ABSTRACT
There have been many clinical trials, systematic reviews/Meta-analysis proving that Xingnaojing Injection has a good clinical efficacy in treatment of cerebral ischaemic stroke, but with fewer comprehensive descriptions. In this study, an overview of systematic reviews/Meta-analysis of Xingnaojing Injection in treating cerebral ischaemic stroke was performed to provide current situation of evidences and basis for clinical practice. CNKI, Wanfang, VIP, CBM, EMbase, PubMed, Cochrane Library, Web of Science were retrieved through computers. A total of 6 literatures were included in this study. By AMSTAR-2 checklist and GRADE, the quality of included systematic reviews and the efficacy of Xingnaojing Injection were evaluated. The results of AMSTAR-2 checklist showed an extremely low quality for all of the 6 systematic reviews. According to the results of GRADE evaluation, among 55 outcomes, there were 2 outcomes with a medium quality, 4 outcomes with a low quality and 49 outcomes with an extremely low quality. The 6 systematic reviews reached a consistent conclusion that Xingnaojing Injection was effective in the treatment of cerebral ischaemic stroke. This therapy could improve the total efficacy, neurological deficit scores, hemodynamic and hemodynamic parameters. However, the methodolo-gical quality of all literatures was extremely low. The evidence levels of outcomes were between extremely low to medium. The effectiveness of Xingnaojing Injection in the treatment of cerebral ischaemic stroke still needs to be further verified by more high-quality studies. In the future, relevant clinical studies and systematic reviews/Meta-analysis shall be carried out in a strict accordance with relevant regulations.
Subject(s)
Humans , Brain Ischemia/drug therapy , Drugs, Chinese Herbal , Ischemic Stroke , Stroke/drug therapy , Systematic Reviews as TopicABSTRACT
There is obvious allele disequilibrium in nasopharyngeal carcinoma at chromosome 3p, 9p, 6q, 11q, 13q and 14q. Nasopharyngeal carcinoma (NPC) susceptibility/suppressor gene candidates were obtained by molecular biology methods,such as cDNA representational difference ana-lysis. The functional research of NPC susceptibility/ suppressor gene candidates indicated: (1) The increased expression of Cx contributed to obstacles of gap junctional intercellular communication (GJIC), and resulted an aberration of GJIC; (2) BRD7, a transcript factor, was associated with cell cycle regulation; (3) NAG7,an estrogen receptor repressor, inhibited the invasive potential of human NPC cells by regulating ERalpha expression and the H-ras/p-c-Raf and JNK/AP-1/MMP1 signaling pathways; (4) NGX6, a metastasis-associated protein, can negative-regulate EGF/Ras/MAPK signaling transduction pathway, and interact with ezrin protein to inhibit invasion and metastasis of NPC cells; (5) SPLUNC1, a secreted protein, can inhibit the bacterium clone formation, and is an innate immune molecule. These data will lay an important foundation for the NPC mechanism.
Subject(s)
Humans , Biomarkers, Tumor , Cell Cycle Proteins , Genetics , Chromosomal Proteins, Non-Histone , Genetics , Genomics , Methods , Glycoproteins , Genetics , Membrane Proteins , Genetics , Nasopharyngeal Neoplasms , Genetics , Metabolism , Pathology , Phosphoproteins , Genetics , RNA, Long Noncoding , RNA, Untranslated , Tumor Cells, Cultured , Tumor Suppressor Proteins , GeneticsABSTRACT
OBJECTIVE@#To explore the effect of all-trans-retinoic acid (ATRA) on the growth inhibition and cellular differentiation of C6 glioma cells.@*METHODS@#Human glioma C6 cells were treated with 5 mg/L ATRA,and the inhibition of cell growth was assessed by methyl thiazolyl tetrazolium assay. The differentiation of C6 cells was determined by flow cytometry, microscopy,transmission electron microscope, and immunohistochemical technique.@*RESULTS@#Treatment of ATRA could result in the growth inhibition of C6 cells, and the cell density significantly decreased(P0.05).Whereas, early apoptosis was observed under the transmission electron microscope, the vacuoles increased, the mitochondria and endoplasmic reticulum were abundant in the cytoplasm, and the cellular structures tended to be normal.The expression of glial fibrillaryacidic protein in C6 cells increased in the treatment group.@*CONCLUSION@#ATRA can inhibit the proliferation, and induce the differentiation of C6 glioma cells.
Subject(s)
Animals , Humans , Mice , Antineoplastic Agents , Pharmacology , Brain Neoplasms , Pathology , Cell Proliferation , Cell Transformation, Neoplastic , Glioma , Pathology , Tretinoin , Pharmacology , Tumor Cells, CulturedABSTRACT
Omics docking study for polygenic inheritance tumors has become an important strategy in oncology research. This review focuses on the conceptions and technologies of omics, and puts forward the central contents and omics docking for polygenic inheritance tumor to reveal the role of molecular changes at different stages of polygenic inheritance tumor at multidisciplinary and multilayer level. It is a new strategy to explore the mechanism of tumor carcinogenesis, and to regulate the network, key molecules, and drug target by combined biology effects.
Subject(s)
Humans , Carrier Proteins , Genetics , Genomics , Methods , Glycoproteins , Genetics , Membrane Proteins , Genetics , Multifactorial Inheritance , Genetics , Neoplasms , Genetics , Metabolism , Phosphoproteins , Genetics , Proteomics , Methods , Tumor Suppressor Proteins , GeneticsABSTRACT
Metabolomics is a new science and technology, which it refers to a holistic analytical approach to all the low molecular weight metabolites in an organism or a cell. In this paper, the definition and objective of metabolomics are provided, and the current application of metabolomic research in malignant tumors (diagnosis and therapy) are summarized.
Subject(s)
Animals , Humans , Biomarkers, Tumor , Genetics , Metabolism , Genomics , Methods , Metabolism , Models, Biological , Neoplasms , Genetics , Metabolism , Proteomics , Methods , Transcription, GeneticABSTRACT
OBJECTIVE@#To explore the effect of LRRC4, a glioma suppressive gene, on blocking U251 cells in G0/G1 by MAPK signaling pathway.@*METHODS@#LRRC4 was transfected into U251 cells, and at 24 hour of post-transfection, cells were split at a 1:3 dilution, challenged with 500 microg /mL G418 and formed a stable transfected clone pool. RT-PCR, Northern blot and Western blot were used to identify the stable transfectants. ERK, JNK and P38 expression changes were analyzed by Western blot. FACS analysis, Luciferase reporter gene assay and Western blot were used to detect the cell cycle and cyclin D1.@*RESULTS@#LRRC4 down-regulated the expression of phosphorylated ERK2 and up-regulated the expression of total protein JNK2 (a key molecule of MAPK signaling pathway) and phosphorylated c-Jun. LRRC4 decreased the expression of mutation P53, cyclin D1 activation and its expression. U251 cells were blocked in G0/G1 by LRRC4.@*CONCLUSION@#LRRC4 can decrease JNK2, up-regulate the phosphoralated c-Jun, down-regulate mutant P53 and cyclin D1, and therefore block U251 cells in G0/G1.
Subject(s)
Humans , Blotting, Northern , Blotting, Western , Cell Line, Tumor , Cyclin D1 , Metabolism , Flow Cytometry , G1 Phase , Genetics , Physiology , Glioma , Genetics , Metabolism , Pathology , Luciferases , Genetics , Metabolism , MAP Kinase Signaling System , Genetics , Physiology , Mitogen-Activated Protein Kinase Kinases , Metabolism , Nerve Tissue Proteins , Genetics , Metabolism , Physiology , RNA, Messenger , Genetics , Recombinant Fusion Proteins , Genetics , Metabolism , Resting Phase, Cell Cycle , Genetics , Physiology , Reverse Transcriptase Polymerase Chain Reaction , TransfectionABSTRACT
OBJECTIVE@#To examine the expression absence of LRRC4 gene in glioblastoma cell lines.@*METHODS@#RT-PCR and Northern blot were used to detect the expression of LRRC4 gene in 6 glioblastomas cells lines. Polymerase chain reaction and DNA sequencing were used to screen the LRRC4 gene mutation, while bioinformation assay was used to search for the reason of LRRC4 gene absence in U251 cell lines.@*RESULTS@#The expression of LRRC4 was absent in 6 malignant glioma cell lines (U251, U87, BT325, SF126, SF767 and M17), which were examined by Northern-blot and RT-PCR assay. All sequencing of PCR products from gDNA of SF126, SF767, and M17 cell lines contained the point mutation at the same position ( LRRC4 geneT977A) (3/5), which was a synonymous mutation. However, PCR products from gDNA of U251 and U87 cell lines (2/5) were not obtained. The expression absence of LRRC4 was ascribed to the loss of homozygosity of 7q32-ter in U251 cell lines.@*CONCLUSION@#The expression of LRRC4 gene is absent in glioblastoma cell lines, and it offers the important experiment proof for LRRC4 to act as a new candidate of brain tumor suppressor gene from glioma. The loss of homozygosity of 7q32-ter contributed to the expression absence of LRRC4 in U251 cell lines.
Subject(s)
Humans , Base Sequence , Blotting, Northern , Brain Neoplasms , Genetics , Pathology , Cell Line, Tumor , DNA Mutational Analysis , Gene Expression Regulation, Neoplastic , Glioblastoma , Genetics , Pathology , Nerve Tissue Proteins , Genetics , Point Mutation , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
OBJECTIVE@#To prepare anti-LRRC4 polyclonal antibody and analyze the correlation between the expression of LRRC4 and pathological grades of gliomas in rabbits.@*METHODS@#Appropriate protein sequence with good hydrophilicity and antigenicity was chosen by analyzing with DS Gene 1.1 software. The corresponding nucleic acid sequence amplified by PCR was used to construct a recombinant pGEX-4T-2/276 bp. E.coli JM109 transformed with the recombinant was induced by IPTG to express GST-fusion protein, and the fusion protein expressed as insoluble inclusion bodies. Then the purified inclusion body was used to immunize rabbits. Once the titer of antiserum reached 1:10(8) by indirect ELISA, the serum was collected and purified. The expression-profile of LRRC4 in embryonic tissues and gliomas with various pathological grades were obtained by western blot and immunohistochemistry with the anti-LRRC4 polyclonal antibody.@*RESULTS@#The highly specific anti-LRRC4 polyclonal antibody whose titer reached 1:10(8) was prepared. The relatively specific expression of LRRC4 was detected in the normal brain, but reduced expression or loss of expression in gliomas was also noticed by immunohistochemistry, and there was a correlation between the expression level of lrrc4 and the pathological grade of gliomas.@*CONCLUSION@#The anti-LRRC4 polyclonal antibody with high titer and specificity has been obtained. A correlation between the expression level of LRRC4 and the pathological grade of gliomas is detected, which lays the foundation for advanced research of LRRC4.
Subject(s)
Animals , Male , Rabbits , Antibodies, Monoclonal , Allergy and Immunology , Antibody Specificity , Allergy and Immunology , Blotting, Western , Brain , Metabolism , Pathology , Brain Neoplasms , Allergy and Immunology , Metabolism , Pathology , Glioma , Allergy and Immunology , Metabolism , Pathology , Immunohistochemistry , Nerve Tissue Proteins , Genetics , Allergy and Immunology , Recombinant Fusion Proteins , Allergy and ImmunologyABSTRACT
OBJECTIVE@#To explore the effect of LRRC4 on the mobility and invasion of glioblastomas U251 cells through the SDF-1alpha/CXCR4 axis.@*METHODS@#RT-PCR, transfilter cell invasion assay, adhesion assay, scraping test, scrape loading, and dye transfer assay were used to determine the effect of LRRC4 on U251 cells.@*RESULTS@#SDF-1 alpha could increase the invasion in U251 which expressed CXCR4. The reintroduction of LRRC4 in U251 cells could inhibit the expression of CXCR4. LRRC4 also inhibited the adhesion ability of U251 to ECV304 as well as the mobility and invasion ability in vitro, which was mediated by the SDF-1alpha/CXCR4 axis. Furthermore, LRRC4 could greatly enhance the gap junctional intercellular communication of U251 cells.@*CONCLUSION@#The reintroduction of LRRC4 in U251 cells can inhibit the expression of CXCR4 and the SDF-1alpha/CXCR4 axis-mediated cell invasion in vitro.
Subject(s)
Humans , Cell Adhesion , Cell Line, Tumor , Cell Movement , Chemokine CXCL12 , Metabolism , Glioblastoma , Pathology , Neoplasm Invasiveness , Nerve Tissue Proteins , Genetics , Receptors, CXCR4 , MetabolismABSTRACT
OBJECTIVE@#To express the recombinant SPLUNC1 protein in HNE1 cells and to study its function of bactericidal and binding to lipopolysaccharide (LPS).@*METHODS@#Full length of SPLUNC1 gene was cloned into pCMV-tag4A vector and stably transfected into HNE1 cell lines, the supernatant of cell cultures was collected. After being treated with the supernatant, the Pseudomonas aeruginosa was seeded to LB soft agar plate, and the bacteria clones were counted and analyzed. For in vitro LPS binding assay, LPS was coated to 96-well plates. We incubated in the plate with SPLUNC1 protein, and detected the binded SPLUNC1 protein by ELISA. Incubating the FITC-LPS with the SPLUNC1 stably transfected or control cells, the intracellular intensity of fluorescence was observed under the fluorescence microscope.@*RESULTS@#SPLUNC1 inhibited the bacteria clone formation obviously. Although the binding efficiency of LPS and SPLUNC1 in vitro was very low, more FITC-LPS entered into the SPLUNC1 stably transfected cells.@*CONCLUSION@#SPLUNC1 can inhibit the growth of Pseudomonas aeruginosa and bind LPS, and play an important defensive role in innate immunity of the upper airway.