24 results on '"Quan, Wei"'
Search Results
2. RIPK1-Induced A1 Reactive Astrocytes in Brain in MPTP-Treated Murine Model of Parkinson's Disease.
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Qiao, Chenmeng, Niu, Guyu, Zhao, Weijiang, Quan, Wei, Zhou, Yu, Zhang, Meixuan, Li, Ting, Zhou, Shengyang, Huang, Wenyan, Zhao, Liping, Wu, Jian, Cui, Chun, and Shen, Yanqin
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PARKINSON'S disease ,ASTROCYTES ,RECEPTOR-interacting proteins ,GENE expression ,PROTEIN kinases ,CARBIDOPA - Abstract
Neuroinflammation is one of the hallmarks of Parkinson's disease, including the massive activation of microglia and astrocytes and the release of inflammatory factors. Receptor-interacting protein kinase 1 (RIPK1) is reported to mediate cell death and inflammatory signaling, and is markedly elevated in the brain in PD mouse models. Here, we aim to explore the role of RIPK1 in regulating the neuroinflammation of PD. C57BL/6J mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 20 mg/kg four times/day), followed by necrostatin-1 treatment (Nec-1, RIPK1 inhibitor; 1.65 mg/kg once daily for seven days. Notably, the first Nec-1 was given 12 h before MPTP modeling). Behavioral tests indicated that inhibition of RIPK1 greatly relieved motor dysfunction and anxiety-like behaviors of PD mice. It also increased striatal TH expression, rescue the loss of dopaminergic neurons, and reduce activation of astrocytes in the striatum of PD mice. Furthermore, inhibition of RIPK1 expression reduced A1 astrocytes' relative gene expression (CFB, H2-T23) and inflammatory cytokine or chemokine production (CCL2, TNF-α, IL-1β) in the striatum of PD mice. Collectively, inhibition of RIPK1 expression can provide neuroprotection to PD mice, probably through inhibition of the astrocyte A1 phenotype, and thus RIPK1 might be an important target in PD treatment. [ABSTRACT FROM AUTHOR]
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- 2023
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3. Cell Heterogeneity Uncovered by Single-Cell RNA Sequencing Offers Potential Therapeutic Targets for Ischemic Stroke.
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Min Qiu, Jia-bin Zong, Quan-wei He, Yu-xiao Liu, Yan Wan, Man Li, Yi-fan Zhou, Jie-hong Wu, and Bo Hu
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RNA sequencing ,ISCHEMIC stroke ,GENE expression - Abstract
Ischemic stroke is a detrimental neurological disease characterized by an irreversible infarct core surrounded by an ischemic penumbra, a salvageable region of brain tissue. Unique roles of distinct brain cell subpopulations within the neurovascular unit and peripheral immune cells during ischemic stroke remain elusive due to the heterogeneity of cells in the brain. Single-cell RNA sequencing (scRNA-seq) allows for an unbiased determination of cellular heterogeneity at high-resolution and identification of cell markers, thereby unveiling the principal brain clusters within the cell-type-specific gene expression patterns as well as cellspecific subclusters and their functions in different pathways underlying ischemic stroke. In this review, we have summarized the changes in differentiation trajectories of distinct cell types and highlighted the specific pathways and genes in brain cells that are impacted by stroke. This review is expected to inspire new research and provide directions for investigating the potential pathological mechanisms and novel treatment strategies for ischemic stroke at the level of a single cell. [ABSTRACT FROM AUTHOR]
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- 2022
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4. The Larix kaempferi genome reveals new insights into wood properties.
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Sun, Chao, Xie, Yun‐Hui, Li, Zhen, Liu, Yan‐Jing, Sun, Xiao‐Mei, Li, Jing‐Jing, Quan, Wei‐Peng, Zeng, Qing‐Yin, Van de Peer, Yves, and Zhang, Shou‐Gong
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BIOLOGICAL evolution ,LARCHES ,WOOD ,GENETIC transcription regulation ,CONIFERS ,RETROTRANSPOSONS ,GENOMES ,PINACEAE - Abstract
Here, through single‐molecule real‐time sequencing, we present a high‐quality genome sequence of the Japanese larch (Larix kaempferi), a conifer species with great value for wood production and ecological afforestation. The assembled genome is 10.97 Gb in size, harboring 45,828 protein‐coding genes. Of the genome, 66.8% consists of repeat sequences, of which long terminal repeat retrotransposons are dominant and make up 69.86%. We find that tandem duplications have been responsible for the expansion of genes involved in transcriptional regulation and stress responses, unveiling their crucial roles in adaptive evolution. Population transcriptome analysis reveals that lignin content in L. kaempferi is mainly determined by the process of monolignol polymerization. The expression values of six genes (LkCOMT7, LkCOMT8, LkLAC23, LkLAC102, LkPRX148, and LkPRX166) have significantly positive correlations with lignin content. These results indicated that the increased expression of these six genes might be responsible for the high lignin content of the larches' wood. Overall, this study provides new genome resources for investigating the evolution and biological function of conifer trees, and also offers new insights into wood properties of larches. [ABSTRACT FROM AUTHOR]
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- 2022
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5. Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease.
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Quan, Wei, Li, Jia, Liu, Li, Zhang, Qinghui, Qin, Yidan, Pei, Xiaochen, and Chen, Jiajun
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KRUSKAL-Wallis Test , *STATISTICS , *FLOW cytometry , *ANALYSIS of variance , *RNA , *CELL physiology , *MANN Whitney U Test , *MICRORNA , *GENE expression , *T-test (Statistics) , *PARKINSON'S disease , *METHYLATION , *DESCRIPTIVE statistics , *ENZYME-linked immunosorbent assay , *TRANSFERASES , *ADENOSINES , *DATA analysis software , *DATA analysis , *TUMOR markers , *PHENOTYPES - Abstract
This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson's disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differentially expressed genes and function enrichment analysis of the two sets of data and found that the expression of the m6A-modification gene HNRNPC was significantly downregulated in the PD group, and it played an important role in DNA metabolism, RNA metabolism, and RNA processing and may be involved in PD. Then, we constructed the HNRNPC differential expression cell line to study the role of this gene in the pathogenesis of PD. The results showed that overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors IFN-β, IL-6, and TNF-α, suggesting that HNRNPC may cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation. Our study also has certain limitations. For example, the data of the experimental group and the validation group come from different cell types, and the data of the experimental group involve individuals with G2019S LRRK2 mutations. In addition, due to the low expression of HNRNPC in PC12 cells, we used the method of overexpressing this gene to study its function. All these factors may cause our conclusions to be biased. Therefore, more research is still needed to corroborate it in the future. [ABSTRACT FROM AUTHOR]
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- 2021
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6. Identification of Potential Core Genes in Parkinson's Disease Using Bioinformatics Analysis.
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Quan, Wei, Li, Jia, Jin, Xiya, Liu, Li, Zhang, Qinghui, Qin, Yidan, Pei, Xiaochen, and Chen, Jiajun
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TISSUE analysis , *DISEASE progression , *METABOLISM , *BIOINFORMATICS , *GENE expression , *PARKINSON'S disease , *GENES , *GENE expression profiling , *MITOGEN-activated protein kinases - Abstract
Purpose. This study aimed to explore new core genes related to the occurrence of Parkinson's disease (PD) and core genes that can lead to the progression of PD. Methods. The expression profile data of GSE42966, which contained six substantia nigra tissues isolated from normal individuals and nine substantia nigra tissues isolated from patients with PD, were obtained from Gene Expression Omnibus. Differentially expressed genes (DEGs) were identified, followed by functional enrichment analysis and protein-protein interaction (PPI) network construction. We then identified 10 hub genes and analyzed their expression in different Braak stages. Results. A total of 773 DEGs were identified that were significantly enriched in metabolic pathways. Ten hub genes were identified through the PPI network, namely, GNG3, MAPK1, FPR1, ATP5B, GNG2, PRKACA, HRAS, HSPA8, PSAP, and GABBR2. The expression of HRAS was different in patients with PD with Braak stages 3 and 4. Conclusion. These 10 hub genes and the metabolic pathways they are enriched in may be involved in the pathogenesis of PD. HRAS may have potential value in predicting the progression of PD. [ABSTRACT FROM AUTHOR]
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- 2021
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7. Identification of gene expression profiles and key genes in subchondral bone of osteoarthritis using weighted gene coexpression network analysis
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Chi Zhang, Si‐Lin Zheng, Jianxiong Wang, Jin Li, Fangyuan Xu, Haiming Wang, Quan Wei, Yujie Xie, Hou‐Qiang Huang, and Guo Shengmin
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0301 basic medicine ,Gene Expression Profiling ,Wnt signaling pathway ,Cell Biology ,Transforming growth factor beta ,Computational biology ,Biology ,Biochemistry ,Extracellular matrix ,03 medical and health sciences ,030104 developmental biology ,Gene Ontology ,Gene Expression Regulation ,Gene expression ,Osteoarthritis ,biology.protein ,Cluster Analysis ,Humans ,Gene Regulatory Networks ,Genetic Predisposition to Disease ,BAMBI ,Signal transduction ,Molecular Biology ,Gene ,PI3K/AKT/mTOR pathway - Abstract
Osteoarthritis (OA) significantly influences the quality life of people around the world. It is urgent to find an effective way to understand the genetic etiology of OA. We used weighted gene coexpression network analysis (WGCNA) to explore the key genes involved in the subchondral bone pathological process of OA. Fifty gene expression profiles of GSE51588 were downloaded from the Gene Expression Omnibus database. The OA-associated genes and gene ontologies were acquired from JuniorDoc. Weighted gene coexpression network analysis was used to find disease-related networks based on 21756 gene expression correlation coefficients, hub-genes with the highest connectivity in each module were selected, and the correlation between module eigengene and clinical traits was calculated. The genes in the traits-related gene coexpression modules were subject to functional annotation and pathway enrichment analysis using ClusterProfiler. A total of 73 gene modules were identified, of which, 12 modules were found with high connectivity with clinical traits. Five modules were found with enriched OA-associated genes. Moreover, 310 OA-associated genes were found, and 34 of them were among hub-genes in each module. Consequently, enrichment results indicated some key metabolic pathways, such as extracellular matrix (ECM)-receptor interaction (hsa04512), focal adhesion (hsa04510), the phosphatidylinositol 3'-kinase (PI3K)-Akt signaling pathway (PI3K-AKT) (hsa04151), transforming growth factor beta pathway, and Wnt pathway. We intended to identify some core genes, collagen (COL)6A3, COL6A1, ITGA11, BAMBI, and HCK, which could influence downstream signaling pathways once they were activated. In this study, we identified important genes within key coexpression modules, which associate with a pathological process of subchondral bone in OA. Functional analysis results could provide important information to understand the mechanism of OA.
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- 2018
8. Tumor-specific oncolytic adenoviruses expressing granulocyte macrophage colony-stimulating factor or anti-CTLA4 antibody for the treatment of cancers
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Gang Shi, Hongwei Tian, Yu Quan Wei, Yunchun Li, Hong Xin Deng, De-Chao Yu, Ting Du, and Junfeng Zhang
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Cancer Research ,Genes, Viral ,Genetic Vectors ,Melanoma, Experimental ,Gene Expression ,Virus Replication ,Adenoviridae ,Mice ,Cytopathogenic Effect, Viral ,Cell Line, Tumor ,Neoplasms ,Gene Order ,medicine ,Animals ,Humans ,Macrophage ,Cytotoxic T cell ,CTLA-4 Antigen ,Cytotoxicity ,Molecular Biology ,Oncolytic Virotherapy ,biology ,Melanoma ,Antibodies, Monoclonal ,Granulocyte-Macrophage Colony-Stimulating Factor ,Genetic Therapy ,medicine.disease ,Xenograft Model Antitumor Assays ,Molecular biology ,Tumor Burden ,Oncolytic virus ,Disease Models, Animal ,Oncolytic Viruses ,Granulocyte macrophage colony-stimulating factor ,Cell culture ,biology.protein ,Molecular Medicine ,Female ,Antibody ,medicine.drug - Abstract
The purpose of this study was to examine the tumor specificity, cytotoxicity and the antitumor activity of two conditionally replicating oncolytic adenoviruses, SKL001 and SKL002, which expressed granulocyte macrophage colony-stimulating factor (GM-CSF) or anti-cytotoxic T lymphocyte-associated antigen-4 (CTLA4) antibody, respectively, and determine their antitumor efficacy in A549 lung tumor model, B16F10 mouse melanoma tumor model and CMT-64 mouse small lung carcinoma tumor model. Virus yield and cytotoxicity were used to determine tumor specificity and virus replication-mediated cytotoxicity of SKL001 and SKL002 in a panel of human tumor cell lines and primary cells in vitro. Two subcutaneous (s.c.) tumor nexograft tumor models were used to assess their antitumor activity. Under the control of the E2F promoter, the expression of E1a genes appeared only in tumor cells, whereas the wild-type Ad5 expressed its E1a genes in both tumor cells and normal cells. GM-CSF and anti-CTLA4 production were significantly higher in tumor cells than normal cells. SKL001 and SKL002 replicated in Rb-defective cell lines as efficiently as wild-type adenovirus but produced 100-fold less virus in normal human cells. SKL001 and SKL002 was up to 1000-fold more cytotoxic in Rb pathway-defective human tumor cells in comparison with normal human cells. Antitumor activity of SKL001 and SKL002 following intravenous administration was shown in a human lung A549 s.c. xenograft tumor model and mouse B16F10 melanoma tumor model when compared with phosphate-buffered saline treatment. In immune-competent mice, the addition of GM-CSF produced a stronger antitumor activity and induced a higher number of mature dendritic cells and macrophages, whereas additive antitumor activity was observed in the group when SKL001 and SKL002 were combined. In vitro and in vivo studies showed the selective replication, cytotoxicity, gene production and antitumor efficacy of SKL001 and SKL002 in human tumor model, suggesting a potential utility of this oncolytic agent for the treatment of human cancer. Further studies are warranted to show the role of human GM-CSF and anti-CTLA4 antibody in the antitumor efficacy of these two oncolytic viruses.
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- 2014
9. FIP200 is Involved in Murine Pseudomonas Infection by Regulating HMGB1 Intracellular Translocation
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Yi, Li, Chang-pei, Gan, Shuang, Zhang, Xi-kun, Zhou, Xue-feng, Li, Yu-quan, Wei, Jin-liang, Yang, and Min, Wu
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Blotting, Western ,Intracellular Space ,Autophagy-Related Proteins ,Gene Expression ,chemical and pharmacologic phenomena ,Article ,lcsh:Physiology ,Cell Line ,lcsh:Biochemistry ,Phagocytosis ,Phagosomes ,Pulmonary infection ,Macrophages, Alveolar ,Autophagy ,Acute lung injury ,Animals ,Pseudomonas Infections ,lcsh:QD415-436 ,FIP200 ,HMGB1 Protein ,Mice, Knockout ,Microscopy, Confocal ,lcsh:QP1-981 ,Reverse Transcriptase Polymerase Chain Reaction ,Intracellular Signaling Peptides and Proteins ,Mice, Inbred C57BL ,Protein Transport ,HMGB1 acetylation ,Host-Pathogen Interactions ,Pseudomonas aeruginosa - Abstract
Background: FIP200, a critical autophagy initiating protein, can participate in numerous cellular functions including cancer development; however, its functional role in P. aeruginosa infection of alveolar macrophages is unknown. Methods: To investigate the role of FIP200 in host defense, we transfected murine alveolar macrophage MH-S cells with FIP200 siRNA. Having confirmed that FIP200 knockdown inhibited PAO1-induced autophagosme formation, we sought to characterize the underlying signaling pathways by immunoblotting. Further, we used fip200 KO mice to study the effects of fip200 deficiency on HMGB1 translocation. Results: We showed that Pseudomonas PAO1 strain infection facilitated autophagosome formation, whereas knockdown of FIP200 inhibited autophagosome formation and HMGB1 expression in MH-S cells. Silencing FIP200 impaired the translocation of HMGB1 to cytosol of MH-S cells and almost abolished acetylation of HMGB1 during PAO1 infection. In contrast, FIP200 overexpression facilitated the cytosol translocation of HMGB1 from nuclei and increased acetylation of HMGB1 in PAO1-infected MH-S cells. Importantly, expression and acetylation of HMGB1 were also significantly down-regulated in fip200 KO mice following PAO1 infection. Conclusions: Collectively, these findings elucidate that FIP200 may regulate expression and translocation of HMGB1 during PAO1 infection, which may indicate novel therapeutic targets to control pulmonary infection.
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- 2014
10. Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats.
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Wang, Quan-wei, Yu, Xiao-feng, Xu, Hua-li, Zhao, Xue-zhong, and Sui, Da-yuan
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ANIMAL experimentation , *BLOOD pressure , *CARRIER proteins , *CELLULAR signal transduction , *COLLAGEN , *GENE expression , *GINSENG , *GLYCOSIDES , *HEART , *LEFT heart ventricle , *HEART failure , *ISOPROTERENOL , *MYOCARDIUM , *ORAL drug administration , *PROLINE , *RATS , *TRANSFORMING growth factors-beta , *FIBROSIS , *BLOOD - Abstract
Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-β1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-β1/Smad3 pathway. [ABSTRACT FROM AUTHOR]
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- 2019
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11. MicroRNA-Modulated Apoptotic and Autophagic Signaling Networks in Cancer
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Yu-quan Wei and Bo Liu
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Programmed cell death ,Apoptosis ,microRNA ,Gene expression ,Autophagy ,medicine ,Cancer ,RNA ,Biology ,medicine.disease ,Carcinogenesis ,medicine.disease_cause ,Cell biology - Abstract
MicroRNAs (miRNAs), small and non-coding RNAs ∼ 22 nucleotides (nt) in length, are estimated to regulate about 30 % human gene expression at the post-transcriptional and the translational levels. MiRNAs are also involved in a series of important cellular processes, such as proliferation, differentiation, apoptosis and autophagy. Of note, apoptosis can invariably contribute to cell death, whereas autophagy can play either a pro-survival or a pro-death role in cancer. Recent evidence has shown that miRNAs can function as oncogenes or tumor suppressive genes in diverse types of human cancers. Also, miRNAs are well-characterized to be crucial in tumorigenesis as either oncogenes or tumor suppressors by targeting apoptosis and autophagy. However, the intricate mechanisms of miRNA-modulated apoptosis and autophagy still remain unclear. In this chapter, we focus on summarizing the dual function of miRNAs in regulation of apoptosis and autophagy; thereby revealing the regulatory mechanisms of miRNA-regulated apoptosis and autophagy, which may shed light on developing novel RNA therapeutic strategy in the near future.
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- 2014
12. Self-assembly of virus-like particles of canine parvovirus capsid protein expressed from Escherichia coli and application as virus-like particle vaccine
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Shi-Chong Han, Huichen Guo, Haiming Wang, Jin Xu, Suizhong Cao, Da Ao, Shiqi Sun, Yan-Quan Wei, Hu Dong, and De-Hui Sun
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Parvovirus, Canine ,animal diseases ,viruses ,Injections, Subcutaneous ,Gene Expression ,Lymphocyte proliferation ,Antibodies, Viral ,complex mixtures ,Applied Microbiology and Biotechnology ,Virus ,Parvoviridae Infections ,Mice ,Dogs ,Virus-like particle ,Escherichia coli ,Animals ,Dog Diseases ,Lymphocytes ,Vaccines, Virus-Like Particle ,Cell Proliferation ,Vaccines, Synthetic ,biology ,Parvovirus ,Immunogenicity ,Viral Vaccine ,Vaccination ,Canine parvovirus ,virus diseases ,Viral Vaccines ,General Medicine ,biochemical phenomena, metabolism, and nutrition ,biology.organism_classification ,Virology ,Recombinant Proteins ,Capsid ,Capsid Proteins ,Protein Multimerization ,Biotechnology - Abstract
Canine parvovirus disease is an acute infectious disease caused by canine parvovirus (CPV). Current commercial vaccines are mainly attenuated and inactivated; as such, problems concerning safety may occur. To resolve this problem, researchers developed virus-like particles (VLPs) as biological nanoparticles resembling natural virions and showing high bio-safety. This property allows the use of VLPs for vaccine development and mechanism studies of viral infections. Tissue-specific drug delivery also employs VLPs as biological nanomaterials. Therefore, VLPs derived from CPV have a great potential in medicine and diagnostics. In this study, small ubiquitin-like modifier (SUMO) fusion motif was utilized to express a whole, naturalVP2 protein of CPV in Escherichia coli. After the cleavage of the fusion motif, the CPV VP2 protein has self-assembled into VLPs. The VLPs had a size and shape that resembled the authentic virus capsid. However, the self-assembly efficiency of VLPs can be affected by different pH levels and ionic strengths. The mice vaccinated subcutaneously with CPV VLPs and CPV-specific immune responses were compared with those immunized with the natural virus. This result showed that VLPs can effectively induce anti-CPV specific antibody and lymphocyte proliferation as a whole virus. This result further suggested that the antigen epitope of CPV was correctly present on VLPs, thereby showing the potential application of a VLP-based CPV vaccine.
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- 2013
13. Ginsenoside Re Attenuates Isoproterenol-Induced Myocardial Injury in Rats.
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Wang, Quan-wei, Yu, Xiao-feng, Xu, Hua-li, Jiang, Yi-chuan, Zhao, Xue-zhong, and Sui, Da-yuan
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SUBCUTANEOUS injections , *ANIMAL experimentation , *BIOLOGICAL assay , *CREATINE kinase , *GENE expression , *GLUTATHIONE , *GLYCOSIDES , *HEART cells , *HYDROCARBONS , *ISOPROTERENOL , *MYOCARDIUM , *ORAL drug administration , *OXIDATION-reduction reaction , *RATS , *TRANSCRIPTION factors , *WESTERN immunoblotting , *MALONDIALDEHYDE , *TROPONIN , *PHARMACODYNAMICS , *WOUNDS & injuries - Abstract
Objective. Panax ginseng is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component ofPanax ginseng . This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats.Methods. Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathological examination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method.Results. Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re.Conclusion. These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes. [ABSTRACT FROM AUTHOR]- Published
- 2018
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14. Inhibition of proliferation and induction of apoptosis by abrogation of heat-shock protein (HSP) 70 expression in tumor cells
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Keisuke Teshigawara, Yu-quan Wei, Xia Zhao, Yoshitaka Kariya, and Atsushi Uchida
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Cancer Research ,Programmed cell death ,Hot Temperature ,Time Factors ,Cell division ,Molecular Sequence Data ,Immunology ,Gene Expression ,Apoptosis ,Biology ,DNA, Antisense ,Flow cytometry ,Heat shock protein ,Tumor Cells, Cultured ,medicine ,Humans ,Immunology and Allergy ,HSP70 Heat-Shock Proteins ,Base Sequence ,medicine.diagnostic_test ,Cell growth ,Molecular biology ,Oncology ,Cell culture ,DNA fragmentation ,Cell Division - Abstract
Tumor cells often express elevated levels of heat-shock protein (HSP) 70. The present study was designed to investigate the role of HSP70 in the proliferation and survival of tumor cells in the human system. When Molt-4 and other tumor cells were treated in vitro with HSP70 antisense oligomer, they displayed propidium-iodide-stained condensed nuclei (intact or fragmented). A ladder-like pattern of DNA fragments was observed with HSP70 antisense-oligomer-treated tumor cells in agrose gel electrophoresis, which was consistent with internucleosomal DNA fragmentation. Flow cytometry analysis revealed the hypodiploid DNA peak of propidium-iodide-stained nuclei in the antisense-oligomer-treated cells. The apoptosis induced by HSP antisense oligomer was dose- and time-dependent. The antisense oligomer induced apoptosis mainly in tumor cells at G1 and S phase, resulting in an inhibition of cell proliferation. HSP70 antisense oligomer caused DNA-sequence-specific inhibition of HSP70 expression, which preceded apparent apoptosis. These results indicate that HSP70 antisense treatment inhibits the expression of HSP70, which in turn inhibits cell proliferation and induces apoptosis in tumor cells and suggest that HSP70 is required for tumor cells to proliferate and survive under normal condition.
- Published
- 1995
15. Adeno associated viral vector-delivered and hypoxia response element-regulated CD151 expression in ischemic rat heart
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Xiao Lin Huang, Yu Jie Fei, Zheng Xiang Liu, Jing Yang Lin, Xin Zhang, and Quan Wei
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Male ,Angiogenesis ,viruses ,Genetic enhancement ,Blotting, Western ,Genetic Vectors ,Myocardial Infarction ,Myocardial Ischemia ,Biology ,Tetraspanin 24 ,Polymerase Chain Reaction ,Viral vector ,Rats, Sprague-Dawley ,Antigens, CD ,Gene expression ,medicine ,Animals ,Humans ,Pharmacology (medical) ,Myocardial infarction ,CD151 ,Pharmacology ,Regulation of gene expression ,General Medicine ,Genetic Therapy ,Dependovirus ,medicine.disease ,Rats ,Blot ,Disease Models, Animal ,Gene Expression Regulation ,Phosphopyruvate Hydratase ,Immunology ,Microvessels ,Cancer research ,Original Article ,Hypoxia-Inducible Factor 1 - Abstract
The aim of this study was to improve the delivery efficacy and target specificity of the pro-angiogenic gene CD151 to the ischemic heart.To achieve the inducible expression of adeno-associated viral (AAV)-delivered CD151 gene in only the ischemic myocardium, we generated an AAV construct in which CD151 expression can be controlled by the hypoxia response element (HRE) sequence from the human Enolase gene. The function of this vector was examined in rat H9C2 cardiac myoblasts and in ischemic rat myocardium. The expression of CD151 in the areas of ischemic myocardium was confirmed at the mRNA level by real-time PCR and on the protein level by Western blot, whereas the CD151 expression in the microvessels within the areas of ischemic myocardium was detected by immunohistochemistry.HRE significantly enhances the expression of CD151 under hypoxic conditions or in the ischemic myocardium, and forced CD151 expression increases the number of microvessels in the ischemic myocardium.The AAV-mediated, HRE regulated delivery of the CD151 gene shows higher expression in the ischemic myocardium and more efficiently targets CD151 to the hypoxic regions after myocardial infarction.
- Published
- 2011
16. Lentiviral vector-mediated doxycycline-inducible iASPP gene targeted RNA interference in hepatocellular carcinoma
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Bo-Hua Li, Yu-Quan Wei, Ya-Jun Guo, Jian Zhao, Xia Chen, Ming-Shu Pang, and Bin Lu
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Carcinoma, Hepatocellular ,Genetic Vectors ,Down-Regulation ,Apoptosis ,Biology ,medicine.disease_cause ,Transfection ,Viral vector ,Small hairpin RNA ,RNA interference ,Gene expression ,medicine ,Humans ,RNA, Small Interfering ,Cell Proliferation ,Gene knockdown ,Oncogene ,Lentivirus ,Liver Neoplasms ,Intracellular Signaling Peptides and Proteins ,Hep G2 Cells ,Molecular biology ,Recombinant Proteins ,Repressor Proteins ,Oncology ,Doxycycline ,RNA Interference ,Carcinogenesis ,Plasmids - Abstract
Background and Objective: iASPP, an inhibitory member of the apoptosis-stimulating proteins of p53 (ASPP) family, has been found to be up-regulated in various human tumor types. This study was to construct an efficient doxycycline-regulated, lentiviral vector-mediated knockdown system for iASPP that will allow for inducible down-regulation of iASPP gene expression and preliminary functional analysis. Methods: A pair of complementary oligos with hairpin structures targeting the iASPP gene and a negative control were synthesized, then ligated with pLVTHM vector and sequenced. The fragment containing the shRNA cassette was cloned to pLVCT-tTR-KRAB plasmid. The recombinant vectors were co-transfected with viral packaging mix into 293T cells, and viral supernatant was harvested to determine the titer. After treatment with or without doxycycline, HepG2 cells infected with virus were harvested and the expression of iASPP was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. Its effects on tumor growth were characterized using MTS assay, soft agar colony formation, and flow cytometry analysis. Results: The lentiviral vector expressing shRNA that targets to the oncogene iASPP was constructed successfully. HepG2 infected with the lentivirus expressing 5hRNA against iASPP inhibited the expression of iASPP in the presence of doxycycline, which resulted in the repression of tumor cell proliferation and anchorage-independent growth potential. Conclusions: The lentiviral vector-mediated tet-on system demonstrates efficient and inducible knockdown of iASPP in hepatocellular carcinoma cells. iASPP gene may be involved in tumorigenesis and progression of human tumors.
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- 2010
17. [Construction and expression of a novel bisbicistronic expression vector: pCMV-Myc-IRES-EGFP]
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Fei, Yan, Xin-Yu, Zhao, Hong-Xin, Deng, and Yu-Quan, Wei
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Base Sequence ,Recombinant Fusion Proteins ,Blotting, Western ,Genetic Vectors ,Green Fluorescent Proteins ,Molecular Sequence Data ,Genes, myc ,Gene Expression ,Transfection ,Cell Line ,Microscopy, Fluorescence ,Carbon-Nitrogen Lyases ,Humans ,Cloning, Molecular ,Apoptosis Regulatory Proteins - Abstract
It is often necessary to construct more than one recombinant plasmids when investigating the characteristics, physchemical features and functional mechanisms of genes or proteins. Repeated sub-cloning procedures including design of primers, enzyme digestion, ligation and verification of recombinant plasmids, have to be involved with. For this reason, it has become a tendency to developing new genetic vectors which can be used in multitude of experiments. Therefore, by using pIRES vector as a backbone, here we reported the construction of a mammalian expression vector: pCMV-Myc-IRES-EGFP which contains the N-terminal c-Myc epitope tag and the enhanced green fluorescent protein (EGFP) translated in an IRES-dependent manner. This novel vector can be used to testify the efficiency of cell transfection, to collect successfully transfected cell population via cytometry, to conduct transcription and translation in vitro, to purify target proteins or to trap their interactional proteins. The availability of this vector can facilitate function study of genes.
- Published
- 2007
18. [Prokaryotic expression, purification and refolding of extracellular ligand binding domains of chick Tie-2 and its immunogenicity]
- Author
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Yan, Luo, Ling, Tian, Yang, Wu, Qiu, Li, Ji-yan, Liu, Bing, Hu, Jing-mei, Su, Qiu-ming, He, Cheng-wen, Liu, Yu-quan, Wei, and Yan-jun, Wen
- Subjects
Mice, Inbred BALB C ,Protein Folding ,Neovascularization, Pathologic ,Recombinant Fusion Proteins ,Gene Expression ,Enzyme-Linked Immunosorbent Assay ,Ligands ,Polymerase Chain Reaction ,Receptor, TIE-2 ,Mice ,Escherichia coli ,Animals ,Cloning, Molecular ,Chickens ,Plasmids - Abstract
To study the prokaryotic expression of extracellular ligand binding domains of chick Tie-2, the purification and refolding conditions of the recombinant protein, and to observe its immunogenicity in mouse.A DNA fragment encoding extracellular ligand binding domains of chick Tie-2 was obtained by PCR from a previous constructed plasmid as a template. The amplified fragment was then inserted into prokaryotic expression vector PQE30, and was expressed in E. coli XL-1 blue by adding isopropyl-beta-D-thiogalactoside(IPTG). The recombinant protein in inclusion bodies was purified by nickel-nitrilotriacetic acid (Ni-NTA) affinity chromatography under denatured conditions. Then the refolding of the purified protein was performed with gradient dialysis. The target protein was injected into mouse subcutaneously, and the antiserum of the mouse was analyzed by ELISA and Western blot analysis.The recombinant protein was highly expressed in E. coli XL-1 blue, and in mouse it produced the antibody which could specifically recognize the recombinant protein.The protein of extracellular ligand binding domains of chick Tie-2 can be highly expressed in prokaryotic expression system, and the expressed protein can induce immune response in mouse. These findings are very important for the further study of this protein in anti-angiogenesis and immunotherapy research.
- Published
- 2004
19. [Anticancer effect of tanshinone and its mechanisms]
- Author
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Shu-Lan, Yuan, Xiu-Jie, Wang, and Yu-Quan, Wei
- Subjects
Abietanes ,Animals ,Gene Expression ,Humans ,Apoptosis ,Salvia miltiorrhiza ,DNA ,Phenanthrenes ,Antineoplastic Agents, Phytogenic ,Telomerase - Abstract
Tanshinone IIA is a derivative of phenanthrene-quinone isolated from Salvia miltiorrhiza BUNGE, which is a traditional herbal medicine that is used to treat cardiovascular diseases. Recent studies showed that Tanshinone IIA possesses cytotoxic activity against many kinds of human carcinoma cell lines, induces differentiation and apoptosis and inhibits invasion and metastasis of cancer cells. Its mechanisms are thought as inhibiting DNA synthesis and proliferation of cancer cells, regulating the expression of genes related to proliferation, differentiation, and apoptosis, inhibiting the telomerase activity of cancer cells, and changing the expression of cellular surface antigen.
- Published
- 2003
20. Recombinant Human Sonic Hedgehog Protein Regulates the Expression of ZO-1 and Occludin by Activating Angiopoietin-1 in Stroke Damage.
- Author
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Xia, Yuan-peng, He, Quan-wei, Li, Ya-nan, Chen, Sheng-cai, Huang, Ming, Wang, Yong, Gao, Yuan, Huang, Yan, Wang, Meng-die, Mao, Ling, and Hu, Bo
- Subjects
- *
RECOMBINANT proteins , *GENE expression , *GENETIC regulation , *CEREBRAL ischemia , *BLOOD-brain barrier , *PERMEABILITY (Biology) , *ARTERIAL occlusions - Abstract
This study examines the regulating effect of Sonic Hedgehog (Shh) on the permeability of the blood-brain barrier (BBB) in cerebral ischemia. By employing permanent middle cerebral artery occlusion (pMCAO) model, we find that Shh significantly decreases brain edema and preserves BBB permeability. Moreover, Shh increases zonula occludens-1 (ZO-1), occludin and angiopiotetin-1 (Ang-1) expression in the ischemic penumbra. Blockage of Shh with cyclopamine abolishes the effects of Shh on brain edema, BBB permeability and ZO-1, occludin, Ang-1 expression. Primary brain microvessel endothelial cells (BMECs) and astrocytes were pre-treated with Shh, cyclopamine, Ang-1-neutralizing antibody, and subjected to oxygen-glucose deprivation (OGD). Results show that the Ang-1 protein level in the culture medium of Shh-treated astrocytes is significantly higher. Shh also increased ZO-1, occludin and Ang-1 expression in BMECs, while cyclopamine and Ang-1-neutralizing antibody inhibited the effects of Shh on the ZO-1 and occludin expression, respectively. This study suggests that, under ischemic insults, Shh triggers Ang-1 production predominantly in astrocytes, and the secreted Ang-1 acts on BMECs, thereby upregulating ZO-1 and occludin to repair the tight junction and ameliorate the brain edema and BBB leakage. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
21. NOXA-Induced Alterations in the Bax/Smac Axis Enhance Sensitivity of Ovarian Cancer Cells to Cisplatin.
- Author
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Chao Lin, Xin-yu Zhao, Lei Li, Huan-yi Liu, Kang Cao, Yang Wan, Xin-yu Liu, Chun-lai Nie, Lei Liu, Ai-ping Tong, Hong-xin Deng, Jiong Li, Zhu Yuan, and Yu-quan Wei
- Subjects
APOPTOTIC protease-activating factor 1 ,CANCER genetics ,OVARIAN cancer ,CANCER cell growth ,CANCER cell analysis ,CISPLATIN ,GENE targeting ,GENE expression - Abstract
Ovarian cancer is the most common cause of death from gynecologic malignancy. Deregulation of p53 and/or p73-associated apoptotic pathways contribute to the platinum-based resistance in ovarian cancer. NOXA, a pro-apoptotic BH3- only protein, is identified as a transcription target of p53 and/or p73. In this study, we found that genetic variants of Bcl-2 proteins exist among cisplatin-sensitive and -resistant ovarian cancer cells, and the responses of NOXA and Bax to cisplatin are regulated mainly by p53. We further evaluated the effect of NOXA on cisplatin. NOXA induced apoptosis and sensitized A2780s and SKOV3 cells to cisplatin in vitro and in vivo. The effects were mediated by elevated Bax expression, enhanced caspase activation, release of Cyt C and Smac into the cytosol. Furthermore, gene silencing of Bax or Smac significantly attenuated NOXA and/or cisplatin-induced apoptosis in chemosensitive A2780s cells, whereas overexpression of Bax or addition of Smac-N7 peptide significantly increased NOXA and/or cisplatin-induced apoptosis in chemoresistant SKOV3 cells. To our knowledge, these data suggest a new mechanism by which NOXA chemosensitized ovarian cancer cells to cisplatin by inducing alterations in the Bax/Smac axis. Taken together, our findings show that NOXA is potentially useful as a chemosensitizer in ovarian cancer therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
22. Enhancement of cisplatin sensitivity in lewis lung carcinoma by liposome-mediated delivery of a survivin mutant.
- Author
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Dan-Dan Yu, Chun-Ting Wang, Hua-Shan Shi, Zhi-Yong Li, Li Pan, Qing-Zhong Yuan, Fei Leng, Yuan Wen, Xiang Chen, and Yu-Quan Wei
- Subjects
CISPLATIN ,LUNG cancer ,LIPOSOMES ,APOPTOSIS ,GENE expression ,CANCER cells ,DRUG therapy ,IMMUNE response ,HEALTH risk assessment - Abstract
Background: A high concentration of cisplatin (CDDP) induces apoptosis in many tumor cell lines. CDDP has been administered by infusion to avoid severe toxicity. Recently, it has been reported that changes in survivin expression or function may lead to tumor sensitization to chemical and physical agents. The aim of this study was to determine whether a dominant-negative mouse survivin mutant could enhance the anti-tumor activity of CDDP. Methods: A plasmid encoding the phosphorylation-defective dominant-negative mouse survivin threonine 34Talanine mutant (survivin T34A) complexed to a DOTAP-chol liposome (Lip-mS) was administered with or without CDDP in Lewis Lung Carcinoma (LLC) cells and in mice bearing LLC tumors, and the effects on apoptosis, tumor growth and angiogenesis were assessed. Data were analyzed using one-way analysis of variance(ANOVA), and a value of P < 0.05 was considered to be statistically significant. Results: LLC cells treated with a combination of Lip-mS and CDDP displayed increased apoptosis compared with those treated with Lip-mS or CDDP alone. In mice bearing LLC tumors and treated with intravenous injections of Lip-mS and/ or CDDP, combination treatment significantly reduced the mean tumor volume compared with either treatment alone. Moreover, the antitumor effect of Lip-mS combined with CDDP was greater than their anticipated additive effects. Conclusion: These data suggest that the dominant-negative survivin mutant, survivin T34A, sensitized LLC cells to chemotherapy of CDDP. The synergistic antitumor activity of the combination treatment may in part result from an increase in the apoptosis of tumor cells, inhibition of tumor angiogenesis and induction of a tumor-protective immune response. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
23. Pharmacophore Modelling and Virtual Screening for Identification of New Aurora-A Kinase Inhibitors.
- Author
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Xiao-Qiang Deng, Hui-Yuan Wang, Ying-Lan Zhao, Ming-Li Xiang, Pei-Du Jiang, Zhi-Xing Cao, Yu-Zhu Zheng, Shi-Dong Luo, Luo-Ting Yu, Yu-Quan Wei, and Sheng-Yong Yang
- Subjects
CANCER treatment ,AURORAS ,MOLECULAR structure ,CANCER cells ,GENE expression ,DATABASE searching - Abstract
Aurora-A has been identified as one of the most attractive targets for cancer therapy and a considerable number of Aurora-A inhibitors have been reported recently. In order to clarify the essential structure–activity relationship for the known Aurora-A inhibitors as well as identify new lead compounds against Aurora-A, 3D pharmacophore models were developed based on the known inhibitors. The best hypothesis, Hypo1, was used to screen molecular structural databases, including Specs and China Natural Products Database for potential lead compounds. The hit compounds were subsequently subjected to filtering by Lipinski’s rules and docking study to refine the retrieved hits and as a result to reduce the rate of false positive. Finally, 39 compounds were purchased for further in vitro assay against several human tumour cell lines including A549, MCF-7, HepG2 and PC-3, in which Aurora-A is overexpressed. Two compounds show very low micromolar inhibition potency against some of these tumour cells. And they have been selected for further investigation. [ABSTRACT FROM AUTHOR]
- Published
- 2008
- Full Text
- View/download PDF
24. Glycyrrhizic acid treatment ameliorates anxiety-like behaviour via GLT1 and Per1/2-dependent pathways.
- Author
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Ma, Shanbo, Chong, Ye, Zhang, Rui, Quan, Wei, Gui, Jiayue, Li, Long, Wang, Jin, Miao, Shan, Shi, Xiaopeng, Zhao, Minggao, and Zhang, Kun
- Subjects
- *
CHINESE medicine , *COMPUTER-assisted molecular modeling , *ANXIETY , *REVERSE transcriptase polymerase chain reaction , *TRANQUILIZING drugs , *PLANT extracts , *MICE , *GENE expression , *MEDICINAL plants , *DRUG efficacy , *ANIMAL experimentation - Abstract
As a traditional Chinese medicinal herb, Glycyrrhiza. Fisch. (licorice root, chinese name: Gancao) has a variety of medicinal values and is widely used clinically. Its main active ingredient, glycyrrhizic acid (GA), is believed to have a neuroprotective effect. However, the underlying biological mechanisms of GA on stress-induced anxiety disorders are still unclear. To investigate the anti-anxiety effect of GA and its underlying mechanism. We selected the anxiety model induced by repeated chronic restraint stress (CRS) for 2 h on each of 7 consecutive days. GA (4, 20, 100 mg/kg) was injected intraperitoneally once daily for 1 week. The potential GA receptors were identified using whole-cell patches and computer-assisted docking of molecules. High-throughput RNA sequencing, adeno-associated virus-mediated gene regulation, Western blotting, and RT-qPCR were used to assess the underlying molecular pathways. GA alleviate depression-like and anxiety-like behaviors in CRS mice. GA decreased synaptic transmission by facilitating glutamate reuptaking in mPFC. Meanwhile, long-term GA treatment increased the expression of clock genes Per1 and Per2. Suppressing both Per1 and Per2 abolished the anxiolytic effects of GA treatment. Our study suggests that GA may be developed for the treatment of stress-induced anxiety disorders, and its mechanism is related to GLT1 and Per1/2-dependent pathways. This presents a novel approach to discovering potent therapeutic drugs. [Display omitted] • GA improves anxiety-like behaviour. • GA reduces neuronal excitability. • Glycyrrhizic acid facilitates glutamate re-uptake in a GLT1-dependent pathway. • GA regulates the expression of Per1 and Per2. • As a traditional Chinese medicinal her, glycyrrhiza has a variety of medicinal values and is widely used clinically. Its main active ingredient, glycyrrhizic acid (GA), is believed to have a neuroprotective effect. However,the underlying biological mechanisms of GA on stress-induced anxiety disorders are still unclear. This study detected the underlying mechanism of anxiolytic effects after short-term and long-term treatments with GA. The results showed that a single GA injection as well as chronic GA treatment elicited a significant anxiolytic effect in mice receiving chronic restraint stress. GA decreased synaptic transmission by facilitating the re-uptake in mPFC. Meanwhile, long-term GA treatment increased the expression of clock genes, Per1 and Per2. Suppressing both Per1 and Per2 reduced anxiolytic effects of long-term GA treatment, suggesting two different mechanisms mediating anxiolytic effects of GA. Our study suggests that GA may be developed to treat stress-induced anxiety disorders. This presents a novel approach towards discovering potent therapeutic drugs. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
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