation of ATP or adenosine (ADO) on TE-13 cell line. The morphological changes of TE-13 cells induced by ATP or ADO were observed under fluorescence light microscope by acridine orange (AO)/ethidium bromide (EB) double stained cells. The internucleosomal fragmentation of genomic DNA was detected by agarose gel electrophoresis. The apoptotic rate and cell cycle after treatment with ATP or ADO were determined by flow cytometry.ATP and ADO produced inhibitory effects on TE-13 cells at the concentration between 0.01 and 1.0 mmol/L. The IC(50) of TE-13 cells exposed to ATP or ADO for 48 and 72 h was 0.71 or 1.05, and 0.21 or 0.19 mmol/L, respectively. The distribution of cell cycle phase and proliferation index (PI) value of TE-13 cells changed, when being exposed to ATP or ADO at the concentrations of 0.01, 0.1, and 1 mmol/L for 48 h. ATP and ADO inhibited the cell proliferation by changing the distribution of cell cycle phase via either G(0)/G(1) phase (ATP or ADO, 1 mmol/L) or S phase (ATP, 0.1 mmol/L) arrest. Under light microscope, the tumor cells exposed to 0.3 mmol/L ATP or ADO displayed morphological changes of apoptosis. A ladder-like pattern of DNA fragmentation was obtained from TE-13 cells treated with 0.1-1 mmol/L ATP or ADO in agarose gel electrophoresis. ATP and ADO induced apoptosis of TE-13 cells in a dose-dependent manner at the concentration between 0.03 and 1 mmol/L. The maximum apoptotic rate of TE-13 cells exposed to ATP or ADO for 48 h was 16.63% or 16.9%, respectively.ATP and ADO inhibit cell proliferation, arrest cell cycle, and induce apoptosis of TE-13 cell line.