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  1. Article ; Online: Based on network pharmacology and molecular docking to explore the molecular mechanism of Ginseng and Astragalus decoction against postmenopausal osteoporosis.

    Fan, Wei / Jiang, Zong-Zhe / Wan, Sheng-Rong

    Medicine

    2023  Volume 102, Issue 46, Page(s) e35887

    Abstract: Traditional Chinese medicine suggests that Ginseng and Astragalus Decoction (GAD) may effectively treat postmenopausal osteoporosis (PMO). However, the exact mechanism of action for GAD remains unclear. This study aims to utilize network pharmacology and ...

    Abstract Traditional Chinese medicine suggests that Ginseng and Astragalus Decoction (GAD) may effectively treat postmenopausal osteoporosis (PMO). However, the exact mechanism of action for GAD remains unclear. This study aims to utilize network pharmacology and molecular docking technology to explore the potential mechanism of GAD in treating PMO. The main chemical components of GAD were identified by consulting literature and traditional Chinese medicine systems pharmacology database. GeneCards and online mendelian inheritance in man were used to identify PMO disease targets, and Cytoscape 3.8.2 software was used to construct a herb-disease-gene-target network. The intersection of drug targets and disease targets was introduced into the search tool for the retrieval of interacting genes platform to construct a protein-protein interaction network. Additionally, we further conducted gene ontology and Kyoto encyclopedia of genes and genomes enrichment analyses, followed by molecular docking between active ingredients and core protein targets. We have identified 59 potential targets related to the treatment of PMO by GAD, along with 33 effective components. Quercetin and kaempferol are the compounds with higher degree. In the protein-protein interaction network, IL6, AKT1, and IL1B are proteins with high degree. The enrichment analysis of gene ontology and KEEG revealed that biological processes involved in treating PMO with GAD mainly include response to hormones, positive regulation of phosphorylation, and regulation of protein homodimerization activity. The signal pathways primarily include Pathways in cancer, PI3K-Akt signaling pathway, and AGE-RAGE signaling pathway. Molecular docking results indicate that kaempferol and quercetin have a high affinity for IL6, AKT1, and IL1B. Our research predicts that IL6, AKT1, and IL1B are highly likely to be potential targets for treating PMO with GAD. PI3K/AKT pathway and AGE-ARGE pathway may play an important role in PMO.
    MeSH term(s) Humans ; Female ; Molecular Docking Simulation ; Kaempferols ; Network Pharmacology ; Panax ; Interleukin-6 ; Osteoporosis, Postmenopausal/drug therapy ; Osteoporosis, Postmenopausal/genetics ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Quercetin ; Astragalus Plant ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use
    Chemical Substances Kaempferols ; Interleukin-6 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Quercetin (9IKM0I5T1E) ; Drugs, Chinese Herbal
    Language English
    Publishing date 2023-11-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80184-7
    ISSN 1536-5964 ; 0025-7974
    ISSN (online) 1536-5964
    ISSN 0025-7974
    DOI 10.1097/MD.0000000000035887
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.171: Show issues Location:
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  2. Article ; Online: Hyperglycemia-induced STING signaling activation leads to aortic endothelial injury in diabetes.

    An, Ying / Geng, Kang / Wang, Hong-Ya / Wan, Sheng-Rong / Ma, Xiu-Mei / Long, Yang / Xu, Yong / Jiang, Zong-Zhe

    Cell communication and signaling : CCS

    2023  Volume 21, Issue 1, Page(s) 365

    Abstract: Hyperglycaemia-induced endothelial dysfunction is a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy. STING, which is a newly discovered regulator of innate immunity, has also been reported to play an important role in ... ...

    Abstract Hyperglycaemia-induced endothelial dysfunction is a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy. STING, which is a newly discovered regulator of innate immunity, has also been reported to play an important role in various metabolic diseases. However, the role of STING in diabetes-induced endothelial cell dysfunction is unknown. In this study, we established a diabetic macroangiopathy mouse model by streptozotocin (STZ) injection combined with high-fat diet (HFD) feeding and a glucotoxicity cell model in high glucose (HG)-treated rat aortic endothelial cells (RAECs). We found that STING expression was specifically increased in the endothelial cells of diabetic arteries, as well as in HG-treated RAECs. Moreover, genetic deletion of STING significantly ameliorated diabetes-induced endothelial cell dysfunction and apoptosis in vivo. Likewise, STING inhibition by C-176 reversed HG-induced migration dysfunction and apoptosis in RAECs, whereas STING activation by DMXAA resulted in migration dysfunction and apoptosis. Mechanistically, hyperglycaemia-induced oxidative stress promoted endothelial mitochondrial dysfunction and mtDNA release, which subsequently activated the cGAS-STING system and the cGAS-STING-dependent IRF3/NF-kB pathway, ultimately resulting in inflammation and apoptosis. In conclusion, our study identified a novel role of STING in diabetes-induced aortic endothelial cell injury and suggested that STING inhibition was a potential new therapeutic strategy for the treatment of diabetic macroangiopathy. Video Abstract.
    MeSH term(s) Mice ; Rats ; Animals ; Endothelial Cells/metabolism ; Signal Transduction ; Hyperglycemia/complications ; Nucleotidyltransferases/metabolism ; Diabetes Complications/metabolism ; Diabetes Mellitus
    Chemical Substances Nucleotidyltransferases (EC 2.7.7.-)
    Language English
    Publishing date 2023-12-21
    Publishing country England
    Document type Video-Audio Media ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-023-01393-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction.

    An, Ying / Xu, Bu-Tuo / Wan, Sheng-Rong / Ma, Xiu-Mei / Long, Yang / Xu, Yong / Jiang, Zong-Zhe

    Cardiovascular diabetology

    2023  Volume 22, Issue 1, Page(s) 237

    Abstract: Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a ... ...

    Abstract Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy, is characterized by a reduction in NO bioavailability. Oxidative stress, which is the main pathogenic factor in diabetes, is one of the major triggers of endothelial dysfunction through the reduction in NO. In this review, we summarize the four sources of ROS in the diabetic vasculature and the underlying molecular mechanisms by which the pathogenic factors hyperglycaemia, hyperlipidaemia, adipokines and insulin resistance induce oxidative stress in endothelial cells in the context of diabetes. In addition, we discuss oxidative stress-targeted interventions, including hypoglycaemic drugs, antioxidants and lifestyle interventions, and their effects on diabetes-induced endothelial dysfunction. In summary, our review provides comprehensive insight into the roles of oxidative stress in diabetes-induced endothelial dysfunction.
    MeSH term(s) Humans ; Endothelial Cells ; Vascular Diseases ; Diabetes Mellitus/diagnosis ; Hyperglycemia ; Oxidative Stress
    Language English
    Publishing date 2023-09-02
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2093769-6
    ISSN 1475-2840 ; 1475-2840
    ISSN (online) 1475-2840
    ISSN 1475-2840
    DOI 10.1186/s12933-023-01965-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Bdh1 overexpression ameliorates hepatic injury by activation of Nrf2 in a MAFLD mouse model.

    Xu, Bu-Tuo / Teng, Fang-Yuan / Wu, Qi / Wan, Sheng-Rong / Li, Xin-Yue / Tan, Xiao-Zhen / Xu, Yong / Jiang, Zong-Zhe

    Cell death discovery

    2022  Volume 8, Issue 1, Page(s) 49

    Abstract: In 2020, a group of experts officially suggested metabolic dysfunction associated with fatty liver disease "MAFLD" as a more appropriate overarching term than NAFLD, indicating the key role of metabolism in fatty liver disease. Bdh1, as the rate-limiting ...

    Abstract In 2020, a group of experts officially suggested metabolic dysfunction associated with fatty liver disease "MAFLD" as a more appropriate overarching term than NAFLD, indicating the key role of metabolism in fatty liver disease. Bdh1, as the rate-limiting enzyme of ketone metabolism, acts as an important metabolic regulator in liver. However, the role of Bdh1 in MAFLD is unclear. In this study, we used the transgenic db/db mice as a MAFLD mouse model and observed the downregulated expression of Bdh1 in fatty liver. In addition, expression of Bdh1 was also reduced by palmitic acid (PA) treatment in LO2 cells. Bdh1 knockdown led to ROS overproduction and ROS-induced inflammation and apoptosis in LO2 cells, while Bdh1 overexpression protected LO2 cells from lipotoxicity by inhibiting ROS overproduction. Mechanistically, Bdh1-mediated βOHB metabolism inhibits ROS overproduction by activation of Nrf2 through enhancement of metabolic flux composed of βOHB-AcAc-succinate-fumarate. Notably, adeno-associated virus (AAV)-mediated Bdh1 overexpression successfully reversed the hepatic function indexes, fibrosis, inflammation, and apoptosis in fatty livers from db/db mice. In conclusion, our study revealed a Bdh1-mediated molecular mechanism in pathogenesis of metabolic dysfunction related liver disease and identified Bdh1 as a novel potential therapeutic target for MAFLD.
    Language English
    Publishing date 2022-02-03
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-022-00840-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: BDH1-mediated βOHB metabolism ameliorates diabetic kidney disease by activation of NRF2-mediated antioxidative pathway.

    Wan, Sheng-Rong / Teng, Fang-Yuan / Fan, Wei / Xu, Bu-Tuo / Li, Xin-Yue / Tan, Xiao-Zhen / Guo, Man / Gao, Chen-Lin / Zhang, Chun-Xiang / Jiang, Zong-Zhe / Xu, Yong

    Aging

    2023  Volume 15, Issue 22, Page(s) 13384–13410

    Abstract: A ketogenic diet (KD) and β-hydroxybutyrate (βOHB) have been widely reported as effective therapies for metabolic diseases. β-Hydroxybutyrate dehydrogenase 1 (BDH1) is the rate-limiting enzyme in ketone metabolism. In this study, we examined the BDH1- ... ...

    Abstract A ketogenic diet (KD) and β-hydroxybutyrate (βOHB) have been widely reported as effective therapies for metabolic diseases. β-Hydroxybutyrate dehydrogenase 1 (BDH1) is the rate-limiting enzyme in ketone metabolism. In this study, we examined the BDH1-mediated βOHB metabolic pathway in the pathogenesis of diabetic kidney disease (DKD). We found that BDH1 is downregulated in the kidneys in DKD mouse models, patients with diabetes, and high glucose- or palmitic acid-induced human renal tubular epithelial (HK-2) cells. BDH1 overexpression or βOHB treatment protects HK-2 cells from glucotoxicity and lipotoxicity by inhibiting reactive oxygen species overproduction. Mechanistically, BDH1-mediated βOHB metabolism activates NRF2 by enhancing the metabolic flux of βOHB-acetoacetate-succinate-fumarate. Moreover,
    MeSH term(s) Animals ; Humans ; Mice ; 3-Hydroxybutyric Acid/pharmacology ; Antioxidants/therapeutic use ; Diabetes Mellitus ; Diabetic Nephropathies/metabolism ; Kidney/pathology ; NF-E2-Related Factor 2/genetics ; Hydroxybutyrate Dehydrogenase/metabolism
    Chemical Substances 3-Hydroxybutyric Acid (TZP1275679) ; Antioxidants ; NF-E2-Related Factor 2 ; Hydroxybutyrate Dehydrogenase (EC 1.1.1.30)
    Language English
    Publishing date 2023-11-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.205248
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Chronic Ethanol Consumption Induces Osteopenia via Activation of Osteoblast Necroptosis.

    Guo, Man / Huang, Yong-Li / Wu, Qi / Chai, Li / Jiang, Zong-Zhe / Zeng, Yan / Wan, Sheng-Rong / Tan, Xiao-Zhen / Long, Yang / Gu, Jun-Ling / Teng, Fang-Yuan / Xu, Yong

    Oxidative medicine and cellular longevity

    2021  Volume 2021, Page(s) 3027954

    Abstract: Chronic high-dose alcohol consumption impairs bone remodeling, reduces bone mass, and increases the risk of osteoporosis and bone fracture. However, the mechanisms underlying alcohol-induced osteoporosis are yet to be elucidated. In this study, we showed ...

    Abstract Chronic high-dose alcohol consumption impairs bone remodeling, reduces bone mass, and increases the risk of osteoporosis and bone fracture. However, the mechanisms underlying alcohol-induced osteoporosis are yet to be elucidated. In this study, we showed that excess intake of ethyl alcohol (EtOH) resulted in osteopenia and osteoblast necroptosis in mice that led to necrotic lesions and reduced osteogenic differentiation in bone marrow mesenchymal stem cells (BMMSCs). We found that EtOH treatment led to the activation of the RIPK1/RIPK3/MLKL signaling, resulting in increased osteoblast necroptosis and decreased osteogenic differentiation and bone formation both in vivo and in vitro. We further discovered that excessive EtOH treatment-induced osteoblast necroptosis might partly depend on reactive oxygen species (ROS) generation; concomitantly, ROS contributed to necroptosis of osteoblasts through a positive feedback loop involving RIPK1/RIPK3. In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro. Collectively, we demonstrated that chronic high-dose alcohol consumption induced osteopenia via osteoblast necroptosis and revealed that RIPK1 kinase may be a therapeutic target for alcohol-induced osteopenia.
    MeSH term(s) Alcohol Drinking/adverse effects ; Animals ; Bone Diseases, Metabolic/etiology ; Bone Diseases, Metabolic/metabolism ; Bone Diseases, Metabolic/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Necroptosis ; Osteoblasts/pathology ; Reactive Oxygen Species/metabolism ; Signal Transduction
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2021-10-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2021/3027954
    Database MEDical Literature Analysis and Retrieval System OnLINE

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