The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform

Rui Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Clemastine Fumarate protects against myocardial ischemia reperfusion injury by activating the tlr4 pi3k akt signaling pathway
    Frontiers in Pharmacology, 2020
    Co-Authors: Xiaoxiao Yuan, Rui Zhang, Ru Yan, Feng Yue, Zhaodong Juan, Yaru Huang, Xiaotong Sun, Xiaohui Xia
    Abstract:

    Our pilot studies have shown that Clemastine Fumarate (CLE) can protect against myocardial ischemia-reperfusion injury (MIRI) through regulation of toll like receptor 4 (TLR4). However, the protective mechanism of CLE and related signaling pathways for MIRI remains unclear. The objective of this study is to determine the mechanism by which CLE relieves MIRI in cardiomyocytes and its relationship with the TLR4/PI3K/Akt signaling pathway. CCK8 analysis was used to test the optimal concentration of TLR4 inhibitor CLI-095 and TLR4 agonist lipopolysaccharide (LPS) on MIRI. The expression of inflammatory factors, oxidative stress response, cell damage, and intracellular calcium redistribution of cardiomyocytes were examined using the ELISA kits, Total Superoxide Dismutase Assay Kit with WST-8 and Lipid Peroxidation MDA Assay Kit, LDH Cytotoxicity Assay Kit, and laser scanning confocal microscope. The expression of TLR4/PI3K/Akt and cleaved caspase-3 were determined by Western blotting and immunofluorescent staining. Our results showed that MIRI aggravated the inflammatory response, oxidative stress, cellular damage of cardiomyocytes, and caused redistribution of intracellular calcium, upregulated the expression of TLR4 protein, cleaved caspase-3 protein, and down-regulated the expression of PI3K/Akt protein. After treatment with CLE, the inflammatory response, oxidative stress, and cellular damage of cardiomyocytes were alleviated, and intracellular calcium ion accumulation decreased. The expression of TLR4 protein, cleaved caspase-3 protein declined, but PI3K/Akt protein expression increased in cardiomyocytes treated with CLE. In addition, after treatment with the TLR4 inhibitor CLI-095, the results were similar to those of CLE treatment. The TLR4 agonist LPS aggravated the reactions caused by MIRI. The role of LPS was reversed after CLE treatment. These results suggested that CLE can attenuate MIRI by activating the TLR4/PI3K/Akt signaling pathway.

  • effect of Clemastine Fumarate on tlr4 pi3k akt signaling pathway during hypoxia reoxygenation in rat cardiomyocytes
    Chinese Journal of Anesthesiology, 2019
    Co-Authors: Ru Yan, Rui Zhang, Feng Yue, Yongxin Liu, Xiaoxiao Yuan, Meiyan Sun, Zhaodong Juan, Yaru Huang
    Abstract:

    Objective To evaluate the effect of Clemastine Fumarate on Toll-like receptor 4/phosphatidylinositol-3-kinase/serine-threonine kinase (TLR4/PI3K/Akt) signaling pathway during hypoxia-reoxygenation(H/R) in rat cardiomyocytes. Methods H9C2 cells of rats cultured in vitro were seeded in culture wells or dishes at a density of 1×105 cells/ml and divided into 3 groups (n=11 each) by using a random number table method: control group (group C), H/R group and Clemastine Fumarate group (CF group). Cardiomyocytes were exposed to 5% CO2-95% N2 in a low-glucose DMEM medium at 37℃ for 4 h followed by 4 h reoxygenation.At 4 h of reoxygenation, the cell viability was detected by CCK-8 assay, the ultrastructure was observed with a transmission electron microscope, the expression of TLR4, PI3K, phosphorylated Akt (p-Akt) and caspase-3 was detected by Western blot, and the expression of TLR4, PI3K and caspase-3 was detected by immunofluorescence. Results Compared with group C, the cell viability was significantly decreased, the expression of TLR4 and caspase-3 was up-regulated, and the expression of PI3K and p-Akt was down-regulated in group H/R (P<0.05). Compared with group H/R, the cell viability was significantly increased, the expression of TLR4 and caspase-3 was down-regulated, the expression of PI3K and p-Akt was up-regulated (P<0.05), and the mitochondrial damage was significantly attenuated in group CF. Conclusion The mechanism by which Clemastine Fumarate alleviates H/R injury to rat cardiomyocytes may be related to inhibiting TLR4 expression and activating PI3K/Akt signaling pathway. Key words: Histamine H1 antagonists; Myocardial reperfusion injury; Toll-like receptor 4; Phosphatidylinositol 3-kinases; Protein-serine-threonine kinases

  • effect of Clemastine Fumarate on lung ischemia reperfusion injury in rabbits
    Chinese Journal of Anesthesiology, 2016
    Co-Authors: Wei Wang, Ning Liu, Huirong Han, Rui Zhang
    Abstract:

    Objective To investigate the effect of Clemastine Fumarate on lung ischemia-reperfusion (I/R) injury in rabbits. Methods Fifty New Zealand white rabbits of both sexes, weighing 2.0-3.0 kg, were divided into 3 groups using a random number table: sham operation group (Sham group, n=10), I/R group (n=20) and Clemastine Fumarate group (Cle group, n=20). The model of lung I/R was established by clamping the left hilum of lung and decreasing the tidal volume followed by restoration of perfusion and ventilation 1 h later in I/R and Cle groups.At 3 h of ventilation in group Sham and 2 and 4 h of reperfusion in I/R and Cle groups, blood samples were collected for determination of serum tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) concentrations by enzyme-linked immunosorbent assay.The left lung was lavaged, and the broncho-alveolar lavage fluid (BALF) was colleted for determination of white blood cell count.Lung specimens were obtained for microscopic examination of the ultrastructure of lung tissues and for determination of wet/dry weight ratio (W/D ratio), expression of IL-1β and IL-6 mRNA (by real-time polymerase chain reaction) and cell apoptosis (by TUNEL). The apoptosis rate was calculated. Results Compared with Sham group, the W/D ratio, white blood cell count in BALF, serum concentrations of TNF-α and IL-8 and apoptosis rate were significantly increased, and the expression of IL-1β and IL-6 mRNA was up-regulated in I/R and Cle groups (P<0.05 or 0.01). Compared with I/R group, the W/D ratio, white blood cell count in BALF, serum concentrations of TNF-α and IL-8 and apoptosis rate were significantly decreased, and the expression of IL-1β and IL-6 mRNA was down-regulated in Cle group (P<0.05 or 0.01). The pathological changes of lung tissues were significantly attenuated in Cle group than in I/R group. Conclusion Clemastine Fumarate can attenuate lung I/R injury in rabbits. Key words: Clemastine; Reperfusion injury; Lung

Yaru Huang - One of the best experts on this subject based on the ideXlab platform.

  • Clemastine Fumarate protects against myocardial ischemia reperfusion injury by activating the tlr4 pi3k akt signaling pathway
    Frontiers in Pharmacology, 2020
    Co-Authors: Xiaoxiao Yuan, Rui Zhang, Ru Yan, Feng Yue, Zhaodong Juan, Yaru Huang, Xiaotong Sun, Xiaohui Xia
    Abstract:

    Our pilot studies have shown that Clemastine Fumarate (CLE) can protect against myocardial ischemia-reperfusion injury (MIRI) through regulation of toll like receptor 4 (TLR4). However, the protective mechanism of CLE and related signaling pathways for MIRI remains unclear. The objective of this study is to determine the mechanism by which CLE relieves MIRI in cardiomyocytes and its relationship with the TLR4/PI3K/Akt signaling pathway. CCK8 analysis was used to test the optimal concentration of TLR4 inhibitor CLI-095 and TLR4 agonist lipopolysaccharide (LPS) on MIRI. The expression of inflammatory factors, oxidative stress response, cell damage, and intracellular calcium redistribution of cardiomyocytes were examined using the ELISA kits, Total Superoxide Dismutase Assay Kit with WST-8 and Lipid Peroxidation MDA Assay Kit, LDH Cytotoxicity Assay Kit, and laser scanning confocal microscope. The expression of TLR4/PI3K/Akt and cleaved caspase-3 were determined by Western blotting and immunofluorescent staining. Our results showed that MIRI aggravated the inflammatory response, oxidative stress, cellular damage of cardiomyocytes, and caused redistribution of intracellular calcium, upregulated the expression of TLR4 protein, cleaved caspase-3 protein, and down-regulated the expression of PI3K/Akt protein. After treatment with CLE, the inflammatory response, oxidative stress, and cellular damage of cardiomyocytes were alleviated, and intracellular calcium ion accumulation decreased. The expression of TLR4 protein, cleaved caspase-3 protein declined, but PI3K/Akt protein expression increased in cardiomyocytes treated with CLE. In addition, after treatment with the TLR4 inhibitor CLI-095, the results were similar to those of CLE treatment. The TLR4 agonist LPS aggravated the reactions caused by MIRI. The role of LPS was reversed after CLE treatment. These results suggested that CLE can attenuate MIRI by activating the TLR4/PI3K/Akt signaling pathway.

  • effect of Clemastine Fumarate on tlr4 pi3k akt signaling pathway during hypoxia reoxygenation in rat cardiomyocytes
    Chinese Journal of Anesthesiology, 2019
    Co-Authors: Ru Yan, Rui Zhang, Feng Yue, Yongxin Liu, Xiaoxiao Yuan, Meiyan Sun, Zhaodong Juan, Yaru Huang
    Abstract:

    Objective To evaluate the effect of Clemastine Fumarate on Toll-like receptor 4/phosphatidylinositol-3-kinase/serine-threonine kinase (TLR4/PI3K/Akt) signaling pathway during hypoxia-reoxygenation(H/R) in rat cardiomyocytes. Methods H9C2 cells of rats cultured in vitro were seeded in culture wells or dishes at a density of 1×105 cells/ml and divided into 3 groups (n=11 each) by using a random number table method: control group (group C), H/R group and Clemastine Fumarate group (CF group). Cardiomyocytes were exposed to 5% CO2-95% N2 in a low-glucose DMEM medium at 37℃ for 4 h followed by 4 h reoxygenation.At 4 h of reoxygenation, the cell viability was detected by CCK-8 assay, the ultrastructure was observed with a transmission electron microscope, the expression of TLR4, PI3K, phosphorylated Akt (p-Akt) and caspase-3 was detected by Western blot, and the expression of TLR4, PI3K and caspase-3 was detected by immunofluorescence. Results Compared with group C, the cell viability was significantly decreased, the expression of TLR4 and caspase-3 was up-regulated, and the expression of PI3K and p-Akt was down-regulated in group H/R (P<0.05). Compared with group H/R, the cell viability was significantly increased, the expression of TLR4 and caspase-3 was down-regulated, the expression of PI3K and p-Akt was up-regulated (P<0.05), and the mitochondrial damage was significantly attenuated in group CF. Conclusion The mechanism by which Clemastine Fumarate alleviates H/R injury to rat cardiomyocytes may be related to inhibiting TLR4 expression and activating PI3K/Akt signaling pathway. Key words: Histamine H1 antagonists; Myocardial reperfusion injury; Toll-like receptor 4; Phosphatidylinositol 3-kinases; Protein-serine-threonine kinases

Ru Yan - One of the best experts on this subject based on the ideXlab platform.

  • Clemastine Fumarate protects against myocardial ischemia reperfusion injury by activating the tlr4 pi3k akt signaling pathway
    Frontiers in Pharmacology, 2020
    Co-Authors: Xiaoxiao Yuan, Rui Zhang, Ru Yan, Feng Yue, Zhaodong Juan, Yaru Huang, Xiaotong Sun, Xiaohui Xia
    Abstract:

    Our pilot studies have shown that Clemastine Fumarate (CLE) can protect against myocardial ischemia-reperfusion injury (MIRI) through regulation of toll like receptor 4 (TLR4). However, the protective mechanism of CLE and related signaling pathways for MIRI remains unclear. The objective of this study is to determine the mechanism by which CLE relieves MIRI in cardiomyocytes and its relationship with the TLR4/PI3K/Akt signaling pathway. CCK8 analysis was used to test the optimal concentration of TLR4 inhibitor CLI-095 and TLR4 agonist lipopolysaccharide (LPS) on MIRI. The expression of inflammatory factors, oxidative stress response, cell damage, and intracellular calcium redistribution of cardiomyocytes were examined using the ELISA kits, Total Superoxide Dismutase Assay Kit with WST-8 and Lipid Peroxidation MDA Assay Kit, LDH Cytotoxicity Assay Kit, and laser scanning confocal microscope. The expression of TLR4/PI3K/Akt and cleaved caspase-3 were determined by Western blotting and immunofluorescent staining. Our results showed that MIRI aggravated the inflammatory response, oxidative stress, cellular damage of cardiomyocytes, and caused redistribution of intracellular calcium, upregulated the expression of TLR4 protein, cleaved caspase-3 protein, and down-regulated the expression of PI3K/Akt protein. After treatment with CLE, the inflammatory response, oxidative stress, and cellular damage of cardiomyocytes were alleviated, and intracellular calcium ion accumulation decreased. The expression of TLR4 protein, cleaved caspase-3 protein declined, but PI3K/Akt protein expression increased in cardiomyocytes treated with CLE. In addition, after treatment with the TLR4 inhibitor CLI-095, the results were similar to those of CLE treatment. The TLR4 agonist LPS aggravated the reactions caused by MIRI. The role of LPS was reversed after CLE treatment. These results suggested that CLE can attenuate MIRI by activating the TLR4/PI3K/Akt signaling pathway.

  • effect of Clemastine Fumarate on tlr4 pi3k akt signaling pathway during hypoxia reoxygenation in rat cardiomyocytes
    Chinese Journal of Anesthesiology, 2019
    Co-Authors: Ru Yan, Rui Zhang, Feng Yue, Yongxin Liu, Xiaoxiao Yuan, Meiyan Sun, Zhaodong Juan, Yaru Huang
    Abstract:

    Objective To evaluate the effect of Clemastine Fumarate on Toll-like receptor 4/phosphatidylinositol-3-kinase/serine-threonine kinase (TLR4/PI3K/Akt) signaling pathway during hypoxia-reoxygenation(H/R) in rat cardiomyocytes. Methods H9C2 cells of rats cultured in vitro were seeded in culture wells or dishes at a density of 1×105 cells/ml and divided into 3 groups (n=11 each) by using a random number table method: control group (group C), H/R group and Clemastine Fumarate group (CF group). Cardiomyocytes were exposed to 5% CO2-95% N2 in a low-glucose DMEM medium at 37℃ for 4 h followed by 4 h reoxygenation.At 4 h of reoxygenation, the cell viability was detected by CCK-8 assay, the ultrastructure was observed with a transmission electron microscope, the expression of TLR4, PI3K, phosphorylated Akt (p-Akt) and caspase-3 was detected by Western blot, and the expression of TLR4, PI3K and caspase-3 was detected by immunofluorescence. Results Compared with group C, the cell viability was significantly decreased, the expression of TLR4 and caspase-3 was up-regulated, and the expression of PI3K and p-Akt was down-regulated in group H/R (P<0.05). Compared with group H/R, the cell viability was significantly increased, the expression of TLR4 and caspase-3 was down-regulated, the expression of PI3K and p-Akt was up-regulated (P<0.05), and the mitochondrial damage was significantly attenuated in group CF. Conclusion The mechanism by which Clemastine Fumarate alleviates H/R injury to rat cardiomyocytes may be related to inhibiting TLR4 expression and activating PI3K/Akt signaling pathway. Key words: Histamine H1 antagonists; Myocardial reperfusion injury; Toll-like receptor 4; Phosphatidylinositol 3-kinases; Protein-serine-threonine kinases

Xiaoxiao Yuan - One of the best experts on this subject based on the ideXlab platform.

  • Clemastine Fumarate protects against myocardial ischemia reperfusion injury by activating the tlr4 pi3k akt signaling pathway
    Frontiers in Pharmacology, 2020
    Co-Authors: Xiaoxiao Yuan, Rui Zhang, Ru Yan, Feng Yue, Zhaodong Juan, Yaru Huang, Xiaotong Sun, Xiaohui Xia
    Abstract:

    Our pilot studies have shown that Clemastine Fumarate (CLE) can protect against myocardial ischemia-reperfusion injury (MIRI) through regulation of toll like receptor 4 (TLR4). However, the protective mechanism of CLE and related signaling pathways for MIRI remains unclear. The objective of this study is to determine the mechanism by which CLE relieves MIRI in cardiomyocytes and its relationship with the TLR4/PI3K/Akt signaling pathway. CCK8 analysis was used to test the optimal concentration of TLR4 inhibitor CLI-095 and TLR4 agonist lipopolysaccharide (LPS) on MIRI. The expression of inflammatory factors, oxidative stress response, cell damage, and intracellular calcium redistribution of cardiomyocytes were examined using the ELISA kits, Total Superoxide Dismutase Assay Kit with WST-8 and Lipid Peroxidation MDA Assay Kit, LDH Cytotoxicity Assay Kit, and laser scanning confocal microscope. The expression of TLR4/PI3K/Akt and cleaved caspase-3 were determined by Western blotting and immunofluorescent staining. Our results showed that MIRI aggravated the inflammatory response, oxidative stress, cellular damage of cardiomyocytes, and caused redistribution of intracellular calcium, upregulated the expression of TLR4 protein, cleaved caspase-3 protein, and down-regulated the expression of PI3K/Akt protein. After treatment with CLE, the inflammatory response, oxidative stress, and cellular damage of cardiomyocytes were alleviated, and intracellular calcium ion accumulation decreased. The expression of TLR4 protein, cleaved caspase-3 protein declined, but PI3K/Akt protein expression increased in cardiomyocytes treated with CLE. In addition, after treatment with the TLR4 inhibitor CLI-095, the results were similar to those of CLE treatment. The TLR4 agonist LPS aggravated the reactions caused by MIRI. The role of LPS was reversed after CLE treatment. These results suggested that CLE can attenuate MIRI by activating the TLR4/PI3K/Akt signaling pathway.

  • effect of Clemastine Fumarate on tlr4 pi3k akt signaling pathway during hypoxia reoxygenation in rat cardiomyocytes
    Chinese Journal of Anesthesiology, 2019
    Co-Authors: Ru Yan, Rui Zhang, Feng Yue, Yongxin Liu, Xiaoxiao Yuan, Meiyan Sun, Zhaodong Juan, Yaru Huang
    Abstract:

    Objective To evaluate the effect of Clemastine Fumarate on Toll-like receptor 4/phosphatidylinositol-3-kinase/serine-threonine kinase (TLR4/PI3K/Akt) signaling pathway during hypoxia-reoxygenation(H/R) in rat cardiomyocytes. Methods H9C2 cells of rats cultured in vitro were seeded in culture wells or dishes at a density of 1×105 cells/ml and divided into 3 groups (n=11 each) by using a random number table method: control group (group C), H/R group and Clemastine Fumarate group (CF group). Cardiomyocytes were exposed to 5% CO2-95% N2 in a low-glucose DMEM medium at 37℃ for 4 h followed by 4 h reoxygenation.At 4 h of reoxygenation, the cell viability was detected by CCK-8 assay, the ultrastructure was observed with a transmission electron microscope, the expression of TLR4, PI3K, phosphorylated Akt (p-Akt) and caspase-3 was detected by Western blot, and the expression of TLR4, PI3K and caspase-3 was detected by immunofluorescence. Results Compared with group C, the cell viability was significantly decreased, the expression of TLR4 and caspase-3 was up-regulated, and the expression of PI3K and p-Akt was down-regulated in group H/R (P<0.05). Compared with group H/R, the cell viability was significantly increased, the expression of TLR4 and caspase-3 was down-regulated, the expression of PI3K and p-Akt was up-regulated (P<0.05), and the mitochondrial damage was significantly attenuated in group CF. Conclusion The mechanism by which Clemastine Fumarate alleviates H/R injury to rat cardiomyocytes may be related to inhibiting TLR4 expression and activating PI3K/Akt signaling pathway. Key words: Histamine H1 antagonists; Myocardial reperfusion injury; Toll-like receptor 4; Phosphatidylinositol 3-kinases; Protein-serine-threonine kinases

Zhaodong Juan - One of the best experts on this subject based on the ideXlab platform.

  • Clemastine Fumarate protects against myocardial ischemia reperfusion injury by activating the tlr4 pi3k akt signaling pathway
    Frontiers in Pharmacology, 2020
    Co-Authors: Xiaoxiao Yuan, Rui Zhang, Ru Yan, Feng Yue, Zhaodong Juan, Yaru Huang, Xiaotong Sun, Xiaohui Xia
    Abstract:

    Our pilot studies have shown that Clemastine Fumarate (CLE) can protect against myocardial ischemia-reperfusion injury (MIRI) through regulation of toll like receptor 4 (TLR4). However, the protective mechanism of CLE and related signaling pathways for MIRI remains unclear. The objective of this study is to determine the mechanism by which CLE relieves MIRI in cardiomyocytes and its relationship with the TLR4/PI3K/Akt signaling pathway. CCK8 analysis was used to test the optimal concentration of TLR4 inhibitor CLI-095 and TLR4 agonist lipopolysaccharide (LPS) on MIRI. The expression of inflammatory factors, oxidative stress response, cell damage, and intracellular calcium redistribution of cardiomyocytes were examined using the ELISA kits, Total Superoxide Dismutase Assay Kit with WST-8 and Lipid Peroxidation MDA Assay Kit, LDH Cytotoxicity Assay Kit, and laser scanning confocal microscope. The expression of TLR4/PI3K/Akt and cleaved caspase-3 were determined by Western blotting and immunofluorescent staining. Our results showed that MIRI aggravated the inflammatory response, oxidative stress, cellular damage of cardiomyocytes, and caused redistribution of intracellular calcium, upregulated the expression of TLR4 protein, cleaved caspase-3 protein, and down-regulated the expression of PI3K/Akt protein. After treatment with CLE, the inflammatory response, oxidative stress, and cellular damage of cardiomyocytes were alleviated, and intracellular calcium ion accumulation decreased. The expression of TLR4 protein, cleaved caspase-3 protein declined, but PI3K/Akt protein expression increased in cardiomyocytes treated with CLE. In addition, after treatment with the TLR4 inhibitor CLI-095, the results were similar to those of CLE treatment. The TLR4 agonist LPS aggravated the reactions caused by MIRI. The role of LPS was reversed after CLE treatment. These results suggested that CLE can attenuate MIRI by activating the TLR4/PI3K/Akt signaling pathway.

  • effect of Clemastine Fumarate on tlr4 pi3k akt signaling pathway during hypoxia reoxygenation in rat cardiomyocytes
    Chinese Journal of Anesthesiology, 2019
    Co-Authors: Ru Yan, Rui Zhang, Feng Yue, Yongxin Liu, Xiaoxiao Yuan, Meiyan Sun, Zhaodong Juan, Yaru Huang
    Abstract:

    Objective To evaluate the effect of Clemastine Fumarate on Toll-like receptor 4/phosphatidylinositol-3-kinase/serine-threonine kinase (TLR4/PI3K/Akt) signaling pathway during hypoxia-reoxygenation(H/R) in rat cardiomyocytes. Methods H9C2 cells of rats cultured in vitro were seeded in culture wells or dishes at a density of 1×105 cells/ml and divided into 3 groups (n=11 each) by using a random number table method: control group (group C), H/R group and Clemastine Fumarate group (CF group). Cardiomyocytes were exposed to 5% CO2-95% N2 in a low-glucose DMEM medium at 37℃ for 4 h followed by 4 h reoxygenation.At 4 h of reoxygenation, the cell viability was detected by CCK-8 assay, the ultrastructure was observed with a transmission electron microscope, the expression of TLR4, PI3K, phosphorylated Akt (p-Akt) and caspase-3 was detected by Western blot, and the expression of TLR4, PI3K and caspase-3 was detected by immunofluorescence. Results Compared with group C, the cell viability was significantly decreased, the expression of TLR4 and caspase-3 was up-regulated, and the expression of PI3K and p-Akt was down-regulated in group H/R (P<0.05). Compared with group H/R, the cell viability was significantly increased, the expression of TLR4 and caspase-3 was down-regulated, the expression of PI3K and p-Akt was up-regulated (P<0.05), and the mitochondrial damage was significantly attenuated in group CF. Conclusion The mechanism by which Clemastine Fumarate alleviates H/R injury to rat cardiomyocytes may be related to inhibiting TLR4 expression and activating PI3K/Akt signaling pathway. Key words: Histamine H1 antagonists; Myocardial reperfusion injury; Toll-like receptor 4; Phosphatidylinositol 3-kinases; Protein-serine-threonine kinases