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  1. Artikel ; Online: Nao-Fu-Cong ameliorates diabetic cognitive dysfunction by inhibition of JNK/CHOP/Bcl2-mediated apoptosis in vivo and in vitro.

    Jing, Guang-Chan / Liu, Di / Liu, Yu-Qin / Zhang, Meng-Ren

    Chinese journal of natural medicines

    2020  Band 18, Heft 9, Seite(n) 704–713

    Abstract: Chinese herbal compound Nao-Fu-Cong (NFC) has been mainly used to treat cognitive disorders in Traditional Chinese Medicine (TCM). The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of JNK/CHOP/ ... ...

    Abstract Chinese herbal compound Nao-Fu-Cong (NFC) has been mainly used to treat cognitive disorders in Traditional Chinese Medicine (TCM). The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of JNK/CHOP/Bcl2-mediated apoptosis pathway or not. We randomly assigned STZ (60 mg·kg
    Mesh-Begriff(e) Acetylcysteine/pharmacology ; Animals ; Anthracenes/pharmacology ; Apoptosis/drug effects ; Cognitive Dysfunction/drug therapy ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/physiopathology ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal/pharmacology ; Hippocampus/drug effects ; MAP Kinase Signaling System/drug effects ; Male ; Membrane Potential, Mitochondrial/drug effects ; Neurons/drug effects ; Neuroprotective Agents/pharmacology ; Proto-Oncogene Proteins c-bcl-2/drug effects ; Random Allocation ; Rats ; Transcription Factor CHOP/antagonists & inhibitors
    Chemische Substanzen Anthracenes ; Bcl2 protein, rat ; Drugs, Chinese Herbal ; Neuroprotective Agents ; Proto-Oncogene Proteins c-bcl-2 ; naofucong ; Transcription Factor CHOP (147336-12-7) ; pyrazolanthrone (1TW30Y2766) ; Acetylcysteine (WYQ7N0BPYC)
    Sprache Englisch
    Erscheinungsdatum 2020-08-12
    Erscheinungsland China
    Dokumenttyp Journal Article
    ZDB-ID 2192577-X
    ISSN 1875-5364 ; 2095-6975 ; 1672-3651
    ISSN (online) 1875-5364
    ISSN 2095-6975 ; 1672-3651
    DOI 10.1016/S1875-5364(20)60009-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Transient Receptor Potential Melastatin 2:an Ion Channel for Oxidative Stress Sensing.

    Jing, Guang-chan / Zhang, Meng-ren

    Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae

    2016  Band 38, Heft 3, Seite(n) 364–367

    Abstract: Transient receptor potential (TRP) channel is a superfamily of cation channels located on the cell membrane. TRP channels are classified into seven subfamilies based on the amino acid sequence homology,and transient receptor potential melastatin 2(TRPM2) ...

    Abstract Transient receptor potential (TRP) channel is a superfamily of cation channels located on the cell membrane. TRP channels are classified into seven subfamilies based on the amino acid sequence homology,and transient receptor potential melastatin 2(TRPM2) is the second member of the TRPM subfamily. More evidences have revealed the important roles of TRPM2 in physiological and pathological events such as release of insulin from pancreatic Β-cells,inflammatory cytokines production from cells,and oxidative stress-induced cell death. As a cellular sensor for oxidative stress channel,TRPM2 is activated by a variety of factors. TRPM2 is a potential therapeutic target for oxidative stress-related diseases.
    Mesh-Begriff(e) Cell Death ; Cytokines ; Humans ; Insulin ; Oxidative Stress ; TRPM Cation Channels/physiology
    Chemische Substanzen Cytokines ; Insulin ; TRPM Cation Channels ; TRPM2 protein, human
    Sprache Englisch
    Erscheinungsdatum 2016--10
    Erscheinungsland China
    Dokumenttyp Journal Article ; Review
    ZDB-ID 604853-5
    ISSN 1000-503X
    ISSN 1000-503X
    DOI 10.3881/j.issn.1000-503X.2016.03.023
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Nao-Fu-Cong ameliorates diabetic cognitive dysfunction by inhibition of JNK/CHOP/Bcl2-mediated apoptosis in vivo and in vitro

    JING, Guang-Chan / LIU, Di / LIU, Yu-Qin / ZHANG, Meng-Ren

    Chinese journal of natural medicines. 2020 Sept., v. 18, no. 9

    2020  

    Abstract: Chinese herbal compound Nao-Fu-Cong (NFC) has been mainly used to treat cognitive disorders in Traditional Chinese Medicine (TCM). The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of JNK/CHOP/ ... ...

    Abstract Chinese herbal compound Nao-Fu-Cong (NFC) has been mainly used to treat cognitive disorders in Traditional Chinese Medicine (TCM). The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of JNK/CHOP/Bcl2-mediated apoptosis pathway or not. We randomly assigned STZ (60 mg·kg⁻¹)-induced diabetic rats into control group, diabetic model group and NFC groups (low-dose, medium-dose and high-dose). The primary culture of hippocampal neurons were transferred into different culture media on the third day. The cells were then divided into control group, high-glucose group, NFC (low-dose, medium-dose and high-dose) groups, CHOP si-RNA intervention group, JNK pathway inhibitor SP600125 group and oxidative stress inhibitor N-acetylcysteine (NAC) group. NFC significantly improved the cognitive function of diabetic rats, and had neuroprotective effect on hippocampal neurons cultured in high glucose. Further research results showed that NFC could reduce the apoptosis of hippocampal neurons in rats with diabetic cognitive dysfunction. NFC had inhibitory effects on CHOP/JNK apoptosis pathway induced by high glucose, and also decreased the levels of ROS and increased the mitochondrial membrane potential. These suggested that the neuroprotective effect of NFC might be related to the inhibition of CHOP and JNK apoptotic signaling pathways, and the cross pathway between oxidative stress and mitochondrial damage pathway.
    Schlagwörter Oriental traditional medicine ; acetylcysteine ; apoptosis ; cells ; cognition ; cognitive disorders ; culture media ; glucose ; membrane potential ; mitochondria ; mitochondrial membrane ; models ; neurons ; neuroprotective effect ; oxidative stress ; rats ; research ; signal transduction
    Sprache Englisch
    Erscheinungsverlauf 2020-09
    Umfang p. 704-713.
    Erscheinungsort Elsevier B.V.
    Dokumenttyp Artikel
    Anmerkung NAL-light
    ZDB-ID 2192577-X
    ISSN 1875-5364 ; 2095-6975 ; 1672-3651
    ISSN (online) 1875-5364
    ISSN 2095-6975 ; 1672-3651
    DOI 10.1016/S1875-5364(20)60009-7
    Datenquelle NAL Katalog (AGRICOLA)

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  4. Artikel: Effect of Chinese herbal compound Naofucong () on the inflammatory process induced by high glucose in BV-2 cells.

    Jing, Guang-Chan / Zhang, Meng-Ren / Ji, Chao / Zuo, Ping-Ping / Liu, Yu-Qin / Gu, Bei

    Chinese journal of integrative medicine

    2016  Band 22, Heft 11, Seite(n) 832–839

    Abstract: Objective: To determine the effect of medicated serum of Chinese herbal compound Naofucong (, NFC) on the microglia BV-2 cells viability and the transcription and expression of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in microglia BV-2 ... ...

    Abstract Objective: To determine the effect of medicated serum of Chinese herbal compound Naofucong (, NFC) on the microglia BV-2 cells viability and the transcription and expression of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in microglia BV-2 cells to further explore the mechanisms underlying the protective effect of NFC on inflammatory process induced by high glucose.
    Methods: The microglia BV-2 cells incubated in vitro were divided into different groups: the control group (25 mmol/L glucose), the model group (75 mmol/L glucose), high glucose media containing different dose medicated serum of NFC. After being cultured for 24 h, changes in IL-6 and TNF-α were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The expression of surface marker CD11b of activated microglia was measured by confocal laser scanning microscope and Western blot. Nuclear factor-κB (NF-κB) p-p65 expression was analyzed by Western blot.
    Results: The model group obviously increased the expression of microglial surface marker CD11b and NF-κB p-p65 (all P<0.01), induced a signifificant up-regulation of release and the mRNA expression of IL-6 and TNF-α (P<0.01 or P<0.05). The medicated serum of NFC could obviously down-regulate the transcription and expression of surface marker CD11 b and NF-κB p-p65 (all P<0.01), and inhibit the mRNA and protein expression (P<0.01 or P<0.05) of inflflammatory cytokines, such as IL-6 and TNF-α, in microglia BV-2 cells cultured with high glucose for 24 h.
    Conclusions: The inhibition of microglial activation and IL-6 and TNF-α expression induced by high glucose may at least partly explain NFC therapeutic effects on diabetes-associated cognitive decline diseases. Its underlying mechanism could probably be related to the inhibition of NFC on NF-κB phosphorylation.
    Mesh-Begriff(e) Animals ; Biomarkers/metabolism ; Blotting, Western ; CD11b Antigen/genetics ; CD11b Antigen/metabolism ; Cell Line ; Cell Shape/drug effects ; Cell Survival/drug effects ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Glucose/toxicity ; Inflammation/drug therapy ; Inflammation/pathology ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Male ; Mice ; Microscopy, Confocal ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Transcription Factor RelA/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
    Chemische Substanzen Biomarkers ; CD11b Antigen ; Drugs, Chinese Herbal ; Interleukin-6 ; RNA, Messenger ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha ; naofucong ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2016-11
    Erscheinungsland China
    Dokumenttyp Journal Article
    ZDB-ID 2171254-2
    ISSN 1993-0402 ; 1672-0415
    ISSN (online) 1993-0402
    ISSN 1672-0415
    DOI 10.1007/s11655-016-2256-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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