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Establishment and drug sensitivity evaluation of murine ascites hepatocarcinoma cell line with high lymphatic

Hongying ZHANG, Jianwu TANG, Wenting ZHU, Chunxiu HU, Guowang XU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 119-129 doi: 10.1007/s11684-009-0022-9

摘要： In order to provide a sensitive cell line model for investigating the mechanisms underlying the lymphatic metastasis of tumors and the effect of medicine against cells, a new murine ascites hepatocarcinoma cell line with high lymphatic metastatic potential (Hca-P/L ) was established and the effect of curcumin on biological behavior of Hca-P/L was observed. Murine ascites hepatocarcinoma cell strain with low lymphatic metastatic potential (Hca-P) was subcutaneously inoculated into the medioventral line of a mouse 615 and the first generation of metastatic tumor cells of inguinal lymph node (Hca-P/L ) was obtained. Then, Hca-P/L was screened by the route of mouse foot pad subcutaneously → lymph node → scale-up culture → mouse foot pad subcutaneously for five times consecutively. The sensitivity of two murine ascites hepatocarcinoma cell lines (Hca-P and Hca-P/L ) and two anchorage-dependent human hepatocarcinoma cell lines (SMC7721 and HepG ) to curcumin were studied by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after these cells had been pretreated by curcumin at the concentration of 15-240 μmol/L for 48 h. After pretreatment by curcumin at the maximum non-cytotoxic dose of 15 μmol/L , the effect of curcumin against cell proliferation of Hca-P and Hca-P/L was observed by inverted microscope, cell growth curve and cell population doubling time; the effects of curcumin on cell cycles of Hca-P/L and Hca-P were studied by flow cytometry (FCM). The results showed Hca-P/L spreading to the lymph nodes at multiple sites in mice was screened from Hca-P. The lymph node metastatic rate was 100%. Curcumin had significant growth inhibiting effect on both murine ascites and human hepatocarcinoma cell lines in a dose-dependent manner ( <0. 05). At concentrations of 30-120 μmol/L, curcumin had more inhibition on murine ascites hepatocarcinoma cell lines than on human anchorage-dependent hepatocarcinoma cell lines. At concentrations of 60-240 μmol/L, curcumin had more inhibition on Hca-P/L with (the 50% inhibitory concentration) IC of 51.48 μmol/L than on Hca-P with IC of 90.87 μmol/L. After pretreatment by curcumin at the maximum non-cytotoxic dose of 15 mol/L for 7 days, the proliferations of Hca-P/L and Hca-P were inhibited ( <0.05) in a time-dependent manner ( <0.01) and the population doubling time of Hca-P/L and Hca-P was prolonged ( <0.01), and curcumin had more inhibition on Hca-P/L than on Hca-P ( <0.05). After pretreatment by 15 μmol/L curcumin for 48 h, the morphous of Hca-P/L was influenced more seriously than that of Hca-P and the cell cycle was redistributed with Hca-P/L being blocked in the S phase and Hca-P in the S and G /M phases. Hca-P/L was validated to be more sensitive to curcumin than Hca-P. Hca-P/L is a novel sensitive cell line model for investigating the mechanisms underlying tumor lymphatic metastasis and the effect of the medicine against cells.

关键词： murine ascites hepatocarcinoma cell line     metastasis     curcumin     drug sensitivity    

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Gene and protein expression of proteinase-activated receptor-1, 2 in a murine model of acute graft host

Quan LI MD , Weiming LI MD , Ping ZOU MD , Jian ZHANG BM ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 309-315 doi: 10.1007/s11684-009-0043-4

摘要： Proteinase-activated receptors (PARs) are a novel subclass of seven transmembrane-spanning, G protein-coupled receptors. PAR-1 and PAR-2 are widely expressed in a variety of cells and are found to be involved in many physiological and pathological processes including inflammation and immune response. However, little is known about the function of PAR-1, 2 in acute graft host disease (GVHD). In the present study, we first detected the expression of PAR-1, 2 protein and mRNA in a murine model of acute GVHD using the methods of immunohistochemistry, Western blot and quantitative real-time polymerase chain reaction (PCR). Syngeneic hematopoietic stem cell transplantation (HSCT) mice served as controls. The relative gene expression level of PAR-1 was significantly increased in the skin, liver, small intestine of allogeneic HSCT mice (in skin: 0.039±0.013 0.008±0.002 of controls, =0.009; in liver: 0.165±0.006 0.017±0.006 of controls, =0.004; in small intestine: 0.215±0.009 0.016±0.002 of controls, =0.003), but not in the stomach, lung and kidney of allogeneic HSCT mice (>0.05). PAR-2 mRNA expression in the liver and small intestine of allogeneic HSCT mice (in liver: 0.010±0.002 0.003±0.001 of controls, =0.008; in small intestine: 0.006±0.001 0.003±0.001 of controls, =0.024) was increased significantly, but PAR-2 mRNA expression in the other organs (>0.05) was not found to be significantly elevated. PAR-1, 2 protein expression was in accordance with the mRNA expression, as shown by Western blot. Using immunohistochemistry the present study demonstrated that there was strong PAR-1, 2 immunoreactivity in the epithelial cell and vascular endothelial cell of target organs of acute GVHD. Our findings of markedly increased expression of PAR-1, 2 in target organs of acute GVHD suggest that PAR-1 and PAR-2 may play an important role in the pathogenesis of acute GVHD.

关键词： graft vs host disease     proteinase-activated receptor     murine model     hematopoietic stem cell transplantation    

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Serum mitochondrial tsRNA serves as a novel biomarker for hepatocarcinoma diagnosis

《医学前沿（英文）》 2022年 第16卷 第2期   页码 216-226 doi: 10.1007/s11684-022-0920-7

摘要： Hepatocellular carcinoma (HCC), which makes up the majority of liver cancer, is induced by the infection of hepatitis B/C virus. Biomarkers are needed to facilitate the early detection of HCC, which is often diagnosed too late for effective therapy. The tRNA-derived small RNAs (tsRNAs) play vital roles in tumorigenesis and are stable in circulation. However, the diagnostic values and biological functions of circulating tsRNAs, especially for HCC, are still unknown. In this study, we first utilized RNA sequencing followed by quantitative reverse-transcription PCR to analyze tsRNA signatures in HCC serum. We identified tRF-Gln-TTG-006, which was remarkably upregulated in HCC serum (training cohort: 24 HCC patients vs. 24 healthy controls). In the validation stage, we found that tRF-Gln-TTG-006 signature could distinguish HCC cases from healthy subjects with high sensitivity (80.4%) and specificity (79.4%) even in the early stage (Stage I: sensitivity, 79.0%; specificity, 74.8%; 155 healthy controls vs. 153 HCC patients from two cohorts). Moreover, in vitro studies indicated that circulating tRF-Gln-TTG-006 was released from tumor cells, and its biological function was predicted by bioinformatics assay and validated by colony formation and apoptosis assays. In summary, our study demonstrated that serum tsRNA signature may serve as a novel biomarker of HCC.

关键词： tsRNA     biomarker     hepatocarcinoma    

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Impact of siRNA targeting pirh2 on proliferation and cell cycle control of the lung adenocarcinoma cellline A549

SU Yuan, JIN Yang, ZHANG Xiaoju, ZHOU Qiong, BAI Ming, ZHU Liping

《医学前沿（英文）》 2007年 第1卷 第4期   页码 359-363 doi: 10.1007/s11684-007-0069-4

摘要： The aim of this study was to investigate the role of pirh2 (p53-induced RING-H2) protein in the proliferation, apoptosis and cell cycle control of the lung cancer cell line A549. Pirh2 expression was detected by immunofluorescence, Western blot analysis and real-time polymerase chain reaction (PCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8). Cell cycle control and apoptosis were analyzed by flow cytometry. The results showed that pirh2 was expressed in the cytoplasm of A549 cells. The inhibition of pirh2 expression by siRNA (psiRNA-pirh2) resulted in reduced cell proliferation and increased apoptosis. In addition, the number of G/G phase cells was increased but G/M cells were not affected significantly. Taken together, the inhibition of pirh2 expression in the lung adenocarcinoma cell line A549 resulted in reduced tumor cell growth via the inhibition of cell proliferation, the activation of apoptosis and the interruption of cell cycle transition.

关键词： control     interruption     cytoplasm     number     growth    

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Natural killer cell lines in tumor immunotherapy

null

《医学前沿（英文）》 2012年 第6卷 第1期   页码 56-66 doi: 10.1007/s11684-012-0177-7

摘要：

Natural killer (NK) cells are considered to be critical players in anticancer immunity. However, cancers are able to develop mechanisms to escape NK cell attack or to induce defective NK cells. Current NK cell-based cancer immunotherapy is aimed at overcoming NK cell paralysis through several potential approaches, including activating autologous NK cells, expanding allogeneic NK cells, usage of stable allogeneic NK cell lines and genetically modifying fresh NK cells or NK cell lines. The stable allogeneic NK cell line approach is more practical for quality-control and large-scale production. Additionally, genetically modifying NK cell lines by increasing their expression of cytokines and engineering chimeric tumor antigen receptors could improve their specificity and cytotoxicity. In this review, NK cells in tumor immunotherapy are discussed, and a list of therapeutic NK cell lines currently undergoing preclinical and clinical trials of several kinds of tumors are reviewed.

关键词： natural killer cell     natural killer cell line     tumor immunotherapy     genetic modification    

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Anlotinib as third- or further-line therapy for short-term relapsed small-cell lung cancer: subgroup

《医学前沿（英文）》 2022年 第16卷 第5期   页码 766-772 doi: 10.1007/s11684-021-0916-8

摘要： Patients with small-cell lung cancer (SCLC) relapse within months after completing previous therapies. This study aimed to investigate the efficacy and safety of anlotinib as third- or further-line therapy in patients with short-term relapsed SCLC from ALTER1202. Patients with short-term relapsed SCLC (disease progression within 3 months after completing ≥ two lines of chemotherapy) in the anlotinib (n = 67) and placebo (n = 34) groups were analyzed. The primary endpoint was progression-free survival (PFS). The secondary endpoints included overall survival, objective response rate (ORR), disease control rate, and safety. Anlotinib significantly improved median PFS/OS (4.0 vs. 0.7 months, P < 0.0001)/(7.3 vs. 4.4 months, P = 0.006) compared with placebo. The ORR was 4.5%/2.9% in the anlotinib/placebo group (P = 1.000). The DCR in the anlotinib group was higher than that in the placebo group (73.1% vs. 11.8%, P < 0.001). The most common adverse events (AEs) were hypertension (38.8%), loss of appetite (28.4%), and fatigue (22.4%) in the anlotinib group and gamma-glutamyl transpeptidase elevation (20.6%) in the placebo group. No grade 5 AEs occurred. For patients with short-term relapsed SCLC, third- or further-line anlotinib treatment was associated with improved survival benefit. Further studies are warranted in this regard.

关键词： anlotinib     chemotherapy     short-term relapsed     small-cell lung cancer    

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Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cellline via ERKs pathway

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

《医学前沿（英文）》 2010年 第4卷 第1期   页码 106-111 doi: 10.1007/s11684-010-0004-y

摘要： Hepatitis B virus X protein (HBx), a 17-kd protein encoded by X gene of hepatitis B virus (HBV), has been shown to function as a transcriptional trans-activator of a variety of viral and cellular promoter/enhancer elements. The aim of the study is to investigate the extracellular regulated protein kinases (ERKs) pathway of HBx on glomerular mesangial cell (GMC) proliferation and tumor necrosis factor-α (TNF-α) expression. The HBV X gene was amplified by polymerase chain reaction (PCR), inserted into the eukaryotic expression vector pCI-neo and confirmed by restriction endonuclease digestion and sequence analysis. PCI-neo containing HBV X gene (pCI-neo-X) was then transfected into cultured GMC line via liposome. GMC proliferation, TNF-α and its mRNA expression were compared in the condition of with or without U0126 in culture media. HBx, ERK and p-ERK expression in GMCs was assessed by Western blotting. TNF-α mRNA expression was assessed by semi-quantitative reverse transcription-PCR (RT-PCR). TNF-α level in supernatants was measured by ELISA. GMC proliferation was detected by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) kit. The results showed that HBx expression was found in transfected GMCs and became prominent at 36th and 48th h after transfection whether with or without U0126 in culture media. TNF-α mRNA expression was significantly decreased in U0126 group compared with U0126-free group. TNF-α levels in supernatants in PCI-neo-X transfection without U0126 group were (189.0±18.1) and (172.3±24.3) pg/mL at 36th and 48th h after transfection, respectively. In contrast, TNF-α levels in supernatants with U0126 were (65.6±11.6) and (84.0±24.6) pg/mL at 36th and 48th h, respectively. The TNF-α levels in the latter groups were significantly lower than those in the former groups (<0.05). GMCs proliferation was also lower in added U0126 group at 36th and 48th h after transfection. From above, we can conclude that HBx could induce GMC proliferation and increase TNF-α mRNA expression and its protein production. HBx upregulates TNF-α expression and induces cell proliferation of GMC line partly through ERK signal transduction pathway.

关键词： hepatitis B virus     X gene     glomerular mesangial cell line     extracellular regulated protein kinases     tumor necrosis factor-α    

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myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission and Ca homeostasis in a murine

《医学前沿（英文）》 doi: 10.1007/s11684-023-0983-0

摘要： Berberine alleviates myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission and Ca homeostasis in a murine model of HFpEF

关键词： mitochondrial fission Ca     Berberine alleviates myocardial     murine model HFpEF    

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Inhibition of NF-kappa B can enhance Fas-mediated apoptosis in leukemia cell line HL-60

Li WANG, Shi ZHAO, Hong-Xiang WANG, Ping ZOU

《医学前沿（英文）》 2010年 第4卷 第3期   页码 323-328 doi: 10.1007/s11684-010-0026-5

摘要： This study explored the effects of nuclear factor-kappa B (NF-κB) inhibitor Bay 11-7082 on Fas/FasL system and Fas-mediated apoptosis in cell line HL-60 cells. The mRNA and protein levels of Fas, FasL, and X-linked inhibitor of apoptosis protein (XIAP) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry (FCM); the level of sFasL was evaluated by enzyme-linked immunosorbent assay (ELISA); and apoptosis was determined by FCM. After treatment with Bay 11-7082, the mRNA and protein levels of FasL and XIAP in HL-60 cells were significantly lower than in the controls ( <0.05), but the mRNA and protein levels of Fas and sFasL did not change significantly ( >0.05). Apoptotic rate of HL-60 cells treated with Bay 11-7082 was significantly higher than in the controls ( <0.05). Therefore, we conclude that Bay 11-7082 can enhance Fas-mediated apoptosis in HL-60 cells by downregulating FasL and XIAP levels.

关键词： nuclear factor-kappa B     Fas/FasL system     HL-60     Bay 11-7082    

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4-1BBL expressed by eukaryotic cells activates immune cells and suppresses the progression of murine

Hui QIU, Hui ZHANG, Zuohua FENG

《医学前沿（英文）》 2009年 第3卷 第1期   页码 20-25 doi: 10.1007/s11684-009-0006-9

摘要： The interaction by co-stimulatory molecules 4-1BB and 4-1BB ligand (4-1BBL) plays an important role in the activation, proliferation and differentiation of T lymphocytes. The function of 4-1BB/4-1BBL expressed by the immune cells has been the focus for many tumor immunotherapy efforts. In this study, 4-1BBL was expressed in non-immune cells and non-tumor cells, and the role of 4-1BBL in lymphocyte activation and tumor suppression was investigated. The plasmid p4-1BBL containing the full length of mouse 4-1BBL cDNA sequence was constructed, and the plasmid was transfected into baby hamster kidney (BHK) cells and murine muscle cells by means of lipofectin-mediated or naked plasmid DNA injection into the muscle directly. The study demonstrated that the molecule 4-1BBL expressed by BHK cells could enhance the proliferation and cytotoxicity of lymphocytes, and it could increase the expression level of IL-2 and IFN-γ. The treatment with plasmid p4-1BBL revealed that the number of CD8 T cells in the peri-tumoral tissue increased markedly, and the growth rate of the tumor was significantly lower than that of control group. These findings suggest that expression of 4-1BBL by normal cells in the tumor microenvironment can enhance the proliferation and other functions of T lymphocytes. This therapeutic method may provide a promising approach for tumor immunotherapy.

关键词： 4-1BB ligand     tumor immunotherapy     tumor microenvironment    

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Blockage of receptor-interacting protein 2 expression by small interfering RNA in murine macrophages

LIU Hongchun, CAO Zhongwei, JIN Jianjun, WANG Jiyao

《医学前沿（英文）》 2008年 第2卷 第2期   页码 166-170 doi: 10.1007/s11684-008-0030-1

摘要： This study aims to demonstrate that blocking the receptor-interacting protein2 (Rip2) expression can decrease inflammatory cytokine production by macrophage and protect mice from endotoxin lethality. Murine Rip2 small interfering RNA (siRNA) plasmids were constructed and transfected into macrophage and Rip2 expression was detected with reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Cell proliferation was assayed with MTT. TNF-? concentration was assayed with ELISA and high-mobility group box 1 protein (HMGB1) level with semi-quantitative western blot after lipopolysaccharide (LPS) stimulation. LPS challenge was given after the plasmids were injected into mice and the survival rate was calculated. Rip2 siRNA plasmid could block the mRNA and protein expression of Rip2 and promote cell proliferation. Blocking Rip2 could attenuate LPS-induced TNF-? and HMGB1 production. The HMGB1 expression in the liver decreased to (40.21 ± 11.03) pg/g, and serum TNF-? level decreased to (300.43 ± 59.26) ng/L ( < 0.05). The survival rate of mice from endotoxemia was also improved ( < 0.05). The results demonstrate that Rip2 siRNA plasmid can block the expression of Rip2, decrease the production of TNF-? and HMGB1 and protect mice from fatal endotoxemia.
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Immunotherapeutic effects on murine pancreatic carcinoma by β-elemene combined with dendritic cells modified

TAN Guang, WANG Zhongyu, CHE Luanqing, YIN Shuo

《医学前沿（英文）》 2007年 第1卷 第1期   页码 41-45 doi: 10.1007/s11684-007-0008-4

摘要： The dendritic cell vaccine is a treatment vaccine with potent clinical applications. Functional cytokines can enhance dendritic cell anti-tumor immune responses. This experiment was conducted to study the effects of bone marrow-deriv

关键词： Functional     experiment     anti-tumor     dendritic     clinical    

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transporter 2 genes for increased retention of metaiodobenzylguanidine labeled with iodine 131 in malignant hepatocarcinoma

null

《医学前沿（英文）》 2017年 第11卷 第1期   页码 120-128 doi: 10.1007/s11684-017-0501-3

摘要：

Norepinephrine transporter (NET) transfection leads to significant uptake of iodine-131-labeled metaiodobenzylguanidine (131I-MIBG) in non-neuroendocrine tumors. However, the use of 131I-MIBG is limited by its short retention time in target cells. To prolong the retention of 131I-MIBG in target cells, we infected hepatocarcinoma (HepG2) cells with Lentivirus-encoding human NET and vesicular monoamine transporter 2 (VMAT2) genes to obtain NET-expressing, NET-VMAT2-coexpressing, and negative-control cell lines. We evaluated the uptake and efflux of 131I-MIBG both in vitro and in vivo in mice bearing transfected tumors. NET-expressing and NET-VMAT2-coexpressing cells respectively showed 2.24 and 2.22 times higher 131I-MIBG uptake than controls. Two hours after removal of 131I-MIBG-containing medium, 25.4% efflux was observed in NET-VMAT2-coexpressing cells and 38.6% in NET-expressing cells. In vivo experiments were performed in nude mice bearing transfected tumors; results revealed that NET-VMAT2-coexpressing tumors had longer 131I-MIBG retention time than NET-expressing tumors. Meanwhile, NET-VMAT2-coexpressing and NET-expressing tumors displayed 0.54% and 0.19%, respectively, of the injected dose per gram of tissue 24 h after 131I-MIBG administration. Cotransfection of HepG2 cells with NET and VMAT2resulted in increased 131I-MIBG uptake and retention. However, the degree of increase was insufficient to be therapeutically effective in target cells.

关键词： norepinephrine transporter     vesicular monoamine transporter 2     -MIBG     gene therapy     lentivirus vector    

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Investigation on the mechanism of ginsenoside Rg3 in treating murine primary mammary tumor

Hongbo TANG MD, Zirong YE MM, Yuping REN MD, Zhanyong ZHU MD, Yiping WU MD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 421-425 doi: 10.1007/s11684-009-0078-6

摘要： A murine primary mammary tumor model was established to investigate the treatment with ginsenosides Rg3. The relationship between ginsenosides Rg3 and primary mammary tumor was explored. Mammary tumor was induced by using the 7,12-dimethybenz(a)anthracene (DMBA). Ginsenoside Rg3 was employed for treatment. The incidence of mammary tumor in every group was compared, and the expressions of vascular endothelial growth factor (VEGF) and microvessel density (MVD) were detected by immunohistochemical method. The cell cycle and apoptosis percentage were determined by means of flow cytometry. The incidence of tumor in treatment group was significantly lower than that in control group (60.00% 33.33%, <0.05). The average diameter of mammary tumor was (0.86±0.27) cm in control group and (0.39±0.09) cm in treatment group, with the difference being significant between control and treatment groups (<0.01). The MVD value was (31.9±5.3) in control group and (20.1±4.9) in treatment group, respectively. There was a significant difference between the two groups (<0.05). The apoptosis percentage in control group was significantly lower than that in treatment group [(2.47±0.69)% (5.67±0.99)%, <0.05]. Ginsenoside Rg3 can play an antitumor role in primary mammary tumor model by inhibiting angiogenesis, cell cycle progression, and promoting cell apoptosis.

关键词： ginsenoside Rg3     mammary tumor     mice    

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Acoustic fault signal extraction via the line-defect phononic crystals

《机械工程前沿（英文）》 2022年 第17卷 第1期   页码 10-10 doi: 10.1007/s11465-021-0666-y

摘要： Rotating machine fault signal extraction becomes increasingly important in practical engineering applications. However, fault signals with low signal-to-noise ratios (SNRs) are difficult to extract, especially at the early stage of fault diagnosis. In this paper, 2D line-defect phononic crystals (PCs) consisting of periodic acrylic tubes with slit are proposed for weak signal detection. The defect band, namely, the formed resonance band of line-defect PCs enables the incident acoustic wave at the resonance frequency to be trapped and enhanced at the resonance cavity. The noise can be filtered by the band gap. As a result, fault signals with high SNRs can be obtained for fault feature extraction. The effectiveness of weak harmonic and periodic impulse signal detection via line-defect PCs are investigated in numerical and experimental studies. All the numerical and experimental results indicate that line-defect PCs can be well used for extracting weak harmonic and periodic impulse signals. This work will provide potential for extracting weak signals in many practical engineering applications.

关键词： phononic crystals     line-defect     fault signal extraction     acoustic enhancement    

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标题 作者 时间 类型 操作

Establishment and drug sensitivity evaluation of murine ascites hepatocarcinoma cell line with high lymphatic

Hongying ZHANG, Jianwu TANG, Wenting ZHU, Chunxiu HU, Guowang XU

期刊论文

Gene and protein expression of proteinase-activated receptor-1, 2 in a murine model of acute graft host

Quan LI MD , Weiming LI MD , Ping ZOU MD , Jian ZHANG BM ,

期刊论文

Serum mitochondrial tsRNA serves as a novel biomarker for hepatocarcinoma diagnosis

期刊论文

Impact of siRNA targeting pirh2 on proliferation and cell cycle control of the lung adenocarcinoma cellline A549

SU Yuan, JIN Yang, ZHANG Xiaoju, ZHOU Qiong, BAI Ming, ZHU Liping

期刊论文

Natural killer cell lines in tumor immunotherapy

null

期刊论文

Anlotinib as third- or further-line therapy for short-term relapsed small-cell lung cancer: subgroup

期刊论文

Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cellline via ERKs pathway

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

期刊论文

myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission and Ca homeostasis in a murine

期刊论文

Inhibition of NF-kappa B can enhance Fas-mediated apoptosis in leukemia cell line HL-60

Li WANG, Shi ZHAO, Hong-Xiang WANG, Ping ZOU

期刊论文

4-1BBL expressed by eukaryotic cells activates immune cells and suppresses the progression of murine

Hui QIU, Hui ZHANG, Zuohua FENG

期刊论文

Blockage of receptor-interacting protein 2 expression by small interfering RNA in murine macrophages

LIU Hongchun, CAO Zhongwei, JIN Jianjun, WANG Jiyao

期刊论文

Immunotherapeutic effects on murine pancreatic carcinoma by β-elemene combined with dendritic cells modified

TAN Guang, WANG Zhongyu, CHE Luanqing, YIN Shuo

期刊论文

transporter 2 genes for increased retention of metaiodobenzylguanidine labeled with iodine 131 in malignant hepatocarcinoma

null

期刊论文

Investigation on the mechanism of ginsenoside Rg3 in treating murine primary mammary tumor

Hongbo TANG MD, Zirong YE MM, Yuping REN MD, Zhanyong ZHU MD, Yiping WU MD,

期刊论文

Acoustic fault signal extraction via the line-defect phononic crystals

期刊论文