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  1. Article: Recombinant interleukin-2 stimulates lymphocyte recovery in patients with severe COVID-19.

    Zhu, Meng-En / Wang, Qian / Zhou, Shaoqiong / Wang, Bin / Ke, Li / He, Ping

    Experimental and therapeutic medicine

    2021  Volume 21, Issue 3, Page(s) 227

    Abstract: A recently identified type of pneumonia, referred to as coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus-2, has rapidly spread worldwide. Lymphopenia and a proinflammatory cytokine storm frequently ... ...

    Abstract A recently identified type of pneumonia, referred to as coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus-2, has rapidly spread worldwide. Lymphopenia and a proinflammatory cytokine storm frequently occur in patients with severe COVID-19. However, to the best of our knowledge, no specific immunomodulatory therapy for COVID-19 has been reported to date. In the present retrospective case-control study, the potential therapeutic effect of recombinant human interleukin-2 (rIL-2) in patients with severe COVID-19 was demonstrated. A total of 59 patients with severe COVID-19 were admitted to the Union Hospital of Tongji Medical College (Wuhan, China) between 29th January 2020 and 29th February 2020 and were included in the present study. In total, 20 patients received subcutaneous injection of rIL-2 (1 million IU per day) for 7-10 days in addition to regular treatment and were classified as the rIL-2 group. Furthermore, 20 of the 39 patients receiving regular treatment, without the intervention of rIL-2, were matched as the control group. Patients in these two groups were subjected to propensity score matching in terms of clinical characteristics such as age, sex, symptoms, signs, laboratory data and comorbidities. Changes in the lymphocyte count, as well as IL-6 and C-reactive protein (CRP) levels, were analyzed at the time of admission and discharge and any differences between the rIL-2 and non-rIL-2 groups were determined. The results demonstrated an increase in the lymphocyte count and a decrease in CRP levels in the rIL-2 group compared with that in the non-rIL-2 group. The difference in the change of the lymphocyte count between the rIL-2 group and non-rIL-2 group was statistically significant (P<0.01). Although CRP levels were decreased to a greater extent in the rIL-2 group, the difference between the two groups was not statistically significant (P>0.05). Collectively, the present results suggested that administration of rIL-2 may be a prospective adjuvant therapy for patients with severe COVID-19 and its effects may be mediated by increasing lymphocyte numbers.
    Language English
    Publishing date 2021-01-18
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2683844-8
    ISSN 1792-1015 ; 1792-0981
    ISSN (online) 1792-1015
    ISSN 1792-0981
    DOI 10.3892/etm.2021.9658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Indirect co‑culture of vascular smooth muscle cells with bone marrow mesenchymal stem cells inhibits vascular calcification and downregulates the Wnt signaling pathways.

    Zhu, Meng'en / Fang, Xin / Zhou, Shaoqiong / Li, Wei / Guan, Siming

    Molecular medicine reports

    2016  Volume 13, Issue 6, Page(s) 5141–5148

    Abstract: Vascular calcification (VC) is widely considered to be a crucial clinical indicator of cardiovascular disease. Recently, certain properties of mesenchymal stem cells (MSCs) have been hypothesized to have potential in treating cardiovascular diseases. ... ...

    Abstract Vascular calcification (VC) is widely considered to be a crucial clinical indicator of cardiovascular disease. Recently, certain properties of mesenchymal stem cells (MSCs) have been hypothesized to have potential in treating cardiovascular diseases. However, their effect on the initiation and progression of VC remains controversial. The present study aimed to investigate whether MSCs indirectly mediate VC and their impact on the Wnt signaling pathways. A Transwell system was selected to establish the indirect co‑culture environment, and hence, vascular smooth muscle cells (VSMCs) were indirectly co‑cultured in the presence or absence of MSCs at a ratio of 1:1. Osteogenic medium (OS) was added to imitate a calcifying environment. Fourteen days later, VSMCs in the lower layers of the Transwell plates were harvested. Alkaline phosphatase activity and calcium nodules were markedly increased in calcific VSMCs induced by OS. However, these parameters were significantly decreased in VSMCs by indirectly co‑culturing with MSCs in the same medium. Furthermore, the messenger RNA expression levels of osteopontin and osteoprotegerin were notably increased in VSMCs cultured in OS, but reduced by indirect interaction with MSCs. In addition, the activities of canonical and noncanonical Wnt ligands, wingless‑type MMTV integration site family, number 5A (Wnt5a), receptor tyrosine kinase‑like orphan receptor 2 (Ror2) and β‑catenin, which are important in the process of VC, were downregulated by indirect contact with MSCs in OS. Thus, indirect co‑culture with MSCs inhibits VC and downregulates the Wnt signaling pathways.
    MeSH term(s) Animals ; Bone Marrow Cells/metabolism ; Bone Marrow Cells/pathology ; Coculture Techniques ; Down-Regulation ; Male ; Mesenchymal Stromal Cells/metabolism ; Mesenchymal Stromal Cells/pathology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Rats ; Vascular Calcification/metabolism ; Vascular Calcification/pathology ; Wnt Signaling Pathway
    Language English
    Publishing date 2016-06
    Publishing country Greece
    Document type Journal Article
    ISSN 1791-3004
    ISSN (online) 1791-3004
    DOI 10.3892/mmr.2016.5182
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Baicalin Attenuates Cardiac Dysfunction and Myocardial Remodeling in a Chronic Pressure-Overload Mice Model.

    Zhang, Yanqing / Liao, Pingping / Zhu, Meng'en / Li, Wei / Hu, Dan / Guan, Siming / Chen, Long

    Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

    2017  Volume 41, Issue 3, Page(s) 849–864

    Abstract: Background/aims: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy ...

    Abstract Background/aims: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy remains unknown. Here we investigated the protective effects of baicalin on cardiac hypertrophy induced by pressure overload and explored the potential mechanisms involved.
    Methods: C57BL/6J-mice were treated with baicalin or vehicle following transverse aortic constriction or Sham surgery for up to 8 weeks, and at different time points, cardiac function and heart size measurement and histological and biochemical examination were performed.
    Results: Mice under pressure overload exhibited cardiac dysfunction, high mortality, myocardial hypertrophy, increased apoptosis and fibrosis markers, and suppressed cardiac expression of PPARα and PPARβ/δ. However, oral administration of baicalin improved cardiac dysfunction, decreased mortality, and attenuated histological and biochemical changes described above. These protective effects of baicalin were associated with reduced heart and cardiomyocyte size, lower fetal genes expression, attenuated cardiac fibrosis, lower expression of profibrotic markers, and decreased apoptosis signals in heart tissue. Moreover, we found that baicalin induced PPARα and PPARβ/δ expression in vivo and in vitro. Subsequent experiments demonstrated that long-term baicalin treatment presented no obvious cardiac lipotoxicity.
    Conclusions: The present results demonstrated that baicalin attenuates pressure overload induced cardiac dysfunction and ventricular remodeling, which would be due to suppressed cardiac hypertrophy, fibrosis, apoptosis and metabolic abnormality.
    MeSH term(s) Animals ; Cardiotonic Agents/pharmacology ; Cell Line ; Cell Size ; Disease Models, Animal ; Endomyocardial Fibrosis/etiology ; Endomyocardial Fibrosis/mortality ; Endomyocardial Fibrosis/pathology ; Endomyocardial Fibrosis/prevention & control ; Flavonoids/pharmacology ; Gene Expression Regulation ; Hypertrophy, Left Ventricular/etiology ; Hypertrophy, Left Ventricular/mortality ; Hypertrophy, Left Ventricular/pathology ; Hypertrophy, Left Ventricular/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; PPAR alpha/agonists ; PPAR alpha/genetics ; PPAR alpha/metabolism ; PPAR delta/agonists ; PPAR delta/genetics ; PPAR delta/metabolism ; PPAR-beta/agonists ; PPAR-beta/genetics ; PPAR-beta/metabolism ; Pressure/adverse effects ; Signal Transduction ; Survival Analysis ; Ventricular Dysfunction, Left/etiology ; Ventricular Dysfunction, Left/mortality ; Ventricular Dysfunction, Left/pathology ; Ventricular Dysfunction, Left/prevention & control
    Chemical Substances Cardiotonic Agents ; Flavonoids ; PPAR alpha ; PPAR delta ; PPAR-beta ; baicalin (347Q89U4M5)
    Language English
    Publishing date 2017-02-16
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1067572-3
    ISSN 1421-9778 ; 1015-8987
    ISSN (online) 1421-9778
    ISSN 1015-8987
    DOI 10.1159/000459708
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3160: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  4. Article: Baicalin Attenuates Cardiac Dysfunction and Myocardial Remodeling in a Chronic Pressure-Overload Mice Model

    Zhang, Yanqing / Liao, Pingping / Zhu, Meng’en / Li, Wei / Hu, Dan / Guan, Siming / Chen, Long

    Cellular Physiology and Biochemistry

    2017  Volume 41, Issue 3, Page(s) 849–864

    Abstract: Background/Aims: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy ... ...

    Institution Department of Geriatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    Clinical Center for Human Genomic Research, Union Hospital, Huazhong University of Science and Technology, Wuhan, China
    Abstract Background/Aims: Baicalin has been shown to be effective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial ischaemic injury. However, whether baicalin plays a role in cardiac hypertrophy remains unknown. Here we investigated the protective effects of baicalin on cardiac hypertrophy induced by pressure overload and explored the potential mechanisms involved. Methods C57BL/6J-mice were treated with baicalin or vehicle following transverse aortic constriction or Sham surgery for up to 8 weeks, and at different time points, cardiac function and heart size measurement and histological and biochemical examination were performed. Results Mice under pressure overload exhibited cardiac dysfunction, high mortality, myocardial hypertrophy, increased apoptosis and fibrosis markers, and suppressed cardiac expression of PPARα and PPARβ/δ. However, oral administration of baicalin improved cardiac dysfunction, decreased mortality, and attenuated histological and biochemical changes described above. These protective effects of baicalin were associated with reduced heart and cardiomyocyte size, lower fetal genes expression, attenuated cardiac fibrosis, lower expression of profibrotic markers, and decreased apoptosis signals in heart tissue. Moreover, we found that baicalin induced PPARα and PPARβ/δ expression in vivo and in vitro. Subsequent experiments demonstrated that long-term baicalin treatment presented no obvious cardiac lipotoxicity. Conclusions The present results demonstrated that baicalin attenuates pressure overload induced cardiac dysfunction and ventricular remodeling, which would be due to suppressed cardiac hypertrophy, fibrosis, apoptosis and metabolic abnormality.
    Keywords Hypertrophy ; Pressure overload ; Baicalin
    Language English
    Publishing date 2017-02-16
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Original Paper ; This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).
    ZDB-ID 1067572-3
    ISSN 1421-9778 ; 1015-8987
    ISSN (online) 1421-9778
    ISSN 1015-8987
    DOI 10.1159/000459708
    Database Karger publisher's database

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3160: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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