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| 1 | 会展活动与旅游活动的比较——兼论会展旅游概念的界定显示文摘本文通过比较会议与展览来界定会展业,通过会展活动与旅游活动的比较来区分会展业和旅游业,通过游客与参加会展的人群的比较来界定会展旅游者,通过会展活动中会展属性与旅游属性的比较来界定会展旅游。得出会展业与旅游业是两个性质完全不同但又关联紧密的行业;会展旅游与旅游业的会展多元化经营是两个不同的概念。会展旅游业是旅游业利用会展业的旅游属性和依托会展业的发展优势形成的新型产业。 | 王云龙 | 2003 | 旅游学刊2003，18，5： | 58 |
| 2 | Metastatic human hepatocellular carcinoma models in nude mice and cell line with metastatic potential显示文摘Metastatic human HCC model is needed for the studies on mechanism and intervention of metastatic recurrence. By using orthotopic implantation of histologically intact tissues of 30 surgical specimens, a patient like metastatic model of human HCC in nude mice (LCI-D20)and a Iow metastatic model of human HCC in nude mice LCI-D35 ) have been established. All mice with transplanted LCI-D20 tumors exhibited extremely high metastatic ability including spontaneous metastasis to liver, lungs, lymph nodes and peritoneal seeding.Remarkable difference was also found in expression of some of the invasiveness related genes and growth factors between the LCI-D20 and LCI-D35 tumors. PAI-Iincreased gradually following tumor progression in LCID20 model, and correlated with tumor size and AFP level,Phasic expression of tissue intercellular adhesion molecule-I in this model was also observed. Using corneal micropocket model, it was demonstrated that the vascular response induced by LCI-D20 tumor was stronger than that induced by LCI-D35 tumor. Similar report on metastatic human HCC model in nude mice and human HCC cell line with metastatic potential was rarely found in the literature. This LCI-D20 model has been widely used for the studies on intervention of metastasis, including antiangiogenesis, antisense approach, metalloproteinase inhibitor, differentiation inducer, etc. It is concluded that the establishment of metastatic human HCC model in nude mice and human HCC cell line with metastatic potential will provide important models for the in vivo and in vitro study of HCC invasiveness, angiogenesis as well as intervention of HCC recurrence. | Zhao-You Tang Fan-Xian Sun Jian Tian Sheng-Long Ye Yin-Kun Liu Kang-Da Liu Qiong Xue Jie Chen Jing-Lin Xia Lun-Xiu Qin Hui-Chuan Sun Lu Wang Jian Zhou Yan Li Zeng-Chen Ma Xin-Da Zhou Zhi-Quan Wu Zhi-Ying Lin Bing-Hui Yang Liver Cancer Institute of Fudan University and Zhongshan Hospital,Shanghai 200032,China | 2001 | World Journal of Gastroenterology2001，7，5： | 34 |
| 3 | Effect of hepatocyte apoptosis induced by TNF-α on acute severe hepatitis in mouse models显示文摘AIM To study the effect of hepatocyteapoptosis and necrosis induced by TNF-α on thepathogenesis of acute severe hepatitis(ASH).METHODS The model of ASH was prepared inD-galactosamine(GAIN)sensitized BALB/c miceby injection of either endotoxin(ET)or tumornecrosis factor-α(TNF-α).Morphologicalchanges of apoptotic hepatocytes were studiedby both light and electron microscope and in siteend labeling method(ISEL).Molecular biologicalchanges of DNA ladder were observed byelectrophoresis of extract from liver tissues.Biochemical changes were measured by alanineaminotransferase(ALT),asparticaminotransferase(AST)and TNF-α.The relationbetween apoptosis and necrosis was evaluatedsimultaneously.RESULTS The sequence of hepatocyteapoptosis,necrosis,and final death from ASHwas observed both in GAIN/ET and GAIN/TNF-agroup.Apoptosis was prominent at 3.5 h and 5 hafter injection of inducer,while necrosis becamedominant at 9 h after challenge.The appearanceof apoptosis was earlier in GAIN/TNF-α groupthan that in GAIN/ ET group.Pretreatment ofmice with antiTNF IgG1 may completely preventthe liver injury induced by GalN/ET.CONCLUSION TNF-α can cause liver damageby inducing hepatic apoptosis and necrosis inmice with endotoxemia. | Guo Qing Zang Xia Qiu Zhou Hong Yu Qing Xie Guo Ming Zhao Bin Wang Qing Guo Yue Qin Xiang Dan Liao Department of Infectious Diseases,Rujin Hospital,Shanghai Second Medical University,Shanghai 200025,China | 2000 | World Journal of Gastroenterology2000，6，5： | 30 |
| 4 | Calycosin improves cognitive function in a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway显示文摘The major pathological changes in Alzheimer's disease are beta amyloid deposits and cognitive impairment. Calycosin is a typical phytoestrogen derived from radix astragali that binds to estrogen receptors to produce estrogen-like effects. Radix astragali Calycosin has been shown to relieve cognitive impairment induced by diabetes mellitus, suggesting calycosin may improve the cognitive function of Alzheimer's disease patients. The protein kinase C pathway is upstream of the mitogen-activated protein kinase pathway and exerts a neuroprotective effect by regulating Alzheimer's disease-related beta amyloid degradation. We hypothesized that calycosin improves the cognitive function of a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway. Various doses of calycosin(10, 20 and 40 mg/kg) were intraperitoneally injected into APP/PS1 transgenic mice that model Alzheimer's disease. Calycosin diminished hippocampal beta amyloid, Tau protein, interleukin-1 beta, tumor necrosis factor-alpha, acetylcholinesterase and malondialdehyde levels in a dose-dependent manner, and increased acetylcholine and glutathione activities. The administration of a protein kinase C inhibitor, calphostin C, abolished the neuroprotective effects of calycosin including improving cognitive ability, and anti-oxidative and anti-inflammatory effects. Our data demonstrated that calycosin mitigated oxidative stress and inflammatory responses in the hippocampus of Alzheimer's disease model mice by activating the protein kinase C pathway, and thereby improving cognitive function. | Lei Song Xiaoping Li Xiao-xue Bai Jian Gao Chun-yan Wang | 2017 | Neural Regeneration Research2017，12，11： | 25 |
| 5 | Exogenous bone morphogenetic protein-7 reduces hepatic fibrosis inSchistosoma japonicum-infected micevia transforming growth factor-β/Smad signaling显示文摘AIM: To investigate the antifibrotic effects of bone morphogenetic protein-7 (BMP-7) on Schistosoma japonicum (S. japonicum )-induced hepatic fibrosis in BALB/C mice. METHODS: Sixty BALB/C mice were randomly divided into three groups, including a control group (group A, n = 20), model group (group B, n = 20) and BMP-7 treated group (group C, n = 20). The mice in group B and group C were abdominally infected with S. japonicum cercariae to induce a schistosomal hepatic fibrosis model. The mice in group C were administered human recombinant BMP-7. Liver samples were extracted from mice sacrificed at 9 and 15 wk after modeling. Hepatic histopathological changes were assessed using Masson's staining. Transforming growth factor-beta 1 (TGF-β1), alpha-smooth muscle actin (α-SMA), phosphorylated Smad2/3 (pSmad2/3) and Smad7 protein levels and localization were measured by Western blotting and immunohistochemistry, respectively, and their mRNA expressions were detected by reverse transcriptionpolymerase chain reaction (RT-PCR). RESULTS: The schistosomal hepatic fibrosis mouse model was successfully established, as the livers of mice in group B and group C showed varying degrees of typical schistosomal hepatopathologic changes such as egg granuloma and collagen deposition. The degree of collagen deposition in group C was higher than that in group A (week 9: 22.95±6.66vs 2.02±0.76; week 15: 12.84±4.36 vs 1.74±0.80; P<0.05), but significantly lower than that in group B (week 9: 22.95±6.66 vs 34.43±6.96; week 15: 12.84±4.36 vs 18.90±5.07;P<0.05) at both time points. According to immunohistochemistry data, the expressions of α-SMA, TGF-β1 and pSmad2/3 protein in group C were higher than those in group A (α-SMA: week 9: 21.24±5.73 vs 0.33±0.20; week 15: 12.42±4.88 vs 0.34±0.27; TGF-β1: week 9: 37.00±13.74 vs 3.73±2.14; week 15: 16.71±9.80 vs 3.08±2.35; pSmad2/3: week 9: 12.92±4.81 vs 0.83±0.48; week 15: 7.87±4.09 vs 0.90±0.45; P<0.05), but significantly lower than those in group B (α-SMA: week 9: 21.24±5.73 vs 34.39±5.74; week 15: 12.42±4.88 vs 25.90±7.01; TGF-β1: week 9: 37.00±13.74 vs 55.66±14.88; week 15: 16.71±9.80 vs 37.10±12.51; pSmad2/3: week 9: 12.92±4.81 vs 19.41±6.87; week 15: 7.87±4.09vs 13.00±4.98;P<0.05) at both time points; the expression of Smad7 protein in group B was higher than that in group A and group C at week 9 (8.46±3.95 vs 1.00±0.40 and 8.46±3.95 vs 0.77±0.42; P<0.05), while there were no differences in Smad7 expression between the three groups at week 15 (1.09±0.38 vs 0.97±0.42 vs 0.89±0.39; P>0.05). Although minor discrepancies were observed, the results of RT-PCR and Western blotting were mainly consistentwith the immunohistochemical results. CONCLUSION: Exogenous BMP-7 significantly decreased the degree of hepatic fibrosis in both the acute and chronic stages of hepato-schistosomiasis, and the regulatory mechanism may involve the TGF-β/Smad signaling pathway. | Bo-Lin Chen Jie Peng Qing-Fu Li Min Yang Yuan Wang Wei Chen | 2013 | World Journal of Gastroenterology2013，19，9： | 21 |
| 6 | The cloning of 3'-truncated preS/S gene from HBV genomic DNA and its expression in transgenic mice显示文摘INTRODUCTIONHepatitis B virus (HBV) is regarded as one of themain etiologic factors involved in the developmentof human hepatocellular carcinoma (HCC).The open reading frame (orf)of X gene of HBVencoded a transactivating factor is the evidence thatstrongly supported the notion that the X gene ofHBV DNA integrated in HCC genomic DNA couldcontribute to the carcinogenesis of liver cells byactivation of some related cellular genes | Yi Ping Hu~1 Yu Cheng Yao~1 Jian Xiu Li~1 Xin Min Wang~1 Hong Li~2 Zhong Hua Wang~1 Zhang Heng Lei~3 1 Department of Cell Biology,Second Military Medical University,Shanghai 200433,China 2 Department of Biology,Department of Basic Medicine,West-China University of Medical Sciences,Chengdu 610041,China 3 Department of Biology,North Sichuan Medical College,Nanchong 637007,China | 2000 | World Journal of Gastroenterology2000，6，5： | 18 |
| 7 | Growth-inhibiting effects of taxol on human liver cancer in vitro and in nude mice显示文摘AIM To investigate the effects of taxol onSMMC-7721 human hepatoma and itsmechanisms.METHODS In vitro cell growth was assessedby trypan blue exclusion method.Experimentalhepatoma model was established by seedingSMMC-7721 cells subcutaneously into Balb/c(nu/nu)nude mice.In vivo tumor growth wasdetermined by measurement of tumor diameterwith Vernier calipers.The syntheses of DNA,RNA and protein were analyzed by incorporationof ~3H-thymidine,~3H-uridine and ~3H-leucinerespectively.Using light and electronmicroscopes to observe the morphologicalchanges of cells including mitosis andapoptosis.RESULTS Taxol was effective against SMMC-7721 human hepatoma cell growth in the rangesof 2.5 nmol/L-10 nmol/L with mitotic arrestand apoptosis in vitro.DNA,RNA and proteinsyntheses in cells were also obviouslysuppressed by in vitro treatment of taxol for72 h.Taxol at 2.5 nmol/L reduced ~3H-thymidineuptake to about 34% of the control value(P<0.05).Increasing the dose of taxol to20 nmol/L resulted in a greater decrease in ~3H-thymidine incorporation to 60% of the controlvalue(P<0.01).At a concentration of 20 nmol/L,the ~3H-uridine and ~3H-leucine uptakeswere reduced to 52%(P<0.05)and 63%(P<0.01),respectively.In vivo,taxolsignificantly inhibited SMMC-7721 tumor growthat 10 mg/kg,i.p.,once daily for 10 d.A morethan 90% decrease in tumor volume wasobserved by day 11(P<0.01)similarly withmitotic arrest and cell apoptosis.CONCLUSION Taxol has a marked anticanceractivity in SMMC-7721 human hepatoma both invitro and in nude mice.Its mechanisms might beassociated with mitotic arrest,subsequently,apoptosis of the hepatoma cells.No obvioustoxicity was observed with in vivoadministration of taxoi. | Jin Hui Yuan Ru Ping Zhang Ru Gang Zhang Li Xia Guo Xing Wang Wang Dan Luo Yong Xie Hong Xie | 2000 | World Journal of Gastroenterology2000，6，2： | 18 |
| 8 | Effect of NF-κB inhibitor PDTC on VEGF and endostatin expression of mice with Lewis lung cancer显示文摘Objective:To investigate the effects of NF-κB inhibitor pyrrolidine dithiocarbamate hydrochloride(PDTC) on vascular endothelial growth factor(VEGF) and endostatin expression in mice with Lewis lung cance;and its mechanism.Methods:Mice survival rate and anti-tumor effects were observed in different concentrations of NF-κB inhibitor PDTC after the Lewis lung cancer mice model was established.VEGF and endostatin expressions were detected by immunohistochemical assay.Results:Lewis lung cancer was be inhibited by 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg of NF-κB inhibitor PDTC(P<0.05).Microvessel density(MVD) in 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg NF-κB inhibitor PDTC groups were significantly lower than the control group(P<0.05).Immunohistochemical assay results showed that VEGF and endostatin expressions in the 0.5 mg/kg.1.5 mg/kg and 3.0 mg/kg NF-κB inhibitor PDTC groups were significantly lower than the control group(P<0.05).Western blot results also showed that NF-κB inhibitor PDTC could inhibit VEGF and endostatin expressions in tumor tissues.Conclusions:NF-κB inhibitor PDTC can inhibit tumor formation and reduce tumor angiogenesis in mice with Lewis lung cancer;and its mechanism maybe associated to VEGF and endostatin down-regulation. | Ping Gao Ya-Jie Gao Hong-Lu Liang | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，3： | 18 |
| 9 | Inhibitory effects of Curcuma aromatica oil on proliferation of hepatoma in mice显示文摘AIM To reveal the inhibitory effects ofCurcuma aromatica oil(CAO)on cellproliferation of hepatoma in mice.METHODS Two tumor inhibitory experimentsof CAO on hepatoma in mice were conducted.The inhibitory effects of CAO on proliferation ofhepatoma in mice were evaluated by DNA imagecytometry and immunohistochemical staining ofproliferating cell nuclear antigen(PCNA).RESULTS The tumor inhibitory rates of CAOwere 52% and 51% in two experiments,respectively.Compared with those of the saline-treated control groups,both differences werestatistically significant(P<0.01).In the groupof mice treated with CAO,the cellular nuclearDNA OD value(249±70),areas(623 μm^2±228 μm^2)and DNA(2.38±0.67)index of hepaticcarcinomas were significantly lower than thoseof the control group(430±160,1073 μm^2±101 μm^2 and 4.48±0.71).CAO also couldincrease diploidy cell rates(29.00%±9.34% vs2.97%±5.69%,P<0.01)and decreasepentaploidy cell exceeding rate(30.04%±15.10% vs 70.89%±14.94%,P<0.01).In thegroup of mice treated with CAO,the labelingindexes of proliferating cell nuclear antigen (PCNA-LI)were 30%±4%,which weresignificantly lower than 40%±6% of the controlgroup(P<0.01).CONCLUSION The inhibition of CAO on thegrowth of hepatoma in mice might be associatedwith its depression on cellular proliferativeactivity. | Wan Yin Wu Qin Xu Ling Chun Shi Wei Bin Zhang | 2000 | World Journal of Gastroenterology2000，6，2： | 16 |
| 10 | Effect of Qinglongyi Polysaccharides on Complex Mobility of Erythrocytes in S_(180) Mice显示文摘Objective To study the effect of Qinglongyi polysaccharides (QP) in the exocarp of Juglans mandshurica on the complex mobility of erythrocytes in S180 mice. Methods Erythrocytes were collected and prepared into suspensions, and the complex mobility of cells was measured using high performance capillary electrophoresis (HPCE). Optimized experimental conditions were as follows: 50 cm × 75 μm capillary, buffer for electrophoresis; phosphate solution containing hydroxypropylmethyl cellulose (0.1 mol/L, pH 7.4), injection pressure 3.448 kPa, injection time 10 s, separation voltage 20 kV, and column temperature 25 ℃. Results The migration time of erythrocytes in S180 mice was longer than that in normal mice, which was 18.09 min for the model group and 12.11 min for the control group, and the complex mobility of erythrocytes in S180 mice was lower than that in normal mice, which was 0.92 × 104 cm2 /(V·s) for the model group and 1.38 × 104 cm2 /(V·s) for the control group. It was also found that S180 mice treated by QP could shorten the migration time and increase the complex mobility of erythrocytes. Conclusion QP could improve the complex mobility of erythrocytes in S180 mice, and HPCE could be used as a powerful tool for determining the physiological state and functions of erythrocytes. | JI Chen-feng YUE Lei JI Yu-bin | 2013 | Chinese Herbal Medicines2013，5，1： | 14 |
| 11 | Study on the anticarcinogenic effect and acutetoxicity of liver-targeting mitoxantrone-nanoparticles显示文摘AIM To study the anticarcinogenic effect and acute toxicity of liver targeting mitoxantrone nanospheres. METHODS The anticarcinogenic effect of mitoxantrone polybutylcyanoacrylate nanoparticles (DHAQ PBCA NP) was investigated by using heterotopic and orthotopic transplantation models of human hepatocellular carcinoma (HCC) in nude mice and was compared with mitoxantrone (DHAQ) and doxorubicin (ADR). The acute toxicity of DHAQ PBCA NP lyophilized injection in mice was also studied. RESULTS The tumor inhibition rates of ADR, DHAQ, DHAQ PBCA NP to orthotopically transplanted HCC were 60 07%, 67 49% and 99 44%, respectively, but regard to heterotopically transplanted HCC, these were 80 03%, 86 18% and 92 90%, which were concordant with the results acquired by mitosis counting and proliferating cell nuclear antigen (PCNA). After iv administration to mice with DHAQ PBCA NP, the LD 50 was 16 9*!mg/*!kg ± 3 9*!mg/*!kg , no obvious local irritation was observed and there was no significant damage to the structure of liver cells, and that of the heart, spleen and kidneys. CONCLUSION The effect of DHAQ PBCA NP was significantly higher than that of DHAQ and ADR in the anti orthotopically transplanted HCC and the acute toxicity was relatively low. | ZHANG Zhi Rong, HE Qin, LIAO Gong Tie and BAI Shao Huai | 1999 | World Journal of Gastroenterology1999，5，6： | 13 |
| 12 | Antiviral effects of Reduning injection against Enterovirus 71 and possible mechanisms of action显示文摘The present study was designed to evaluate the protective effects of Reduning injection against Enterovirus 71(EV71) in Vero cells and in mice. The Vero cells were infected with 100 and 50 TCID50(50% tissue culture infective dose) of EV71, respectively. The inhibition of Reduning injection on cytopathic effect(CPE) was detected. Meanwhile, a mouse model produced by intraperitoneal EV71-infection(106 TCID50), was used to investigate the protective effects of Reduning injection. The total survival rate, living time, daily survival rate, weight ratio, and score for symptoms were examined. The viral loads in Vero cells and muscle tissues were detected using real-time PCR. Finally, the content of cytokines was analyzed by ELISA. In the Vero cells, 2.5 mg crude drug·m L-1 of Reduning injection inhibited CPE induced by EV71 infection. In the mice, 1.3 g crude drug·kg-1 of Reduning injection rescued death triggered by infection, in comparison with model group. Moreover, the survival rate, weight ratio, and clinical scores were also improved. The viral RNA copies in the Vero cells and the mice muscle tissues were reduced. Besides, the steep EV71-induced accumulations of TNF-α and MCP-1 were decreased by Reduning injection. In conclusion, Reduning injection showed promising protective effects against EV71 in Vero cells and in mice. | CAO Ze-Yu CHANG Xiu-Juan ZHAO Zhong-Peng CAO Liang XIAO Wei | 2015 | Chinese Journal of Natural Medicines2015，13，12： | 13 |
| 13 | Caffeine is responsible for the bloodglucose-lowering effects of green tea and Puer tea extractsin BALB/c mice显示文摘The present study was designed to determine the effects of Puer tea and green tea on blood glucose level. Male BALB/c mice were administered green tea extract(GTE) or Puer tea extract(PTE), either intragastrically or in their drinking water. The major components of these teas are epigallocatechin gallate(EGCG) and caffeine, respectively. Blood glucose measurement results showed that mice fed intragastrically or mice that drank GTE, PTE or caffeine showed significantly lower blood glucose levels compared to the control group. However, EGCG exhibited no influence on the blood glucose levels. When caffeine was eliminated from the GTE and PTE, the effect on the blood glucose levels was abolished, but the effect was recovered when caffeine was re-introduced into the extracts. Evaluation of hematological and biochemical indices at the time of the greatest caffeine-induced decrease in blood glucose levels showed that the effect of caffeine was specific. Microarray analyses were performed in 3T3-L1 preadipocytes and mature adipocytes treated with 0.1 mg·m L-1 caffeine to identify factors that might be involved in the mechanisms underlying these effects. The results showed that few genes were changed after caffeine treatment in adipocytes, and of them only phospholipid transfer protein(PLTP) may be ralated to blood glucose. In conclusion, this study indicates that caffeine may be the key constituent of tea that decreases blood glucose levels, and it may be used to treat type 2 diabetes. | FANG Chong-Ye WANG Xuan-Jun HUANG Ye-Wei HAO Shu-Mei SHENG Jun | 2015 | Chinese Journal of Natural Medicines2015，13，8： | 12 |
| 14 | Triptolide prolonged allogeneic islet graft survival in chemically induced and spontaneously diabetic mice without impairment of islet function显示文摘BACKGROUND:Triptolide(TPT)is a diterpenoid triepoxide extracted from the Chinese herb Tripterygium wilfordii Hook.F.It exhibits potent immunosuppressive and anti-inflammatory properties.This study was undertaken to investigate its effects on prolongation of islet allograft survival in rodents.Additionally,we investigated whether TPT would be toxic to islet function in vivo.METHODS:We transplanted BALB/c islets to either chemically induced diabetic C57BL/6 mice or spontaneously diabetic nonobese diabetic(NOD)mice.TPT was injected within 2 weeks or continuously,until rejection,in the two combinations.Then, we evaluated the toxicity of TPT on islet function by daily injection to naive BALB/c or diabetic BALB/c that was cured by syngeneic islet transplantation under the kidney capsule.Mice injected with cyclosporine A(CsA)or vehicle served as controls.Intraperitoneal glucose tolerance tests(IPGTTs)performed at 4 and 8 weeks in the na?ve BALB/c group,and at 2,4,6,and 8 weeks in the syngeneic transplanted group.RESULTS:The medium survival time of islets allograft from TPT treated C57BL/6 and NOD recipients were 28.5 days(range 24-30 days,n=10)and 33.0 days(range 15-47 days,n=6), respectively,and they were significantly different from those of the vehicle treated controls,which were 14.0 days(range 13-16 days,n=6)and 5.0 days(range 4-10 days,n=6),respectively(all P<0.0001).The IPGTT demonstrated that there was no difference between the TPT treated and vehicle treated groups, either in the normal or syngeneic transplanted islet BALB/c mice.However,CsA injection impaired islet function in both normal and syngeneic transplanted mice as early as 4 weeks.CONCLUSION:TPT prolonged islets allograft survival in a chemically induced diabetic or an autoimmune diabetic murine model without impairment of islet function. | Xin, Ming-Jun Cui, Shi-Hua Liu, Shuang Sun, Hai-Chen Li, Fei Sun, Jia-Bang Luo, Bin | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，3： | 11 |
| 15 | ERK1/2-HNF4α axis is involved in epigallocatechin-3-gallate inhibition of HBV replication显示文摘Epigallocatechin gallate(EGCG),a major polyphenol in green tea,exhibits diverse biological activities.Previous studies show that EGCG could effectively suppress HBV gene expression and replication,but the role of EGCG in HBV replication and its underlying mechanisms,especially the signaling pathways involved,remain unclear.In this study we investigated the mechanisms underlying EGCG inhibition on HBV replication with a focus on the signaling pathways.We showed that EGCG(12.5?50μM)dose-dependently inhibited HBV gene expression and replication in HepG2.2.15 cells.Similar results were observed in HBV mice receiving EGCG(25 mg·kg^?1·d^?1,ip)for 5 days.In HepG2.2.15 cells,we showed that EGCG(12.5?50μM)significantly activate ERK1/2 MAPK signaling,slightly activate p38 MAPK and JAK2/STAT3 signaling,while had no significant effect on the activation of JNK MAPK,PI3K/AKT/mTOR and NF-κB signaling.By using specific inhibitors of these signaling pathways,we demonstrated that ERK1/2 signaling pathway,but not other signaling pathways,was involved in EGCG-mediated inhibition of HBV transcription and replication.Furthermore,we showed that EGCG treatment dose-dependently decreased the expression of hepatocyte nuclear factor 4α(HNF4α)both at the mRNA and protein levels,which could be reversed by pretreatment with the ERK1/2 inhibitor PD98059(20μM).Moreover,we revealed that EGCG treatment dose-dependently inhibited the activity of HBV core promoter and the following HBV replication.In summary,our results demonstrate that EGCG inhibits HBV gene expression and replication,which involves ERK1/2-mediated downregulation of HNF4α.These data reveal a novel mechanism for EGCG to inhibit HBV gene expression and replication. | Zi-yu Wang Yu-qi Li Zhi-wei Guo Xing-hao Zhou Mu-dan Lu Tong-chun Xue Bo Gao | 2020 | Acta Pharmacologica Sinica2020，41，2： | 11 |
| 16 | Effect of combined treatment with cyclophosphamidum and allicin on neuroblastoma-bearing mice显示文摘Objective:To evaluate the efficacy of allicin combined with cyclophosphamide on neuroblastoma(NB)-bearing mice and explore the immunological mechanism in it.Methods:A total of 30NB-bearing mice were equally randomized into model group,cyclophosphamide group and combined therapy group,10 nudemice were set as normal saline(NS) group.Cyclophosphamide group and combined therapy group were weekly injected with 60 mg/kg cyclophosphamide for four weeks;besides,combined therapy group was given with allicin(10 mg/kg/d) by gastric perfusion for 4 weeks;model group and NS group were given with the same volume of NS.Serum VEGF content was detected by ELISA pre-treating(0 d) and on the 3rd d.14 th d and 28 th d;on29th d,all mice were sacrificed and the tumor,liver,spleen and thymic tissues were weighted.Tumors were made into paraffin section for detecting tumor cell apoptosis and proliferation by TUNEI.and BrdU method,respectively.Survival curves were drawn by Kaplan-Meier method.Results:After treatment,both treatment groups relieved on viscera indexes,VEGF level,T cell subsets distribution and tumor growth and each index of combined therapy group was better than cyclophosphamide group(P<0.05 or 0.01);only combined therapy group could significantly increase the lifetime of NB-bearing mice(χ~2=5.667,P=0.017).Conclusions:Allicin can improve T cell subsets distribution and inhibit VEGF expression through its immunomodulatory activity,thereby improve the efficiency on NB in coordination with cyclophosphamide. | Xiang-Yang Gao Xian-Jie Geng Wen-Long Zhai Xian-Wei Zhang Yuan Wei Guang-Jun Hou | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，2： | 11 |
| 17 | Improved method for inducing chronic atrophic gastritis in mice显示文摘BACKGROUND Chronic atrophic gastritis(CAG)is a common disease of the digestive system with pathological characteristics of a decreasing number,or disappearance,of inherent glands of the gastric mucosa.CAG has been defined as a precancerous condition of gastric cancer.Intestinal metaplasia or intraepithelial neoplasia accompanying atrophied glands of the stomach is regarded as one of the most important precancerous lesions of gastric cancer.As a common malignant tumour,gastric cancer remains without a satisfactory therapy and its pathogenesis remains unclear,seriously threatening human life.Therefore,some scholars have proposed to prevent the incidence of gastric cancer by avoiding precancerous lesions.If CAG can be reversed,the incidence of gastric cancer can be substantially reduced.To reverse and prevent CAG and study its pathogenesis and therapy,it is necessary to develop an ideal,safe,stable,animal model.AIM To study a rapid,stable,and safe method of establishing a mouse model of human CAG.METHODS Six-week-old Kunming mice were divided into a phosphate buffered solution control group,a Helicobacter pylori(H.pylori)group,an N-methyl-N'-nitroguanidine(MNNG)group,an ammonia water group,and a group combining H.pylori,MNNG,and ammonia water(hereinafter referred to as the combined group).The mice were administrated with drinking water containing ammonia or infected with H.pylori through gavage.At the 30th,60th,90th,and 120th day after the last H.pylori infection,mice were selected randomly to collect their gastric mucosa for hematoxylin eosin staining,terminal nick-end labelling staining detection,and immunohistochemical staining for Bax and Bcl-2.In addition,H.pylori was isolated,cultured,and identified,and its extent of colonisation calculated.Blood was collected to detect inflammatory factors interleukin(IL)-1β,IL-8,and tumor necrosis factor(TNF)-αand immune function markers CD4 and CD8 to confirm successful establishment of the CAG model.RESULTS The combined group showed slight CAG at the 90th day and moderate CAG at the 120th day,while other groups did not show CAG at that time.CONCLUSION The combination of H.pylori,MNNG,and ammonia is an effective method of developing a mouse model of human CAG. | Xian Wei Xue-Ping Feng Lu-Yao Wang Yan-Qiang Huang Ling-Ling Liang Xiao-Qiang Mo Hong-Yu Wei | 2019 | World Journal of Gastrointestinal Oncology2019，11，12： | 10 |
| 18 | 关于成都发展会展旅游的初步探讨显示文摘会展旅游是当今国际旅游业开发的重要方向 ,也是我国各城市旅游开发的一个不可或缺的组成部分。文章就成都发展会展旅游的优劣条件进行分析之后 ,提出了成都会展旅游的开发方向及一系列对策措施。 | 王元珑 江娟丽 | 2003 | 经济师2003，，5： | 9 |
| 19 | Knockout mouse models of insulin signaling: Relevance past and future显示文摘Insulin resistance is a hallmark of type 2 diabetes. In an effort to understand and treat this condition, re searchers have used genetic manipulation of mice to uncover insulin signaling pathways and determine the effects of their perturbation. After decades of research much has been learned, but the pathophysiology o insulin resistance in human diabetes remains contro versial, and treating insulin resistance remains a chal lenge. This review will discuss limitations of mouse models lacking select insulin signaling molecule genes In the most influential mouse models, glucose metabo lism differs from that of humans at the cellular, organ and whole-organism levels, and these differences limi the relevance and benefit of the mouse models both in terms of mechanistic investigations and therapeutic development. These differences are due partly to im mutable differences in mouse and human biology, and partly to the failure of genetic modifications to produce an accurate model of human diabetes. Several fac tors often limit the mechanistic insights gained from experimental mice to the particular species and strain including: developmental effects, unexpected meta bolic adjustments, genetic background effects, and technical issues. We conclude that the limitations and weaknesses of genetically modified mouse models of insulin resistance underscore the need for redirection of research efforts toward methods that are more directly relevant to human physiology. | Anne E Bunner P Charukeshi Chandrasekera Neal D Barnard | 2014 | World Journal of Diabetes2014，5，2： | 9 |
| 20 | Effects of targeting magnetic drug nanoparticles on human cholangiocarcinoma xenografts in nude mice显示文摘BACKGROUND:Targeting is a new therapeutic tool for malignant tumor as a result of combining nanotechnology with chemotherapeutics.The aim of our study was to investigate the effects of magnetic nanoparticles enveloping a chemotherapeutic drug on human cholangiocarcinoma xenografts in nude mice. METHODS:The human cholangiocarcinoma xenograft model was established in nude mice with the QBC939 cell line.The nude mice were randomly assigned to 7 groups. 0.9%saline or magnetic nanoparticles,including high (group 2),medium(group 4)and low(group 5)dosages, were given to nude mice through the tail vein 20 days after the QBC939 cell line was implanted.Calculations were made 35 days after treatment in order to compare the volumes,inhibition ratios and growth curves of the tumors in each group.Mice in each group were sacrificed randomly to collect tumor tissues and other organs for electron microscopy and pathological examination. RESULTS:The high and medium dosage groups were significantly different from the control group(P<0.05). The tumor inhibition ratios for the high,medium and low dosage groups were 39.6%,14.6%and 7.9%,respectively. The tumor growth curve of groups 5,4,and 2 changed slowly in turn.The high and medium groups showed cell apoptosis under an electron microscope.CONCLUSION:Magnetic nanoparticles can inhibit the growth of human cholangiocarcinoma xenografts in nude mice. | Tang, Tao Zheng, Jian-Wei Chen, Bo Li, Hong Li, Xi Xue, Ke-Ying Ai, Xing Zou, Sheng-Quan | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，3： | 8 |
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