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| 1 | 城市雨洪模型应用现状及对比分析显示文摘在总结国内外城市雨洪模型研究进展的基础上,分析了适用性较好的SWMM、InfoWorksCS、MOUSE的雨洪模型在国内应用现状,从前处理程序、核心模型、数据接口等几方面将三个模型进行对比,找到各自优势与缺点,指出共同存在的问题,展望城市雨洪模型的发展前景,为现阶段国内城市雨洪模型的应用提供选择依据。 | 王海潮 陈建刚 张书函 来海亮 苏东彬 | 2011 | 水利水电技术2011，42，11： | 55 |
| 2 | Andrographolide sulfonate ameliorates lipopolysaccharide-induced acute lung injury in mice by down-regulating MAPK and NF-κB pathways显示文摘Acute lung injury(ALI) or acute respiratory distress syndrome(ARDS) is a severe, lifethreatening medical condition characterized by widespread inflammation in the lungs, and is a significant source of morbidity and mortality in the patient population. New therapies for the treatment of ALI are desperately needed. In the present study, we examined the effect of andrographolide sulfonate, a water-soluble form of andrographolide(trade name: Xi-Yan-Ping Injection), on lipopolysaccharide(LPS)-induced ALI and inflammation. Andrographolide sulfonate was administered by intraperitoneal injection to mice with LPS-induced ALI. LPS-induced airway inflammatory cell recruitment and lung histological alterations were significantly ameliorated by andrographolide sulfonate. Protein levels of pro-inflammatory cytokines in bronchoalveolar lavage fluid(BALF) and serum were reduced by andrographolide sulfonate administration. m RNA levels of pro-inflammatory cytokines in lung tissue were also suppressed. Moreover, andrographolide sulfonate markedly suppressed the activation of mitogen-activated protein kinase(MAPK) as well as p65 subunit of nuclear factor-κB(NF-κB). In summary, these results suggest that andrographolide sulfonate ameliorated LPS-induced ALI in mice by inhibiting NF-κB and MAPK-mediated inflammatory responses. Our study shows that water-soluble andrographolide sulfonate may represent a new therapeutic approach for treating inflammatory lung disorders. | Shuang Peng Nan Hang Wen Liu Wenjie Guo Chunhong Jiang Xiaoling Yang Qiang Xu Yang Sun | 2016 | Acta Pharmaceutica Sinica B2016，6，3： | 38 |
| 3 | Effect of a cancer vaccine prepared by fusions of hepatocarcinoma cells with dendritic cells显示文摘AIM To prepare a cancer vaccine (H22-DC) expressing high levels of costimulatory molecules based on fusions of hepatocarcinoma cells ( H22 ) with dendritic cells (DC) of mice and to analyze the biological characteristics and induction of specific CTL activity of H22-DC.``METHODS DCs were isolated from murine spleen by metrizamide density gradient centrifugation, purified based on its characteristics of semi-adhesion to culture plates and FcR , and were cultured in the medium containing GM. CSF and IL-4. A large number of DC were harvested. DCs were then fused with H22 cells by PEG and the fusion cells were marked with CDllc MicroBeads. The H22-DC was sorted with Mimi MACS sorter. The techniques of cell culture, immunocytochemistry and light microscopy were also used to test the characteristice of growth and morphology of H22-DC in vitro. As the immunogen, H22-DC was inoculated subcutaneously into the right armpit of BALB/C mice, and their tumorigenicity in vive was observed. MTT was used to test the CTL activity of murine spleen in vitro.``RESULTS DC cells isolated and generated were CD1 lc +cells with irregular shape, and highly expressed CD80,CD86 and CD54 molecules. H22 cells were CDllc cells with sphericel shape and bigger volume, and did not express CD80, CD86 and CD54 molecules. H22-DC was CDllc+ cells with bigger volume, being spherical, flat or irregular in shape, and highly expressed CD80, CD86 and CD54 molecules, too. H22-DC was able to divide and proliferate in vitro, but its activity of proliferation was significantly decreased as compared with H22 cells and its growth curve was flatter than H22 cells. After subcutaneous inoculation over 60 days, 1-12_2-DC showed no tumorigenecity in mice, which was significantly different from control groups (P< 0.01 ) . The spleen CTL activity against H22 cells in mice implanted with fresh H22-DC was significantly higher than control groups (P< 0.0l).``CONCLUSION H22-DC could significantly stimulate the specific CTL activity of murine spleen, which suggests that the fusion cells have already obtained the function of antigen presenting of parental DC and could present H22specific antigen which has not been identified yet, and H22-DC could induce antitumor immune response; although simply mixed H22 cells with DC could stimulate the specific CTL activity which could inhibit the growth of tumor in some degree, it could not prevent the generation of tumor. It shows that the DC vaccine is likely to become a helpful approach in immunotherapy of hepstocarcinoma. | Juan Zhang~1 Jin-Kun Zhang~2 Shao-Hong Zhuo~3 Hai-Bin Chen~2 1 Clinical Laboratory,The First Affiliated Hospital of Shantou University Medical College,Shantou 515041,Guangdong Province,China2 Cancer Pathology Laboratory,Shantou University Medical College,Shantou 515031,Guangdong Province,China3 Department of Gastroenterology,Third Municipal Hospital of Shantou,Shantou 515073,Guangdong Province,China | 2001 | World Journal of Gastroenterology2001，7，5： | 26 |
| 4 | Mutant p53 in colon cancer显示文摘The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, KRAS, TGFBR2, and TP53, whose mutations are frequently found in human colorectal cancers. Among them, the p53 mutation is found in ~60% of colorectal cancers, and a majority of mutations are missense-type at ‘hot spots’, suggesting an oncogenic role of mutant p53 by ‘gain-of-function’ mechanisms. Mouse model studies have shown that one of these missense-type mutations, p53 R270H (corresponding to human R273H), causes submucosal invasion of intestinal tumors, while the loss of wild-type p53 has a limited effect on the invasion process. Furthermore, the same mutant p53 promotes metastasis when combined with Kras activation and TGF-β suppression. Importantly, either missense-type p53 mutation or loss of wild-type p53 induces NF-κB activation by a variety of mechanisms, such as increasing promoter accessibility by chromatin remodeling, which may contribute to progression to epithelial–mesenchymal transition. These results indicate that missense-type p53 mutations together with loss of wild-type p53 accelerate the late stage of colorectal cancer progression through the activation of both oncogenic and inflammatory pathways. Accordingly, the suppression of the mutant p53 function via the inhibition of nuclear accumulation is expected to be an effective strategy against malignant progression of colorectal cancer. | Mizuho Nakayama Masanobu Oshima | 2019 | Journal of Molecular Cell Biology2019，11，4： | 22 |
| 5 | Effects of salvianolic acid B on proliferation, neurite outgrowth and differentiation of neural stem cells derived from the cerebral cortex of embryonic mice显示文摘Salvianolic acid B is isolated from Salvia miltiorrhiza,the root of which is widely used as a traditional Chinese medicine to treat stroke.However,little is known about how salvianolic acid B influences growth characteristics of neural stem cells (NSCs).The purpose of the present study was to evaluate the effects of salvianolic acid B on proliferation,neurite outgrowth and differentiation of NSCs derived from the cerebral cortex of embryonic mice using MTT,flow cytometry,immunofluorescence and RT-PCR.It was found that 20 μg mL·1 and 40 μg mL·1 salvianolic acid B had similar effects on proliferation of NSCs,and a suitable concentration of salvianolic acid B increased the number of NSCs and their derivative neurospheres.The growth-promoting activity of salvianolic acid B was dependent on and associated with an accumulation in the G2/S-phase cell population.Salvianolic acid B also promoted the neurite outgrowth of NSCs and their differentiation into neurons.The mRNA for tau,GFAP and nestin were present in differentiating neurospheres induced by salvianolic acid B.However,high-level expression of tau mRNA and low-level expression of GFAP mRNA was detected in differentiated cells,in contrast to the control conditions.This collective evidence indicates that exogenous salvianolic acid B is capable of promoting proliferation of neurospheres and differentiation towards the neuronal lineage in vitro and may act in the proliferation of NSCs and may promote NSC differentiation into neuronal cells. | GUO GuoQing1,LI Bin1,WANG YuanYuan1,SHAN AiJing1,SHEN WeiZai1,YUAN Lin2 & ZHONG ShiZhen2 1Department of Anatomy,Medical College of Jinan University,Guangzhou 510630,China 2Institute of Clinical Anatomy,Key Laboratory of Tissue Construction and Detection of Guangdong Province,Southern Medical University,Guangzhou 510150,China | 2010 | Science China(Life Sciences)2010，53，6： | 21 |
| 6 | T cell–associated immunoregulation and antiviral effect of oxymatrine in hydrodynamic injection HBV mouse model显示文摘Although oxymatrine(OMT) has been shown to directly inhibit the replication of hepatitis B virus(HBV) in vitro, limited research has been done with this drug in vivo. In the present study, the antiviral effect of OMT was investigated in an immunocompetent mouse model of chronic HBV infection.The infection was achieved by tail vein injection of a large volume of DNA solution. OMT(2.2, 6.7 and20 mg/kg) was administered by daily intraperitoneal injection for 6 weeks. The efficacy of OMT was evaluated by the levels of HBV DNA, hepatitis B surface antigen(HBs Ag), hepatitis B e antigen(HBe Ag)and hepatitis B core antigen(HBc Ag). The immunoregulatory activity of OMT was evaluated by serum ELISA and flow cytometry. Results shows that OMT at 20 mg/kg inhibited HBV replication, and it was more efficient than entecavir(ETV) in the elimination of serum HBs Ag and intrahepatic HBc Ag. Inaddition, OMT accelerated the production of interferon-γ(IFN-γ) in a dose-dependent manner in CD4^+T cells. Our findings demonstrate the beneficial effects of OMT on the enhancement of immunological function and in the control of HBV antigens. The findings suggest this drug to be a good antiviral therapeutic candidate for the treatment of HBV infection. | Xiuxiu Sang Ruilin Wang Yanzhong Han Cong’en Zhang Honghui Shen Zhirui Yang Yin Xiong Huimin Liu Shijing Liu Ruisheng Li Ruichuang Yang Jiabo Wang Xuejun Wang Zhaofang Bai Xiaohe Xiao | 2017 | Acta Pharmaceutica Sinica B2017，7，3： | 20 |
| 7 | Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer’s disease显示文摘Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived exosomes on neurogenesis and cognitive capacity in a mouse model of Alzheimer’s disease.Alzheimer’s disease mouse models were established by injection of beta amyloid 1?42 aggregates into dentate gyrus bilaterally.Morris water maze and novel object recognition tests were performed to evaluate mouse cognitive deficits at 14 and 28 days after administration.Afterwards,neurogenesis in the subventricular zone was determined by immunofluorescence using doublecortin and PSA-NCAM antibodies.Results showed that mesenchymal stem cells-derived exosomes stimulated neurogenesis in the subventricular zone and alleviated beta amyloid 1?42-induced cognitive impairment,and these effects are similar to those shown in the mesenchymal stem cells.These findings provide evidence to validate the possibility of developing cell-free therapeutic strategies for Alzheimer’s disease.All procedures and experiments were approved by Institutional Animal Care and Use Committee(CICUAL)(approval No.CICUAL 2016-011)on April 25,2016. | Edwin E. Reza-Zaldivar Mercedes A. Hernández-Sapiéns Yanet K. Gutiérrez-Mercado Sergio Sandoval-ávila Ulises Gomez-Pinedo Ana L. Márquez-Aguirre Estefanía Vázquez-Méndez Eduardo Padilla-Camberos Alejandro A. Canales-Aguirre | 2019 | Neural Regeneration Research2019，14，9： | 19 |
| 8 | Qingfei Xiaoyan Wan,a traditional Chinese medicine formula, ameliorates Pseudomonas aeruginosa–induced acute lung inflammation by regulation of PI3K/AKT and Ras/MAPK pathways显示文摘Gram-negative pathogen–induced nosocomial infections and resistance are a most serious menace to global public health. Qingfei Xiaoyan Wan(QF), a traditional Chinese medicine(TCM)formula, has been used clinically in China for the treatment of upper respiratory tract infections, acute or chronic bronchitis and pulmonary infection. In this study, the effects of QF on Pseudomonas aeruginosa–induced acute pneumonia in mice were evaluated. The mechanisms by which four typical antiinflammatory ingredients from QF, arctigenin(ATG), cholic acid(CLA), chlorogenic acid(CGA) and sinapic acid(SPA), regulate anti-inflammatory signaling pathways and related targets were investigated using molecular biology and molecular docking techniques. The results showed that pretreatment with QF significantly inhibits the release of cytokines(TNF-α and IL-6) and chemokines(IL-8 and RANTES),reduces leukocytes recruitment into inflamed tissues and ameliorates pulmonary edema and necrosis. In addition, ATG was identified as the primary anti-inflammatory agent with action on the PI3K/AKT and Ras/MAPK pathways. CLA and CGA enhanced the actions of ATG and exhibited synergistic NF-κB inactivation effects possibly via the Ras/MAPK signaling pathway. Moreover, CLA is speculated to target FGFR and MEK firstly. Overall, QF regulated the PI3K/AKT and Ras/MAPK pathways to inhibit pathogenic bacterial infections effectively. | Yuanyuan Hou Yan Nie Binfeng Cheng Jin Tao Xiaoyao Ma Min Jiang Jie Gao Gang Bai | 2016 | Acta Pharmaceutica Sinica B2016，6，3： | 17 |
| 9 | Protective links between vitamin D,inflammatory boweldisease and colon cancer显示文摘Vitamin D deficiency has been associated with a wide range of diseases and multiple forms of cancer including breast, colon, and prostate cancers. Relatively recent work has demonstrated vitamin D to be critical in immune function and therefore important in inflammatory diseases such as inflammatory bowel disease(IBD). Because vitamin D deficiency or insufficiency is increasingly prevalent around the world, with an estimated 30%-50% of children and adults at risk for vitamin D deficiency worldwide, it could have a significant impact on IBD. Epidemiologic studies suggest that low serum vitamin D levels are a risk factor for IBD and colon cancer, and vitamin D supplementation is associated with decreased colitis disease activity and/or alleviated symptoms. Patients diagnosed with IBD have a higher incidence of colorectal cancer than the general population, which supports the notion that inflammation plays a key role in cancer development and underscores the importance of understanding how vitamin D influences inflammation and its cancer-promoting effects. In addition to human epidemiological data, studies utilizing mouse models of colitis have shown that vitamin D is beneficial in preventing or ameliorating inflammation and clinical disease. The precise role of vitamin D on colitis is unknown; however, vitamin D regulates immune cell trafficking and differentiation, gut barrier function and antimicrobial peptide synthesis, all of which may be protective from IBD and colon cancer. Here we focus on effects of vitamin D on inflammation and inflammation-associated colon cancer and discuss the potential use of vitamin D for protection and treatment of IBD and colon cancer. | Stacey Meeker Audrey Seamons Lillian Maggio-Price Jisun Paik | 2016 | World Journal of Gastroenterology2016，22，3： | 15 |
| 10 | Integrative single-cell analysis of transcriptome,DNA methylome and chromatin accessibility in mouse oocytes显示文摘Oocyte growth is a key step in forming mature eggs that are ready to be fertilized.The states and modifications of chromatin represent critical sources of information for this process.However,the dynamics and interrelations of these chromatin characteristics remain elusive.In this study,we developed an improved scCOOL-seq technique (iscCOOL-seq),which is a multiomics,single-cell and single-base resolution method with high mapping rates,and explored the chromatin accessibility landscape and its relationship to DNA methylation in growing mouse oocytes.The most dramatic change in chromatin accessibility occurs during oocyte growth initiation,accompanied with prominent transcriptome alterations and an elevated variation in DNA methylation levels among individual oocytes.Unlike CpG islands (CGIs),partially methylated domains (PMDs)are associated with a low density of nucleosome-depleted regions (NDRs)during the whole maturation period.Surprisingly,highly expressed genes are usually associated with NDRs at their transcriptional end sites (TESs).In addition,genes with de novo methylated gene bodies during oocyte maturation are already open at their promoters before oocyte growth initiation.Furthermore,epigenetic and transcription factors that might be involved in oocyte maturation are identified.Our work paves the way for dissecting the complex, yet highly coordinated,epigenetic alterations during mouse oocyte growth and the establishment of totipotency. | Chan Gu Shanling Liu Qihong Wu Lin Zhang Fan Guo | 2019 | Cell Research2019，29，2： | 14 |
| 11 | Uncarboxylated osteocalcin ameliorates hepatic glucose and lipid metabolism in KKAy mice via activating insulin signaling pathway显示文摘Osteocalcin,expressed in osteoblasts of the bone marrow,undergoes post-translational carboxylation and deposits in mineralized bone matrix.A portion of osteocalcin remains uncarboxylated(uncarboxylated osteocalcin,GluOC)that is released into blood where it functions as a hormone to regulate insulin secretion and insulin sensitivity.As insulin resistance is closely associated with metabolic syndrome,this study is aimed to elucidate how GluOC regulates glucose and lipid metabolism in KKAy mice,an animal model displaying obese,hyperglycemia,hyperinsulinemia,insulin resistance,and hepatic steatosis.GluOC(3,30 ng/g per day,ig)was orally administered to female KKAy mice for 4 weeks.Whole-body insulin sensitivity,glucose metabolism,hepatic steatosis,dyslipidemia were examined using routine laboratory assays.We found that GluOC administration significantly enhanced insulin sensitivity in KKAy mice by activating hepatic IRβ/PI3K/Akt pathway and elevated the whole-body insulin sensitivity with decreased FPI and HOMA-IR index.Furthermore,GluOC administration alleviated hyperglycemia through suppressing gluconeogenesis and promoting glycogen synthesis in KKAy mice and in cultured hepatocytes in vitro.Moreover,GluOC administration dose-dependently ameliorated dyslipidemia and attenuated hepatic steatosis in KKAy mice by inhibiting hepatic de novo lipogenesis and promoting fatty-acidβ-oxidation.These results demonstrate that GluOC effectively enhances hepatic insulin sensitivity,improves hyperglycemia and ameliorates hepatic steatosis in KKAy mice,suggesting that GluOC could be a promising drug candidate for treating metabolic syndrome. | Xiao-lin Zhang Ya-nan Wang Lu-yao Ma Zhong-sheng Liu Fei Ye Jian-hong Yang | 2020 | Acta Pharmacologica Sinica2020，41，3： | 13 |
| 12 | Irisin attenuates intestinal injury,oxidative and endoplasmic reticulum stress in mice with L-arginine-induced acute pancreatitis显示文摘BACKGROUND Acute pancreatitis(AP)is often associated with intestinal injury,which in turn exaggerates the progression of AP.Our recent study has shown that a low level of serum irisin,a novel exercise-induced hormone,is associated with poor outcomes in patients with AP and irisin administration protects against experimental AP.However,the role of irisin in intestinal injury in AP has not been evaluated.AIM To investigate the effect of irisin administration on intestinal injury in experimental AP.METHODS AP was induced in male adult mice by two hourly intraperitoneal injections of Larginine.At 2 h after the last injection of L-arginine,irisin(50 or 250μg/kg body weight)or 1 mL normal saline(vehicle)was administered through intraperitoneal injection.The animals were sacrificed at 72 h after the induction of AP.Intestinal injury,apoptosis,oxidative and endoplasmic reticulum(ER)stress were evaluated.RESULTS Administration of irisin significantly mitigated intestinal damage,reduced apoptosis,and attenuated oxidative and ER stress in AP mice.In addition,irisin treatment also effectively downregulated serum tumor necrosis factor-alpha and interleukin-6 levels and alleviated injury in the pancreas,liver and lung of AP mice.CONCLUSION Irisin-mediated multiple physiological events attenuate intestinal injury following an episode of AP.Irisin has a great potential to be further developed as an effective treatment for patients with AP. | Yi-Fan Ren Meng-Zhou Wang Jian-Bin Bi Jia Zhang Lin Zhang Wu-Ming Liu Sha-Sha Wei Yi Lv Zheng Wu Rong-Qian Wu | 2019 | World Journal of Gastroenterology2019，25，45： | 12 |
| 13 | Intravoxel incoherent motion diffusion-weighted imaging for monitoring chemotherapeutic efficacy in gastric cancer显示文摘AIM: To assess intravoxel incoherent motion diffusionweighted imaging(IVIM-DWI) for monitoring early efficacy of chemotherapy in a human gastric cancer mouse model.METHODS: IVIM-DWI was performed with 12 b-values(0-800 s/mm2) in 25 human gastric cancer-bearing nude mice at baseline(day 0), and then they were randomly divided into control and 1-, 3-, 5- and 7-d treatment groups(n = 5 per group). The control group underwent longitudinal MRI scans at days 1, 3, 5 and 7, and the treatment groups underwent subsequent MRI scans after a specified 5-fluorouracil/calciumfolinate treatment. Together with tumor volumes(TV), the apparent diffusion coefficient(ADC) and IVIM parameters [true water molecular diffusion coefficient(D), perfusion fraction(f) and pseudo-related diffusion coefficient(D*)] were measured. The differences in those parameters from baseline to each measurement(ΔTV%, ΔADC%, ΔD%, Δf% and ΔD*%) were calculated. After image acquisition, tumor necrosis, microvessel density(MVD) and cellular apoptosis were evaluated by hematoxylin-eosin(HE), CD31 and terminal-deoxynucleotidyl transferase mediated nick end labeling(TUNEL) staining respectively, to confirm the imaging findings. Mann-Whitney test and Spearman's correlation coefficient analysis were performed.RESULTS: The observed relative volume increase(ΔTV%) in the treatment group were significantly smaller than those in the control group at day 5(ΔTV_(treatment)% = 19.63% ± 3.01% and ΔTVcontrol% = 83.60% ± 14.87%, P = 0.008) and day 7(ΔTV_(treatment)% = 29.07% ± 10.01% and ΔTV_(control)% = 177.06% ± 63.00%, P = 0.008). The difference in ΔTV% between the treatment and the control groups was not significant at days 1 and 3 after a short duration of treatment. Increases in ADC in the treatment group(ΔADC%_(treatment), median, 30.10% ± 18.32%, 36.11% ± 21.82%, 45.22% ± 24.36%) were significantly higher compared with the control group(ΔADC%_(control), median, 4.98% ± 3.39%, 6.26% ± 3.08%, 9.24% ± 6.33%) at days 3, 5 and 7(P = 0.008, P = 0.016, P = 0.008, respectively). Increases in D in the treatment group(ΔD%_(treatment), median 17.12% ± 8.20%, 24.16% ± 16.87%, 38.54% ± 19.36%) were higher than those in the control group(ΔD%_(control), median-0.13% ± 4.23%, 5.89% ± 4.56%, 5.54% ± 4.44%) at days 1, 3, and 5(P = 0.032, P = 0.008, P = 0.016, respectively). Relative changes in f were significantly lower in the treatment group compared with the control group at days 1, 3, 5 and 7 follow-up(median,-34.13% ± 16.61% vs 1.68% ± 3.40%, P = 0.016;-50.64% ± 6.82% vs 3.01% ± 6.50%, P = 0.008;-49.93% ± 6.05% vs 0.97% ± 4.38%, P = 0.008, and-46.22% ± 7.75% vs 8.14% ± 6.75%, P = 0.008, respectively). D* in the treatment group decreased significantly compared to those in the control group at all time points(median,-32.10% ± 12.22% vs 1.85% ± 5.54%, P = 0.008;-44.14% ± 14.83% vs 2.29% ± 10.38%, P = 0.008;-59.06% ± 19.10% vs 3.86% ± 5.10%, P = 0.008 and-47.20% ± 20.48% vs 7.13% ± 9.88%, P = 0.016, respectively). Furthermore, histopathologic findings showed positive correlations with ADC and D and tumor necrosis(r_s = 0.720, P < 0.001; r_s = 0.522, P = 0.007, respectively). The cellular apoptosis of the tumor also showed positive correlations with ADC and D(r_s = 0.626, P = 0.001; r_s = 0.542, P = 0.005, respectively). Perfusionrelated parameters(f and D*) were positively correlated to MVD(r_s = 0.618, P = 0.001; r_s = 0.538, P = 0.006, respectively), and negatively correlated to cellular apoptosis of the tumor(r_s =-0.550, P = 0.004; r_s =-0.692, P < 0.001, respectively).CONCLUSION: IVIM-DWI is potentially useful for predicting the early efficacy of chemotherapy in a human gastric cancer mouse model. | Xiao-Li Song Heoung Keun Kang Gwang Woo Jeong Kyu Youn Ahn Yong Yeon Jeong Yang Joon Kang Hye Jung Cho Chung Man Moon | 2016 | World Journal of Gastroenterology2016，22，24： | 12 |
| 14 | Current humanized mouse models for studying human immunology and HIV-1 immuno-pathogenesis显示文摘A robust animal model for 'hypothesis-testing/mechanistic' research in human immunology and immuno-pathology should meet the following criteria.First,it has well-studied hemato-lymphoid organs and target cells similar to those of humans.Second,the human pathogens establish infection and lead to relevant diseases.Third,it is genetically inbred and can be manipulated via genetic,immunological and pharmacological means.Many human-tropic pathogens such as HIV-1 fail to infect murine cells due to the blocks at multiple steps of their life cycle.The mouse with a reconstituted human immune system and other human target organs is a good candidate.A number of human-mouse chimeric models with human immune cells have been developed in the past 20 years,but most with only limited success due to the selective engraftment of xeno-reactive human T cells in hu-PBL-SCID mice or the lack of significant human immune responses in the SCID-hu Thy/Liv mouse.This review summarizes the current understanding of HIV-1 immuno-pathogenesis in human patients and in SIV-infected primate models.It also reviews the recent progress in the development of humanized mouse models with a functional human immune system,especially the recent progress in the immunodeficient mice that carry a defective gammaC gene.NOD/SCID/gammaC-/(NOG or NSG) or the Rag2-/-/gammaC-/double knockout (DKO) mice,which lack NK as well as T and B cells (NTB-null mice),have been used to reconstitute a functional human immune system in central and peripheral lymphoid organs with human CD34+ HSC.These NTB-hu HSC humanized models have been used to investigate HIV-1 infection,immuno-pathogenesis and therapeutic interventions.Such models,with further improvements,will contribute to study human immunology,human-tropic pathogens as well as human stem cell biology in the tissue development and function in vivo. | MEISSNER Eric | 2010 | Science China(Life Sciences)2010，53，2： | 11 |
| 15 | Effects of Angelica dahurica on obesity and fatty liver in mice显示文摘Angelica dahurica(A. dahurica) is a traditional Chinese medicinal plant being used in clinical practice. The present study demonstrated that A. dahurica could reduce white-fat weight in high-fat-diet hyperlipidemic mice, decrease total cholesterol and triglyceride concentrations in the livers of both high-fat-diet and Triton WR1339 induced hyperlipidemic mice, and enhance the total hepatic lipase activities of them. These findings were further supported by the results derived from the experiments with Hep G2 cells in vitro. In addition, the proteins related to lipids metabolism were investigated using LC-MS/MS, indicating that genes of lipid metabolism and lipid transport were regulated by A. dhurica. The results from LC-MS/MS were further conformed by Western blot and real time PCR assays. A. dahurica could down-regulate the expression of catalase(CAT) and sterol carrier protein2(SCP2) and up-regulate the expression of lipid metabolism related genes-lipase member C(LIPC) and peroxisome proliferator-activated receptor gamma(PPARγ). In the Triton WR1339 mouse liver and Hep G2 cells in vitro, A. dahurica was able to increase the expression of LIPC and PPARγ, confirming the results from in vivo experiments. Imperatorin showed the same activity as A. dahurica, suggesting it was one of the major active ingredients of the herb. In conclusion, our work represented a first investigation demonstrating that A. dahurica was able to regulate lipid metabolism and could be developed as a novel approach to fighting against fatty liver and obesity. | LU Xi YUAN Zhi-Yi YAN Xiao-Jin LEI Fan JIANG Jing-Fei YU Xuan YANG Xiu-Wei XING Dong-Ming DU Li-Jun | 2016 | Chinese Journal of Natural Medicines2016，14，9： | 11 |
| 16 | Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts via upregulating metastasis associated protein 3显示文摘Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction(TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II(AngII). Emodin upregulated expression of metastasis associated protein 3(MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis;in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis via upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis. | Dan Xiao Yue Zhang Rui Wang Yujie Fu Tong Zhou Hongtao Diao Zhixia Wang Yuan Lin Zhange Li Lin Wen Xujuan Kang Philipp Kopylov Dmitri Shchekochikhin Yong Zhang Baofeng Yang | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 11 |
| 17 | E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo显示文摘AIM: To evaluate the influence of E2F-1 on the growth of human gastric cancer(GC) cells in vivo and the mechanism involved. METHODS: E2F-1 recombinant lentiviral vectors were injected into xenograft tumors of MGC-803 cells in nude mice, and then tumor growth was investigated. Overexpression of transcription factor E2F-1 was assessed by reverse transcription-polymerase chain reaction(RT-PCR) and Western blotting analysis. Apoptosis rates were determined using a terminal deoxynucleotidyl transferase-mediated d UTP-biotin nick end labeling(TUNEL) assay. Expression levels of certain cell cycle regulators and apoptosis-related proteins, such as Bax, survivin, Bcl-2, cyclin D1, S-phase kinaseassociated protein 2, and c-Myc were examined by Western blotting and RT-PCR. RESULTS: Xenograft tumors of MGC-803 cells in nude mice injected with E2F-1 recombinant lentiviral vectors stably overexpressed the E2F-1 gene as measured by semi-quantitative RT-PCR(relative m RNA expression: 0.10 ± 0.02 vs 0.05 ± 0.02 for control vector and 0.06 ± 0.03 for no infection; both P < 0.01) and Western blotting(relative protein expression: 1.90 ± 0.05 vs 1.10 ± 0.03 in control vector infected and 1.11 ± 0.02 for no infection; both P < 0.01). The growth-curve of tumor volumes revealed that infection with E2F-1 recombinant lentiviral vectors significantly inhibited the growth of human GC xenografts(2.81 ± 1.02 vs 6.18 ± 1.15 in control vector infected and 5.87 ± 1.23 with no infection; both P < 0.05) at 15 d after treatment. TUNEL analysis demonstrated that E2F-1 overexpression promoted tumor cell apoptosis(18.6% ± 2.3% vs 6.7% ± 1.2% in control vector infected 6.3% ± 1.2% for no infection; both P < 0.05). Furthermore, lentiviral vector-mediated E2F-1 overexpression increased theexpression of Bax and suppressed survivin, Bcl-2, cyclin D1, Skp2, and c-Myc expression in tumor tissue.CONCLUSION: E2F-1 inhibits growth of GC cells via regulating multiple signaling pathways, and may play an important role in targeted therapy for GC. | Wei-Yuan Wei Lin-Hai Yan Xiao-Tong Wang Lei Li Wen-Long Cao Xiao-Shi Zhang Ze-Xu Zhan Han Yu Yu-Bo Xie Qiang Xiao | 2015 | World Journal of Gastroenterology2015，21，2： | 10 |
| 18 | TLR4-HMGB1-, MyD88- and TRIF-dependent signaling in mouse intestinal ischemia/reperfusion injury显示文摘AIM: To characterize high-mobility group protein 1-toll-like receptor 4(HMGB1-TLR4) and downstream signaling pathways in intestinal ischemia/reperfusion(I/R) injury.METHODS: Forty specific-pathogen-free male C57BL/6 mice were randomly divided into five groups(n = 8 per group): sham, control, anti-HMGB1, anti-myeloid differentiation gene 88(My D88), and anti-translocatingchain-associating membrane protein(TRIF) antibody groups. Vehicle with the control Ig G antibody, antiHMGB1, anti-My D88, or anti-TRIF antibodies(all 1 mg/kg, 0.025%) were injected via the caudal vein 30 min prior to ischemia. After anesthetization, the abdominal wall was opened and the superior mesenteric artery was exposed, followed by 60 min mesenteric ischemia and then 60 min reperfusion. For the sham group, the abdominal wall was opened for 120 min without I/R. Levels of serum nuclear factor(NF)-κB p65, interleukin(IL)-6, and tumor necrosis factor(TNF)-α were measured, along with myeloperoxidase activity in the lung and liver. Inaddition,morphologic changes that occurred in the lung and intestinal tissues were evaluated. Levels of m RNA transcripts encoding HMGB1 and NF-κB were measured by real-time quantitative PCR, and levels of HMGB1 and NF-κB protein were measured by Western blot. Results were analyzed using one-way analysis of variance.RESULTS: Blocking HMGB 1, MyD 8 8, and TRIF expression by injecting anti-HMGB1, anti-My D88, or anti-TRIF antibodies prior to ischemia reduced the levels of inflammatory cytokines in serum; NF-κB p65: 104.64 ± 11.89, 228.53 ± 24.85, 145.00 ± 33.63, 191.12 ± 13.22, and 183.73 ± 10.81(P < 0.05); IL-6: 50.02 ± 6.33, 104.91 ± 31.18, 62.28 ± 6.73, 85.90 ± 17.37, and 78.14 ± 7.38(P < 0.05); TNF-α, 43.79 ± 4.18, 70.81 ± 6.97, 52.76 ± 5.71, 63.19 ± 5.47, and 59.70 ± 4.63(P < 0.05) for the sham, control, anti-HMGB1, anti-My D88, and anti-TRIF groups, respectively(all in pg/m L).Antibodies also alleviated tissue injury in the lung and small intestine compared with the control group in the mouse intestinal I/R model. The administration of antiHMGB1, anti-My D88, and anti-TRIF antibodies markedly reduced damage caused by I/R, for which anti-HMGB1 antibody had the most obvious effect.CONCLUSION: HMGB1 and its downstream signaling pathway play important roles in the mouse intestinal I/R injury, and the effect of the TRIF-dependent pathway is slightly greater. | Jie Wang Gui-Zhen He Yu-Kang Wang Qian-Kun Zhu Wei Chen Tai Guo | 2015 | World Journal of Gastroenterology2015，21，27： | 10 |
| 19 | Effects of urotensin-Ⅱ on cytokines in early acute liver failure in mice显示文摘AIM:To investigate urotensin-Ⅱ(UⅡ) and its effects on tumor necrosis factor(TNF)-α and interleukin(IL)-1β in early acute liver failure(ALF).METHODS:We investigated the time-dependent alteration in UⅡ levels and its effects on TNF-αand IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF.RESULTS:After lipopolysaccharide/D-galactosamine challenge,UⅡ rose very rapidly and reached a maximal level 0.5 h,and the level remained significantly elevated after 2 h(P < 0.05).Six hours after challenge,UⅡ began to degrade,but remained higher than at 0 h(P < 0.05).Pretreatment with urantide,an inhibitor of the UⅡ receptor,suppressed the degree of UⅡ increase in liver and blood at 6 h after challenge(P < 0.05 vs paired controls).In addition,liver and blood TNF-α increased from 1 to 6 h,and reached a peak at 1 and 2 h,respectively; however,IL-1β did not rise until 6 h after challenge.Urantide pretreatment inhibited the degree of TNF-α and IL-1β increase following downregulation of UⅡ post-challenge(all P < 0.05).CONCLUSION:UⅡ plays a role in the pathogenesis and priming of ALF by triggering an inflammatory cascade and driving the early release of cytokines in mice. | Liang-Ming Liu Liang Zhao Dong-Yu Liang Fang-Ping Yu Chang-Gen Ye Wen-Juan Tu Tong Zhu | 2015 | World Journal of Gastroenterology2015，21，11： | 9 |
| 20 | GABAergic Abnormalities Associated with Sensorimotor Corticostriatal Community Structural Deficits in ErbB4 Knockout Mice and First-Episode Treatment-Naive Patients with Schizophrenia显示文摘The current study was designed to explore how disruption of specific molecular circuits in the cerebral cortex may cause sensorimotor cortico-striatal community structure deficits in both a mouse model and patients with schizophrenia.We used prepulse inhibition(PPI)and brain structural and diffusion MRI scans in 23 mice with conditional ErbB4 knockout in parvalbumin interneurons and 27 matched controls.Quantitative real-time PCR was used to assess the differential levels of GABA-related transcripts in brain regions.Concurrently,we measured structural and diffusion MRI and the cumulative contribution of risk alleles in the GABA pathway genes in firstepisode treatment-naı¨ve schizophrenic patients(n=117)and in age-and sex-matched healthy controls(n=86).We present the first evidence of gray and white matter impairment of right sensorimotor cortico-striatal networks and reproduced the sensorimotor gating deficit in a mouse model of schizophrenia.Significant correlations between gray matter volumes(GMVs)in the somatosensory cortex and PPI as well as glutamate decarboxylase 1 mRNA expression were found in controls but not in knockout mice.Furthermore,these findings were confirmed in a human sample in which we found significantly decreased gray and white matter in sensorimotor cortico-striatal networks in schizophrenic patients.The psychiatric risk alleles of the GABA pathway also displayed a significant negative correlation with the GMVs of the somatosensory cortex in patients.Our study identified that ErbB4 ablation in parvalbumin interneurons induced GABAergic dysregulation,providing valuable mechanistic insights into the sensorimotor cortico-striatal community structure deficits associated with schizophrenia. | Chengcheng Zhang Peiyan Ni Yikang Liu Yang Tian Jinxue Wei Bo Xiang Liansheng Zhao Xiaojing Li Xiaohong Ma Wei Deng Wanjun Guo Rongjun Ni Yamin Zhang Qiang Wang Hailiang Huang Nanyin Zhang Tao Li | 2020 | Neuroscience Bulletin2020，36，2： | 9 |
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