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  1. Article ; Online: The challenge of safe anesthesia in developing countries: defining the problems in a medical center in Cambodia.

    Tao, Kun-Ming / Sokha, Sann / Yuan, Hong-Bin

    BMC health services research

    2020  Volume 20, Issue 1, Page(s) 204

    Abstract: Background: The International Standards for a Safe Practice of Anesthesia (ISSPA) were developed on behalf of the World Federation of Societies of Anaesthesiologists and the World Health Organization. It has been recommend as an assessment tool that ... ...

    Abstract Background: The International Standards for a Safe Practice of Anesthesia (ISSPA) were developed on behalf of the World Federation of Societies of Anaesthesiologists and the World Health Organization. It has been recommend as an assessment tool that allows anesthetic providers in developing countries to assess their compliance and needs. This study was performed to describe the anesthesia service in one main public hospital during an 8-month medical mission in Cambodia and evaluate its anesthetic safety issues according to the ISSPA.
    Methods: We conduct a retrospective study involving 1953 patients at the Preah Ket Mealea hospital. Patient demographics, anesthetic techniques, and complications were reviewed according to the registers of the anesthetic services and questionnaires. The inadequacies in personnel, facilities, equipment, medications, and conduct of anesthesia drugs were recorded using a checklist based on the ISSPA.
    Results: A total of 1792 patients received general and regional anesthesia in the operating room, while 161 patients receiving sedation for gastroscopy. The patients' mean age was 45.0 ± 16.6 years (range, 17-87 years). The three most common surgical procedures were abdominal (52.0%; confidence interval [CI], 49.3-54.7), orthopedic (27.6%; CI, 25.2-29.9), and urological surgery (14.7%; CI, 12.8-16.6). General anesthesia, spinal anesthesia, and brachial plexus block were performed in 54.3% (CI, 51.7-56.8), 28.2% (CI, 25.9-30.5), and 9.4% (CI, 7.9-10.9) of patients, respectively. One death occurred. Twenty-six items related to professional aspects, monitoring, and conduct of anesthesia did not meet the ISSPA-recommended standards. A lack of commonly used drugs and monitoring equipment was noted, posing major threats to the safety of anesthesia practice, especially in emergency situations.
    Conclusions: This study adds to the scarce literature on anesthesia practice in low- and middle-income countries such as Cambodia. Future medical assistance should help to strengthen these countries' inadequacies, allowing for the adoption of international standards for the safe practice of anesthesia.
    MeSH term(s) Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anesthesia/standards ; Cambodia ; Developing Countries ; Female ; Health Services Research ; Hospitals, Public/organization & administration ; Humans ; Male ; Medical Missions ; Middle Aged ; Retrospective Studies ; Safety Management/organization & administration ; Safety Management/standards ; World Health Organization ; Young Adult
    Keywords covid19
    Language English
    Publishing date 2020-03-12
    Publishing country England
    Document type Journal Article
    ISSN 1472-6963
    ISSN (online) 1472-6963
    DOI 10.1186/s12913-020-5068-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sphygmomanometer for Invasive Blood Pressure Monitoring in a Medical Mission.

    Tao, Kun-Ming / Sokha, Sann / Yuan, Hong-Bin

    Anesthesiology

    2018  Volume 130, Issue 2, Page(s) 312

    MeSH term(s) Blood Pressure ; Blood Pressure Determination/instrumentation ; Blood Pressure Determination/methods ; Humans ; Hypertension/diagnosis ; Hypotension/diagnosis ; Medical Missions ; Monitoring, Physiologic ; Sphygmomanometers
    Language English
    Publishing date 2018-09-27
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 269-0
    ISSN 1528-1175 ; 0003-3022
    ISSN (online) 1528-1175
    ISSN 0003-3022
    DOI 10.1097/ALN.0000000000002469
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway.

    Ding, Peng / Yang, Rui / Li, Cheng / Fu, Hai-Long / Ren, Guang-Li / Wang, Pei / Zheng, Dong-Yu / Chen, Wei / Yang, Li-Ye / Mao, Yan-Fei / Yuan, Hong-Bin / Li, Yong-Hua

    Critical care (London, England)

    2023  Volume 27, Issue 1, Page(s) 196

    Abstract: Background: Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor ... ...

    Abstract Background: Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor 21 (FGF21), a metabolic regulator secreted by the liver, in VILI development.
    Methods: Serum FGF21 concentrations were determined in patients undergoing mechanical ventilation during general anesthesia and in a mouse VILI model. Lung injury was compared between FGF21-knockout (KO) mice and wild-type (WT) mice. Recombinant FGF21 was administrated in vivo and in vitro to determine its therapeutic effect.
    Results: Serum FGF21 levels in patients and mice with VILI were significantly higher than in those without VILI. Additionally, the increment of serum FGF21 in anesthesia patients was positively correlated with the duration of ventilation. VILI was aggravated in FGF21-KO mice compared with WT mice. Conversely, the administration of FGF21 alleviated VILI in both mouse and cell models. FGF21 reduced Caspase-1 activity, suppressed the mRNA levels of Nlrp3, Asc, Il-1β, Il-18, Hmgb1 and Nf-κb, and decreased the protein levels of NLRP3, ASC, IL-1β, IL-18, HMGB1 and the cleaved form of GSDMD.
    Conclusions: Our findings reveal that endogenous FGF21 signaling is triggered in response to VILI, which protects against VILI by inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These results suggest that boosting endogenous FGF21 or the administration of recombinant FGF21 could be promising therapeutic strategies for the treatment of VILI during anesthesia or critical care.
    MeSH term(s) Animals ; Mice ; Caspase 1/metabolism ; Disease Models, Animal ; HMGB1 Protein ; Inflammasomes ; Interleukin-18 ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Ventilator-Induced Lung Injury/drug therapy ; Ventilator-Induced Lung Injury/prevention & control ; Humans
    Chemical Substances Caspase 1 (EC 3.4.22.36) ; fibroblast growth factor 21 ; HMGB1 Protein ; Inflammasomes ; Interleukin-18 ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
    Language English
    Publishing date 2023-05-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/s13054-023-04488-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Global distribution of publications in anesthesiology : A bibliometric analysis from 1999 to 2018.

    Chen, Qian-Bo / Yang, Huai-Yu / Chen, Da-Shuang / Lv, Yan-Wei / Hu, Liang-Hao / Yuan, Hong-Bin

    Der Anaesthesist

    2021  Volume 70, Issue 10, Page(s) 854–862

    Abstract: Purpose: Only few studies have analyzed the global distribution of anesthesia research. This study was designed to reveal the current global research status of anesthesiology.: Methods: Articles published between 1999 and 2018 in international ... ...

    Title translation Globale Verbreitung von Publikationen über Anästhesiologie : Eine bibliometrische Analyse von 1999 bis 2018.
    Abstract Purpose: Only few studies have analyzed the global distribution of anesthesia research. This study was designed to reveal the current global research status of anesthesiology.
    Methods: Articles published between 1999 and 2018 in international journals in the field of anesthesiology were retrieved from the PubMed database. The top 20 ranked countries were identified. The gross domestic product (GDP) of each country was also retrieved to reveal the correlation between research outputs and the economy. The total outputs and outputs per 10 million inhabitants in each country were calculated and compared. To analyze the quality of publications among the top 10 ranked countries, the impact factor (IF), article influence score (AIS), and immediacy index (ImI) were calculated and analyzed. In addition, the keywords of publications were retrieved to conduct co-occurrence analysis in order to determine the research focus in anesthesiology.
    Results: A total of 112,918 articles were published in 30 selected journals from 1999 to 2018. There was a positive correlation between research outputs and GDP of 10 countries (p < 0.001, r = 0.825). The USA ranked 1st with 21,703 articles, followed by the UK (8393 articles) and Germany (6504 articles). Canada had the highest number of publications per 10 million inhabitants in 2018. The UK had the highest average IF (4.70), average AIS (1.16), and average ImI (1.64) among the 10 countries. The research highlights in the field of anesthesiology included "mechanism and management of pain", "cardiac anesthesia", "pediatric anesthesia and airway management", "analgesia" and "anesthetic agents".
    Conclusion: Regarding quantity trend, the output of global production in anesthesiology increased continuously as the number of articles from the high-output countries showed an increasing trend; however, there was still a gap between developing and developed countries in research quality. High-quality research should be encouraged in developing countries.
    MeSH term(s) Anesthesia ; Anesthesiology ; Bibliometrics ; Child ; Germany ; Humans
    Language English
    Publishing date 2021-05-18
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 260-4
    ISSN 1432-055X ; 0003-2417
    ISSN (online) 1432-055X
    ISSN 0003-2417
    DOI 10.1007/s00101-021-00969-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Propofol reduces hypoxia‑induced autophagic cell death through downregulating HIF 1α in alveolar epithelial type II cells of rats.

    Ning, Hui-Jie / Yuan, Hong-Bin / Xu, Hai-Tao / He, Xing-Ying

    Molecular medicine reports

    2017  Volume 16, Issue 2, Page(s) 1509–1515

    Abstract: Propofol (2,6‑diisopropylphenol) exerts protective effects on alveolar epithelial type II (ATII) cells, partly through attenuating hypoxia‑induced apoptosis. Autophagy is involved in the activation of apoptosis. Therefore, the present study investigated ... ...

    Abstract Propofol (2,6‑diisopropylphenol) exerts protective effects on alveolar epithelial type II (ATII) cells, partly through attenuating hypoxia‑induced apoptosis. Autophagy is involved in the activation of apoptosis. Therefore, the present study investigated the modulating effect of propofol against autophagy in ATII cells under hypoxia. Western blot analysis was performed to detect the protein expression of the autophagy molecular marker, microtubule‑associated protein 1 light chain 3 (LC3)‑II, under various conditions. The effects of propofol on the accumulation of other autophagy‑associated proteins and apoptosis‑associated proteins were also determined using western blot analysis. The interactions between proteins were determined by co‑immunoprecipitation. Apoptosis of the ATII cells was monitored using FITC‑conjugated AV/PI staining. Furthermore, hypoxia‑inducible factor 1α (HIF 1α) small interfering (si) RNA was designed to construct si‑HIF 1α ATII cells. The efficiency of interference was measured using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Following pre‑treatment with propofol, the hypoxia‑induced accumulation of LC3‑II, HIF 1α and B‑cell lymphoma‑2 interacting protein 3 (Bnip3) were markedly decreased, accompanied with the activation of mammalian target of rapamycin. In addition, cleaved‑poly ADP‑ribose polymerase was suppressed, and hypoxia‑induced autophagic cell death was inhibited by propofol pre‑treatment. HIF 1α was inhibited by si‑HIF 1α, which simultaneously suppressed Bnip3 and LC3‑II under hypoxia. Taken together, propofol reduced hypoxia‑induced autophagic cell death through reducing the expression of HIF 1α in ATII cells, indicating a novel strategy for modulating autophagy via propofol in hypoxic ATII cells.
    Language English
    Publishing date 2017-08
    Publishing country Greece
    Document type Journal Article
    ISSN 1791-3004
    ISSN (online) 1791-3004
    DOI 10.3892/mmr.2017.6697
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The novel exercise-induced hormone irisin protects against neuronal injury via activation of the Akt and ERK1/2 signaling pathways and contributes to the neuroprotection of physical exercise in cerebral ischemia.

    Li, Dong-Jie / Li, Yong-Hua / Yuan, Hong-Bin / Qu, Le-Feng / Wang, Pei

    Metabolism: clinical and experimental

    2017  Volume 68, Page(s) 31–42

    Abstract: Background: Irisin is a novel exercise-induced myokine involved in the regulation of adipose browning and thermogenesis. In this study, we investigated the potential role of irisin in cerebral ischemia and determined whether irisin is involved in the ... ...

    Abstract Background: Irisin is a novel exercise-induced myokine involved in the regulation of adipose browning and thermogenesis. In this study, we investigated the potential role of irisin in cerebral ischemia and determined whether irisin is involved in the neuroprotective effect of physical exercise in mice.
    Materials and methods: The middle cerebral artery occlusion (MCAO) model was used to produce cerebral ischemia in mice. First, the plasma irisin levels and changes in expression of the irisin precursor protein FNDC5 in skeletal muscle were determined post ischemic stroke. Second, the association between plasma irisin levels and the neurological deficit score, brain infarct volume, or plasma concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β in mice with MCAO were evaluated. Third, the therapeutic effect of irisin on ischemic brain injury was evaluated in vivo and in vitro. Recombinant irisin was injected directly into the tail vein 30min after the MCAO operation, and then the effects of irisin treatment on brain infarct volume, neurological deficit, neuroinflammation, microglia activation, monocyte infiltration, oxidative stress and intracellular signaling pathway activation (Akt and ERK1/2) were measured. Irisin was also administered in cultured PC12 neuronal cells with oxygen and glucose deprivation (OGD). Finally, to assess the potential involvement of irisin in the neuroprotection of physical exercise, mice were exercised for 2weeks and an irisin neutralizing antibody was injected into these mice to block irisin 1h before the MCAO operation.
    Results: The plasma irisin concentration and intramuscular FNDC5 protein expression decreased after ischemic stroke. Plasma irisin levels were negatively associated with brain infarct volume, the neurological deficit score, plasma TNF-α and plasma IL-6 concentrations. In OGD neuronal cells, irisin protected against cell injury. In mice with MCAO, irisin treatment reduced the brain infarct volume, neurological deficits, brain edema and the decline in body weight. Irisin treatment inhibited activation of Iba-1
    Conclusion: Irisin reduces ischemia-induced neuronal injury via activation of the Akt and ERK1/2 signaling pathways and contributes to the neuroprotective effect of physical exercise against cerebral ischemia, suggesting that irisin may be a factor linking metabolism and cardio-cerebrovascular diseases.
    MeSH term(s) Animals ; Behavior, Animal ; Brain Ischemia/pathology ; Brain Ischemia/prevention & control ; Fibronectins/metabolism ; Fibronectins/pharmacology ; Humans ; Infarction, Middle Cerebral Artery/pathology ; MAP Kinase Signaling System/drug effects ; Mice ; Mice, Inbred C57BL ; Nervous System Diseases/pathology ; Neurons/pathology ; Neuroprotective Agents/pharmacology ; Oncogene Protein v-akt/drug effects ; PC12 Cells ; Physical Conditioning, Animal ; Rats ; Signal Transduction/drug effects ; Stroke/prevention & control
    Chemical Substances FNDC5 protein, mouse ; Fibronectins ; Neuroprotective Agents ; Oncogene Protein v-akt (EC 2.7.11.1)
    Language English
    Publishing date 2017-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2016.12.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Activation of GABA

    Liu, Peng / Yuan, Hong-Bin / Zhao, Shuang / Liu, Fei-Fei / Jiang, Yu-Qing / Guo, Yue-Xian / Wang, Xiu-Li

    Mediators of inflammation

    2018  Volume 2018, Page(s) 6016272

    Abstract: Diabetic neuropathic pain (DNP) is a prevalent complication in diabetes patients. Neuronal inflammation and activation of Toll-like receptor 4 (TLR4) are involved in the occurrence of DNP. However, the underlying mechanisms remain unclear. Downregulation ...

    Abstract Diabetic neuropathic pain (DNP) is a prevalent complication in diabetes patients. Neuronal inflammation and activation of Toll-like receptor 4 (TLR4) are involved in the occurrence of DNP. However, the underlying mechanisms remain unclear. Downregulation of gamma-aminobutyric acid B (GABA
    MeSH term(s) Animals ; Blotting, Western ; Diabetic Neuropathies/metabolism ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/metabolism ; Signal Transduction/physiology ; Spinal Cord Dorsal Horn/metabolism ; Toll-Like Receptor 4/metabolism
    Chemical Substances Receptors, GABA-B ; Toll-Like Receptor 4
    Language English
    Publishing date 2018-12-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2018/6016272
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Fibroblast growth factor 10 protects neuron against oxygen–glucose deprivation injury through inducing heme oxygenase-1

    Li, Yong-Hua / Yang, Li-Ye / Chen, Wei / Li, Ying-Ke / Yuan, Hong-Bin

    Biochemical and biophysical research communications. 2015 Jan. 02, v. 456

    2015  

    Abstract: Fibroblast growth factors (FGFs) are a family of structurally related heparin-binding proteins with diverse biological functions. FGFs participate in mitogenesis, angiogenesis, cell proliferation, development, differentiation and cell migration. Here, we ...

    Abstract Fibroblast growth factors (FGFs) are a family of structurally related heparin-binding proteins with diverse biological functions. FGFs participate in mitogenesis, angiogenesis, cell proliferation, development, differentiation and cell migration. Here, we investigated the potential effect of FGF10, a member of FGFs, on neuron survival in oxygen–glucose deprivation (OGD) model. In primary cultured mouse cortical neurons upon OGD, FGF10 treatment (100 and 1000ng/ml) attenuated the decrease of cell viability and rescued the LDH release. Tuj-1 immunocytochemistry assay showed that FGF10 promoted neuronal survival. Apoptosis assay with Annexin V+PI by flow cytometry demonstrated that FGF10 treatment reduced apoptotic cell proportion. Moreover, immunoblotting showed that FGF10 alleviated the cleaved caspase-3 upregulation caused by OGD. FGF10 treatment also depressed the OGD-induced increase of caspase-3, -8 and -9 activities. At last, we found FGF10 triggered heme oxygenase-1 (HO-1) protein expression rather than hypoxia-inducible factor-1 (HIF-1), AMP-activated protein kinase (AMPK) signaling and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling. Knockdown of HO-1 by siRNA partly abolished the neuroprotection of FGF10 in OGD model. In summary, our observations provide the first evidence for the neuroprotective function of FGF10 against ischemic neuronal injury and suggest that FGF10 may be a promising agent for treatment of ischemic stroke.
    Keywords AMP-activated protein kinase ; angiogenesis ; apoptosis ; caspase-3 ; cell differentiation ; cell movement ; cell proliferation ; cell viability ; fibroblast growth factors ; flow cytometry ; heme oxygenase (biliverdin-producing) ; hypoxia-inducible factor 1 ; immunoblotting ; immunocytochemistry ; mice ; mitogen-activated protein kinase ; mitogenesis ; models ; neurons ; neuroprotective effect ; protein synthesis ; small interfering RNA ; stroke
    Language English
    Dates of publication 2015-0102
    Size p. 225-231.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2014.11.063
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: EP4 activation ameliorates liver ischemia/reperfusion injury via ERK1/2‑GSK3β‑dependent MPTP inhibition.

    Cai, Lin-Lin / Xu, Hai-Tao / Wang, Qi-Long / Zhang, Ya-Qing / Chen, Wei / Zheng, Dong-Yu / Liu, Fang / Yuan, Hong-Bin / Li, Yong-Hua / Fu, Hai-Long

    International journal of molecular medicine

    2020  Volume 45, Issue 6, Page(s) 1825–1837

    Abstract: Prostaglandin E receptor subtype 4 (EP4) is widely distributed in the heart, but its role in hepatic ischemia/reperfusion (I/R), particularly in mitochondrial permeability transition pore (MPTP) modulation, is yet to be elucidated. In the present study, ... ...

    Abstract Prostaglandin E receptor subtype 4 (EP4) is widely distributed in the heart, but its role in hepatic ischemia/reperfusion (I/R), particularly in mitochondrial permeability transition pore (MPTP) modulation, is yet to be elucidated. In the present study, an EP4 agonist (CAY10598) was used in a rat model to evaluate the effects of EP4 activation on liver I/R and the mechanisms underlying this. I/R insult upregulated hepatic EP4 expression during early reperfusion. In addition, subcutaneous CAY10598 injection prior to the onset of reperfusion significantly increased hepatocyte cAMP concentrations and decreased serum ALT and AST levels and necrotic and apoptotic cell percentages, after 6 h of reperfusion. Moreover, CAY10598 protected mitochondrial morphology, markedly inhibited mitochondrial permeability transition pore (MPTP) opening and decreased liver reactive oxygen species levels. This occurred via activation of the ERK1/2‑GSK3β pathway rather than the janus kinase (JAK)2‑signal transducers and activators of transcription (STAT)3 pathway, and resulted in prevention of mitochondria‑associated cell injury. The MPTP opener carboxyatractyloside (CATR) and the ERK1/2 inhibitor PD98059 also partially reversed the protective effects of CAY10598 on the liver and mitochondria. The current findings indicate that EP4 activation induces ERK1/2‑GSK3β signaling and subsequent MPTP inhibition to provide hepatoprotection, and these observations are informative for developing new molecular targets and preventative therapies for I/R in a clinical setting.
    MeSH term(s) Animals ; Glycogen Synthase Kinase 3 beta/metabolism ; Liver/metabolism ; MAP Kinase Signaling System/physiology ; Male ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore/metabolism ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Reperfusion Injury/metabolism ; Signal Transduction/physiology
    Chemical Substances Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Reactive Oxygen Species ; Receptors, Prostaglandin E, EP4 Subtype ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Gsk3b protein, rat (EC 2.7.11.1)
    Language English
    Publishing date 2020-03-17
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 1444428-8
    ISSN 1791-244X ; 1107-3756
    ISSN (online) 1791-244X
    ISSN 1107-3756
    DOI 10.3892/ijmm.2020.4544
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Fibroblast growth factor 10 protects neuron against oxygen-glucose deprivation injury through inducing heme oxygenase-1.

    Li, Yong-Hua / Yang, Li-Ye / Chen, Wei / Li, Ying-Ke / Yuan, Hong-Bin

    Biochemical and biophysical research communications

    2015  Volume 456, Issue 1, Page(s) 225–231

    Abstract: Fibroblast growth factors (FGFs) are a family of structurally related heparin-binding proteins with diverse biological functions. FGFs participate in mitogenesis, angiogenesis, cell proliferation, development, differentiation and cell migration. Here, we ...

    Abstract Fibroblast growth factors (FGFs) are a family of structurally related heparin-binding proteins with diverse biological functions. FGFs participate in mitogenesis, angiogenesis, cell proliferation, development, differentiation and cell migration. Here, we investigated the potential effect of FGF10, a member of FGFs, on neuron survival in oxygen-glucose deprivation (OGD) model. In primary cultured mouse cortical neurons upon OGD, FGF10 treatment (100 and 1000 ng/ml) attenuated the decrease of cell viability and rescued the LDH release. Tuj-1 immunocytochemistry assay showed that FGF10 promoted neuronal survival. Apoptosis assay with Annexin V+PI by flow cytometry demonstrated that FGF10 treatment reduced apoptotic cell proportion. Moreover, immunoblotting showed that FGF10 alleviated the cleaved caspase-3 upregulation caused by OGD. FGF10 treatment also depressed the OGD-induced increase of caspase-3, -8 and -9 activities. At last, we found FGF10 triggered heme oxygenase-1 (HO-1) protein expression rather than hypoxia-inducible factor-1 (HIF-1), AMP-activated protein kinase (AMPK) signaling and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling. Knockdown of HO-1 by siRNA partly abolished the neuroprotection of FGF10 in OGD model. In summary, our observations provide the first evidence for the neuroprotective function of FGF10 against ischemic neuronal injury and suggest that FGF10 may be a promising agent for treatment of ischemic stroke.
    MeSH term(s) Animals ; Apoptosis ; Blood Glucose/metabolism ; Brain Ischemia/pathology ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Cerebral Cortex/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblast Growth Factor 10/metabolism ; Flow Cytometry ; Heme Oxygenase-1/metabolism ; Humans ; Immunohistochemistry ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Neurons/metabolism ; Oxygen/metabolism ; PC12 Cells ; RNA, Small Interfering/metabolism ; Rats ; Reactive Oxygen Species/metabolism ; Stroke/pathology
    Chemical Substances Blood Glucose ; FGF10 protein, human ; Fibroblast Growth Factor 10 ; Membrane Proteins ; RNA, Small Interfering ; Reactive Oxygen Species ; Heme Oxygenase-1 (EC 1.14.14.18) ; Hmox1 protein, mouse (EC 1.14.14.18) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2015-01-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2014.11.063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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