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  1. Article ; Online: Cycloastragenol suppresses M1 and promotes M2 polarization in LPS-stimulated BV-2 cells and ischemic stroke mice.

    Chen, Ting / Li, Ziqing / Li, Shichun / Zou, Yingxiang / Gao, Xinyi / Shu, Shi / Wang, Zhifei

    International immunopharmacology

    2022  Volume 113, Issue Pt A, Page(s) 109290

    Abstract: There are two distinct phenotypes of activated microglia, pro-inflammatory M1 and anti-inflammatory M2. Accumulating evidence indicates that shifting the microglial polarization from M1 to M2 is a potential strategy for the treatment of neuroinflammation- ...

    Abstract There are two distinct phenotypes of activated microglia, pro-inflammatory M1 and anti-inflammatory M2. Accumulating evidence indicates that shifting the microglial polarization from M1 to M2 is a potential strategy for the treatment of neuroinflammation-associated brain diseases, including ischemic stroke. Cycloastragenol (CAG) is a hydrolysis product of astragaloside IV, the major active component of Astragalus radix. We have previously demonstrated that CAG has anti-inflammatory effect in a mouse model of ischemic stroke. This study investigated the effect of CAG on the phenotype polarization of microglia in lipopolysaccharide (LPS)-stimulated BV-2 mouse microglial cells and ischemic stroke mice. In LPS-treated BV-2 cells, we found that CAG significantly reduced the expression of M1 markers, including pro-inflammatory cytokines and enzymes. In contrast, CAG promoted the expression of M2 markers, including anti-inflammatory cytokines and growth factor. In addition, CAG inhibited the activation of nuclear factor-κB (NF-κB) and enhanced the activation of nuclear factor E2-related factor 2 (Nrf2) and the expression of its downstream heme oxygenase-1 (HO-1). Furthermore, CAG also inhibited levels of M1 markers, promoted those of M2 markers, and enhanced Nrf2 activation and HO-1 expression in ischemic mouse brain. Importantly, the effect of CAG on M2 markers, but not M1 markers, was reversed by Nrf2 siRNA in LPS-stimulated BV-2 cells. Together, our results suggested that CAG promoted microglial M2 and suppressed M1 polarization through activating Nrf2 and inhibiting NF-κB, respectively, in LPS-stimulated BV-2 cells and ischemic mouse brain. CAG is a promising candidate for the treatment of neuroinflammation-related diseases, including ischemic stroke.
    MeSH term(s) Animals ; Mice ; Anti-Inflammatory Agents/pharmacology ; Cytokines/metabolism ; Ischemic Stroke ; Lipopolysaccharides ; Microglia ; NF-E2-Related Factor 2/metabolism ; NF-kappa B/metabolism ; Sapogenins/pharmacology
    Chemical Substances Anti-Inflammatory Agents ; cycloastragenol (X37D9F2L0V) ; Cytokines ; Lipopolysaccharides ; NF-E2-Related Factor 2 ; NF-kappa B ; Sapogenins
    Language English
    Publishing date 2022-10-14
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2022.109290
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5408: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Astragaloside IV ameliorates peripheral immunosuppression induced by cerebral ischemia through inhibiting HPA axis.

    Zou, Yingxiang / Li, Shichun / Chen, Ting / Li, Ziqing / Gao, Xinyi / Wang, Zhifei

    International immunopharmacology

    2022  Volume 105, Page(s) 108569

    Abstract: Post-ischemic peripheral immunosuppression increases vulnerability to infection which is a common complication and worsens outcome in ischemic stroke patients. Hypothalamic-pituitary-adrenal (HPA) axis plays a key role in post-ischemic immunosuppression. ...

    Abstract Post-ischemic peripheral immunosuppression increases vulnerability to infection which is a common complication and worsens outcome in ischemic stroke patients. Hypothalamic-pituitary-adrenal (HPA) axis plays a key role in post-ischemic immunosuppression. Astragaloside IV (ASIV), isolated from Astragalus membranaceus, possesses immunomodulatory and neuroprotective effects against cerebral ischemic injury. This study investigated the effect of ASIV on cerebral ischemia-induced peripheral immunosuppression and the underlying mechanism in a mouse model of middle cerebral artery occlusion (MCAO). Our results showed that ASIV significantly prevented the atrophy of spleen and the reduction of splenic cell count. Meanwhile, ASIV preserved cell numbers of splenic NK, T, and B cells in the spleen. ASIV also suppressed apoptosis of splenic cells and preserved their proliferation ability. In addition, ASIV robustly reduced the mRNA expression of TNF-α, IL-1β, IL-6 and CRH in the hypothalamus, as well as the enlargement of adrenal gland and the increase of corticosterone in blood, indicating the inhibition of HPA axis by ASIV. Furthermore, ASIV did not enhance the effect of HPA inhibition on reducing splenic atrophy and preserving splenic NK, T, and B cell numbers in MCAO mice. Of note, ASIV did not attenuate splenic cell apoptosis induced by prednisolone, suggesting that ASIV may ameliorate splenic apoptosis through reducing peripheral glucocorticoid level. Our findings demonstrate that ASIV ameliorates post-ischemic peripheral immunosuppression through inhibiting the activation of HPA axis and targeting HPA activation to ameliorate peripheral immunosuppression may be a promising strategy to improve clinical outcomes of ischemic stroke.
    MeSH term(s) Animals ; Humans ; Hypothalamo-Hypophyseal System ; Immunosuppression Therapy ; Infarction, Middle Cerebral Artery/drug therapy ; Mice ; Pituitary-Adrenal System ; Saponins/pharmacology ; Saponins/therapeutic use ; Triterpenes/pharmacology ; Triterpenes/therapeutic use
    Chemical Substances Saponins ; Triterpenes ; astragaloside A (3A592W8XKE)
    Language English
    Publishing date 2022-01-25
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2022.108569
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Corrigendum to "Fei-Yan-Qing-Hua decoction decreases hyperinflammation by inhibiting HMGB1/RAGE signaling and promotes bacterial phagocytosis in the treatment of sepsis" [J. Ethnopharmacol. (2024 Mar 1) 321:117553].

    Zhang, Huan / Xu, Guihua / Wu, Xiao / Xu, Yanwu / Xu, Lirong / Zou, Yingxiang / Yang, Xiaodong / Pan, Lingyun / Lei, Biao / Mu, Jingwen / Huang, Qilin / Ma, Yuhe / Duan, Naifan / Zhang, Wei / Zheng, Yuejuan

    Journal of ethnopharmacology

    2024  Volume 326, Page(s) 117978

    Language English
    Publishing date 2024-03-05
    Publishing country Ireland
    Document type Published Erratum
    ZDB-ID 134511-4
    ISSN 1872-7573 ; 0378-8741
    ISSN (online) 1872-7573
    ISSN 0378-8741
    DOI 10.1016/j.jep.2024.117978
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1494: Show issues Location:
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  4. Article ; Online: Dehydrozaluzanin C- derivative protects septic mice by alleviating over-activated inflammatory response and promoting the phagocytosis of macrophages.

    Zou, Ying-Xiang / Xiang, Tian-Nan / Xu, Li-Rong / Zhang, Huan / Ma, Yu-He / Zhang, Lu / Zhou, Chun-Xian / Wu, Xiao / Huang, Qi-Lin / Lei, Biao / Mu, Jing-Wen / Qin, Xiang-Yang / Jiang, Xin / Zheng, Yue-Juan

    International immunopharmacology

    2024  Volume 132, Page(s) 111889

    Abstract: Host-directed therapy (HDT) is a new adjuvant strategy that interfere with host cell factors that are required by a pathogen for replication or persistence. In this study, we assessed the effect of dehydrozaluzanin C-derivative (DHZD), a modified ... ...

    Abstract Host-directed therapy (HDT) is a new adjuvant strategy that interfere with host cell factors that are required by a pathogen for replication or persistence. In this study, we assessed the effect of dehydrozaluzanin C-derivative (DHZD), a modified compound from dehydrozaluzanin C (DHZC), as a potential HDT agent for severe infection. LPS-induced septic mouse model and Carbapenem resistant Klebsiella pneumoniae (CRKP) infection mouse model was used for testing in vivo. RAW264.7 cells, mouse primary macrophages, and DCs were used for in vitro experiments. Dexamethasone (DXM) was used as a positive control agent. DHZD ameliorated tissue damage (lung, kidney, and liver) and excessive inflammatory response induced by LPS or CRKP infection in mice. Also, DHZD improved the hypothermic symptoms of acute peritonitis induced by CRKP, inhibited heat-killed CRKP (HK-CRKP)-induced inflammatory response in macrophages, and upregulated the proportions of phagocytic cell types in lungs. In vitro data suggested that DHZD decreases LPS-stimulated expression of IL-6, TNF-α and MCP-1 via PI3K/Akt/p70S6K signaling pathway in macrophages. Interestingly, the combined treatment group of DXM and DHZD had a higher survival rate and lower level of IL-6 than those of the DXM-treated group; the combination of DHZD and DXM played a synergistic role in decreasing IL-6 secretion in sera. Moreover, the phagocytic receptor CD36 was increased by DHZD in macrophages, which was accompanied by increased bacterial phagocytosis in a clathrin- and actin-dependent manner. This data suggests that DHZD may be a potential drug candidate for treating bacterial infections.
    MeSH term(s) Animals ; Mice ; Phagocytosis/drug effects ; Klebsiella Infections/drug therapy ; Klebsiella Infections/immunology ; Klebsiella pneumoniae/drug effects ; Macrophages/drug effects ; Macrophages/immunology ; RAW 264.7 Cells ; Sepsis/drug therapy ; Sepsis/immunology ; Male ; Lipopolysaccharides ; Disease Models, Animal ; Mice, Inbred C57BL ; Signal Transduction/drug effects ; Cytokines/metabolism ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use
    Chemical Substances Lipopolysaccharides ; Cytokines ; Anti-Inflammatory Agents
    Language English
    Publishing date 2024-03-26
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2024.111889
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5408: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Irisflorentin promotes bacterial phagocytosis and inhibits inflammatory responses in macrophages during bacterial infection.

    Xiang, Tiannan / Zou, Yingxiang / Jiang, Xinru / Xu, Lirong / Zhang, Lu / Zhou, Chunxian / Hu, You / Ye, Xiaolan / Yang, Xiao-Dong / Jiang, Xin / Zheng, Yuejuan

    Heliyon

    2023  Volume 10, Issue 1, Page(s) e23225

    Abstract: Bacterial infection remains a big concern in the patients of ICU, which is the main cause of life-threatening organ dysfunction, or even sepsis. The poor control of bacterial infection caused by antibiotic resistance, etc. or the overwhelming immune ... ...

    Abstract Bacterial infection remains a big concern in the patients of ICU, which is the main cause of life-threatening organ dysfunction, or even sepsis. The poor control of bacterial infection caused by antibiotic resistance, etc. or the overwhelming immune response are the most important patho genic factors in intensive care unit (ICU) patients. As main pathogens, antibiotic-resistant bacteria, such as methicillin-resistant
    Language English
    Publishing date 2023-12-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2023.e23225
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Fei-Yan-Qing-Hua decoction decreases hyperinflammation by inhibiting HMGB1/RAGE signaling and promotes bacterial phagocytosis in the treatment of sepsis.

    Zhang, Huan / Xu, Guihua / Wu, Xiao / Xu, Yanwu / Xu, Lirong / Zou, Yingxiang / Yang, Xiaodong / Pan, Lingyun / Lei, Biao / Mu, Jingwen / Huang, Qilin / Ma, Yuhe / Duan, Naifan / Zhang, Wei / Zheng, Yuejuan

    Journal of ethnopharmacology

    2023  Volume 321, Page(s) 117553

    Abstract: Ethnopharmacological relevance: Fei-Yan-Qing-Hua decoction (FYQHD), derived from the renowned formula Ma Xing Shi Gan tang documented in Zhang Zhong Jing's "Treatise on Exogenous Febrile Disease" during the Han Dynasty, has demonstrated notable efficacy ...

    Abstract Ethnopharmacological relevance: Fei-Yan-Qing-Hua decoction (FYQHD), derived from the renowned formula Ma Xing Shi Gan tang documented in Zhang Zhong Jing's "Treatise on Exogenous Febrile Disease" during the Han Dynasty, has demonstrated notable efficacy in the clinical treatment of pneumonia resulting from bacterial infection. However, its molecular mechanisms underlying the therapeutic effects remains elusive.
    Aim of the study: This study aimed to investigate the protective effects of FYQHD against lipopolysaccharide (LPS) and carbapenem-resistant Klebsiella pneumoniae (CRKP)-induced sepsis in mice and to elucidate its specific mechanism of action.
    Materials and methods: Sepsis models were established in mice through intraperitoneal injection of LPS or CRKP. FYQHD was administered via gavage at low and high doses. Serum cytokines, bacterial load, and pathological damage were assessed using enzyme-linked immunosorbent assay (ELISA), minimal inhibitory concentration (MIC) detection, and hematoxylin and eosin staining (H&E), respectively. In vitro, the immunoregulatory effects of FYQHD on macrophages were investigated through ELISA, MIC, quantitative real-time PCR (Q-PCR), immunofluorescence, Western blot, and a network pharmacological approach.
    Results: The application of FYQHD in the treatment of LPS or CRKP-induced septic mouse models revealed significant outcomes. FYQHD increased the survival rate of mice exposed to a lethal dose of LPS to 33.3%, prevented hypothermia (with a rise of 3.58 °C), reduced pro-inflammatory variables (including TNF-α, IL-6, and MCP-1), and mitigated tissue damage in LPS or CRKP-induced septic mice. Additionally, FYQHD decreased bacterial load in CRKP-infected mice. In vitro, FYQHD suppressed the expression of inflammatory cytokines in macrophages activated by LPS or HK-CRKP. Mechanistically, FYQHD inhibited the PI3K/AKT/mTOR/4E-BP1 signaling pathway, thereby suppressing the translational level of inflammatory cytokines. Furthermore, it reduced the expression of HMGB1/RAGE, a positive feedback loop in the inflammatory response. Moreover, FYQHD was found to enhance the phagocytic activity of macrophages by upregulating the expression of phagocytic receptors such as CD169 and SR-A1.
    Conclusion: FYQHD provides protection against bacterial sepsis by concurrently inhibiting the inflammatory response and augmenting the phagocytic ability of immune cells.
    MeSH term(s) Mice ; Animals ; Lipopolysaccharides/pharmacology ; HMGB1 Protein/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction ; Cytokines/metabolism ; Phagocytosis ; Sepsis/drug therapy
    Chemical Substances Lipopolysaccharides ; HMGB1 Protein ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Cytokines
    Language English
    Publishing date 2023-12-06
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 134511-4
    ISSN 1872-7573 ; 0378-8741
    ISSN (online) 1872-7573
    ISSN 0378-8741
    DOI 10.1016/j.jep.2023.117553
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1494: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Cycloastragenol upregulates SIRT1 expression, attenuates apoptosis and suppresses neuroinflammation after brain ischemia.

    Li, Man / Li, Shi-Chun / Dou, Bao-Kai / Zou, Ying-Xiang / Han, Hao-Zhen / Liu, Dong-Xiang / Ke, Zun-Ji / Wang, Zhi-Fei

    Acta pharmacologica Sinica

    2020  Volume 41, Issue 8, Page(s) 1025–1032

    Abstract: Cycloastragenol (CAG) is the active form of astragaloside IV isolated from Astragalus Radix, which displays multiple pharmacological effects. Silent information regulator 1 (SIRT1), a class III histone deacetylase, has been shown to play an important ... ...

    Abstract Cycloastragenol (CAG) is the active form of astragaloside IV isolated from Astragalus Radix, which displays multiple pharmacological effects. Silent information regulator 1 (SIRT1), a class III histone deacetylase, has been shown to play an important role in neuroprotection against cerebral ischemia. In this study, we investigated whether CAG protected against ischemic brain injury and, if so, whether the beneficial effects were associated with the regulation of SIRT1 in the ischemic brain. Mice were subjected to 45 min of middle cerebral artery occlusion (MCAO) followed by reperfusion. CAG (5, 10, 20 mg/kg) was injected intraperitoneally at the onset of reperfusion, 12 h later and then twice daily for up to three days. CAG dose-dependently reduced brain infarct volume, significantly ameliorated functional deficits, and prevented neuronal cell loss in MCAO mice. Meanwhile, CAG significantly reduced matrix metalloproteinase-9 activity, prevented tight junction degradation and subsequently ameliorated blood-brain barrier disruption. Moreover, CAG significantly upregulated SIRT1 expression in the ischemic brain but did not directly activate its enzymatic activity. Concomitant with SIRT1 upregulation, CAG reduced p53 acetylation and the ratio of Bax to Bcl-2 in the ischemic brain. CAG also inhibited NF-κB p65 nuclear translocation. As a result, CAG suppressed the mRNA expression of pro-inflammatory cytokines, including TNF-α and IL-1β, and inhibited the activation of microglia and astrocytes in the ischemic brain. Our findings suggest that CAG is neuroprotective against ischemic brain injury in mice and that its beneficial effect may involve SIRT1 upregulation and the inhibition of apoptosis and neuroinflammation in the ischemic brain.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Blood-Brain Barrier/drug effects ; Infarction, Middle Cerebral Artery/drug therapy ; Inflammation/drug therapy ; Male ; Matrix Metalloproteinase 9/metabolism ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit/metabolism ; Neuroprotective Agents/therapeutic use ; Sapogenins/therapeutic use ; Signal Transduction/drug effects ; Sirtuin 1/metabolism ; Tight Junctions/metabolism ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation/drug effects
    Chemical Substances NF-kappa B p50 Subunit ; Neuroprotective Agents ; Sapogenins ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Nfkb1 protein, mouse (147257-52-1) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; cycloastragenol (X37D9F2L0V)
    Keywords covid19
    Language English
    Publishing date 2020-03-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1360774-1
    ISSN 1745-7254 ; 0253-9756 ; 1671-4083
    ISSN (online) 1745-7254
    ISSN 0253-9756 ; 1671-4083
    DOI 10.1038/s41401-020-0386-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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