The Experts below are selected from a list of 1905 Experts worldwide ranked by ideXlab platform

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

  • Escin ameliorates the impairments of neurological function and blood brain barrier by inhibiting systemic inflammation in intracerebral hemorrhagic mice.
    Experimental neurology, 2020
    Co-Authors: Yu-xin Ding, Leiming Zhang, Sijin Duan, Gao-wa Eerduna, Rong-xia Liu, Tian Wang
    Abstract:

    Abstract This study aims to investigate whether Escin ameliorates the impairments of neurological function by ameliorating systemic inflammation instead of targeting the brain directly in intracerebral hemorrhage (ICH) mice. It showed that Escin did not cross the blood brain barrier (BBB). Compared with the ICH group, the Garcia test scores in the Escin groups were significantly increased. Brain water contents and Evans blue extravasation of the right basal ganglia in the ICH group were augmented, and significantly reduced by Escin. Escin abated the increases of monocyte counts and serum IL-1β levels induced by ICH. IL-1β administration reversed the effect of Escin on Garcia test scores, the brain water contents, and the Evans blue extravasation. Escin ameliorated the increasing levels of RhoA, ROCK1, nuclear NF-κB and the decreasing expression of IκBα, cytosolic NF-κB, occludin, claudin-5 in the ICH group. IL-1β administration blocked not only Escin-mediated increases of IκBα, cytosolic NF-κB, occludin, and claudin-5, but also Escin-caused decreases of RhoA, ROCK1, and nuclear NF-κB. The results indicate that Escin improves neurological outcomes and the BBB function in ICH mice, which is associated with attenuating ICH-induced peripheral system inflammation, and therefore, inhibiting IL-1β/RhoA/NF-κB signaling pathway in BBB, at least in part. These findings suggest that it may be useful to ameliorate brain injury by inhibiting systemic inflammation instead of aiming to target the brain directly after ICH.

  • network pharmacology based research on the combination mechanism between Escin and low dose glucocorticoids in anti rheumatoid arthritis
    Frontiers in Pharmacology, 2019
    Co-Authors: Leiming Zhang, Tian Wang, Yanan Huang, Meiling Wang, Xinlin Wang, Yanfang Wang, Yanfei Hao, Baofeng Fan, Zhuye Gao
    Abstract:

    Rheumatoid arthritis (RA) is characterized by chronic progressive symmetrical synovitis and destruction of multiple joints. Glucocorticoids (GCs) are widely used in the treatment of RA. However, their adverse effects can be serious. Escin, which is isolated from Aesculus hippocastanum L., has been reported to have anti-inflammatory effects. We investigated the anti-RA effect of Escin combined with low dose GCs (dexamethasone, Dex) and the underlying mechanism. Adjuvant-induced rheumatoid arthritis rats and lipopolysaccharides (LPS)-injured RAW 264.7 cells were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. The results showed that Escin combined with low-dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α levels, reduced paw swelling, and ameliorated the joint pathology and immune organ pathology. Gene chip results revealed that Nr3c1 (GR) expression was significantly altered, and that GR was activated by Escin and low dose Dex in vivo and in vitro. Additionally, Escin combined with low dose Dex also significantly increased GR mRNA expression. However, when GR expression was suppressed by its specific inhibitor, the anti-RA effect of Escin combined with low-dose Dex was abolished. The data in this study demonstrated that Escin combined with Dex reduced the dose of Dex, and exerted significant anti-RA effects, which could also reduce the adverse effects of Dex. This combination might result from GR activation. This study might provide a new combination of drugs for the treatment of RA.

  • Network Pharmacology Based Research on the Combination Mechanism Between Escin and Low Dose Glucocorticoids in Anti-rheumatoid Arthritis
    Frontiers Media S.A., 2019
    Co-Authors: Leiming Zhang, Yanan Huang, Meiling Wang, Xinlin Wang, Yanfang Wang, Yanfei Hao, Tian Wang
    Abstract:

    Rheumatoid arthritis (RA) is characterized by chronic progressive symmetrical synovitis and destruction of multiple joints. Glucocorticoids (GCs) are widely used in the treatment of RA. However, their adverse effects can be serious. Escin, which is isolated from Aesculus hippocastanum L., has been reported to have anti-inflammatory effects. We investigated the anti-RA effect of Escin combined with low dose GCs (dexamethasone, Dex) and the underlying mechanism. Adjuvant-induced RA rats and lipopolysaccharides (LPS)-injured RAW264.7 cells were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. The results showed that Escin combined with low-dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α levels, reduced paw swelling, and ameliorated the joint pathology and immune organ pathology. Gene chip results revealed that Nr3c1 (GR) expression was significantly altered, and that GR was activated by Escin and low dose Dex in vivo and in vitro. Additionally, Escin combined with low dose Dex also significantly increased GR mRNA expression. However, when GR expression was suppressed by its specific inhibitor, the anti-RA effect of Escin combined with low-dose Dex was abolished. The data in this study demonstrated that Escin combined with Dex reduced the dose of Dex, and exerted significant anti-RA effects, which could also reduce the adverse effects of Dex. This combination might result from GR activation. This study might provide a new combination of drugs for the treatment of RA

  • Research Article Oral Administration of Escin Inhibits Acute Inflammation and Reduces Intestinal Mucosal Injury in Animal Models
    2016
    Co-Authors: Leiming Zhang, Jianqiao Zhang, Sijin Duan, Tian Wang
    Abstract:

    which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Thepresent study aimed to investigate the effects of oral administration of Escin on acute inflammation and intestinalmucosal injury in animal models. The effects of Escin on carrageenan-induced paw edema in a rat model of acute inflammation, cecal ligation and puncture (CLP) induced intestinal mucosal injury in a mouse model, were observed. It was shown that oral administration of Escin inhibits carrageenan-induced paw edema and decreases the production of prostaglandin E2 (PGE2) and cyclooxygenase- (COX-) 2. In CLP model, low dose of Escin ameliorates endotoxin induced liver injury and intestinal mucosal injury and increases the expression of tight junction protein claudin-5 in mice.These findings suggest that Escin effectively inhibits acute inflammation and reduces intestinal mucosal injury in animal models. 1

  • Oral Administration of Escin Inhibits Acute Inflammation and Reduces Intestinal Mucosal Injury in Animal Models
    Evidence-based complementary and alternative medicine : eCAM, 2015
    Co-Authors: Leiming Zhang, Jianqiao Zhang, Sijin Duan, Tian Wang
    Abstract:

    The present study aimed to investigate the effects of oral administration of Escin on acute inflammation and intestinal mucosal injury in animal models. The effects of Escin on carrageenan-induced paw edema in a rat model of acute inflammation, cecal ligation and puncture (CLP) induced intestinal mucosal injury in a mouse model, were observed. It was shown that oral administration of Escin inhibits carrageenan-induced paw edema and decreases the production of prostaglandin E2 (PGE2) and cyclooxygenase- (COX-) 2. In CLP model, low dose of Escin ameliorates endotoxin induced liver injury and intestinal mucosal injury and increases the expression of tight junction protein claudin-5 in mice. These findings suggest that Escin effectively inhibits acute inflammation and reduces intestinal mucosal injury in animal models.

Jingrong Cui - One of the best experts on this subject based on the ideXlab platform.

  • β Escin sodium inhibits inducible nitric oxide synthase expression via downregulation of the jak stat pathway in a549 cells
    Molecular Carcinogenesis, 2011
    Co-Authors: Jing Tao Liu, Fu Xiang Ran, Jingrong Cui
    Abstract:

    β-Escin, a triterpene saponin, is one of the major active compounds extracted from horse chestnut (Aesculus hippocastanum) seed. Previous work has found that β-Escin sodium has antiinflammatory and antitumor effects. In the present study, we investigated its effect on cell proliferation and inducible nitric-oxide synthase (iNOS) expression in human lung carcinoma A549 cells. β-Escin sodium (5-40 µg/mL) inhibited cytokine mixture (CM)-induced nitric oxide (NO) production in A549 cells by reducing the expression of iNOS. β-Escin sodium suppressed phosphorylation and nuclear translocation of STAT1 (Tyr701) and STAT3 (Tyr705) induced by CM but did not affect the activation of c-Jun and NF-κB. β-Escin sodium inhibited the activation of protein tyrosine kinase JAK2. Pervanadate treatment reversed the β-Escin sodium-induced downregulation of STAT3 and STAT1. β-Escin sodium treatment enhanced an activating phosphorylation of the phosphatase SHP2. Small interfering RNA-mediated knockdown of SHP2 inhibited β-Escin sodium-induced phospho-STAT dephosphorylation. Moreover β-Escin sodium reduced the activation of p38 MAPK. Finally, β-Escin sodium inhibited the proliferation of A549 cells, did not change the cell membrane's permeability, nuclear morphology and size and the mitochondria's transmembrane potential of A549 cells. Taken together, these results demonstrate that β-Escin sodium could downregulate iNOS expression through inhibiting JAK/STAT signaling and p38 MAPK activation in A549 cells. β-Escin sodium has a marked antiproliferative effect on A549 cells at least in part by inhibiting the JAK/STAT signaling pathway, but not by a cytotoxic effect. β-Escin sodium would be useful as a chemopreventive agent or a therapeutic against inflammatory-associated tumor. © 2011 Wiley Periodicals, Inc.

  • β-Escin sodium inhibits inducible nitric oxide synthase expression via downregulation of the JAK/STAT pathway in A549 cells.
    Molecular carcinogenesis, 2011
    Co-Authors: Jing Tao Liu, Fu Xiang Ran, Jingrong Cui
    Abstract:

    β-Escin, a triterpene saponin, is one of the major active compounds extracted from horse chestnut (Aesculus hippocastanum) seed. Previous work has found that β-Escin sodium has antiinflammatory and antitumor effects. In the present study, we investigated its effect on cell proliferation and inducible nitric-oxide synthase (iNOS) expression in human lung carcinoma A549 cells. β-Escin sodium (5-40 µg/mL) inhibited cytokine mixture (CM)-induced nitric oxide (NO) production in A549 cells by reducing the expression of iNOS. β-Escin sodium suppressed phosphorylation and nuclear translocation of STAT1 (Tyr701) and STAT3 (Tyr705) induced by CM but did not affect the activation of c-Jun and NF-κB. β-Escin sodium inhibited the activation of protein tyrosine kinase JAK2. Pervanadate treatment reversed the β-Escin sodium-induced downregulation of STAT3 and STAT1. β-Escin sodium treatment enhanced an activating phosphorylation of the phosphatase SHP2. Small interfering RNA-mediated knockdown of SHP2 inhibited β-Escin sodium-induced phospho-STAT dephosphorylation. Moreover β-Escin sodium reduced the activation of p38 MAPK. Finally, β-Escin sodium inhibited the proliferation of A549 cells, did not change the cell membrane's permeability, nuclear morphology and size and the mitochondria's transmembrane potential of A549 cells. Taken together, these results demonstrate that β-Escin sodium could downregulate iNOS expression through inhibiting JAK/STAT signaling and p38 MAPK activation in A549 cells. β-Escin sodium has a marked antiproliferative effect on A549 cells at least in part by inhibiting the JAK/STAT signaling pathway, but not by a cytotoxic effect. β-Escin sodium would be useful as a chemopreventive agent or a therapeutic against inflammatory-associated tumor. © 2011 Wiley Periodicals, Inc.

  • Effect of β-Escin sodium on endothelial cells proliferation, migration and apoptosis
    Vascular Pharmacology, 2008
    Co-Authors: Xu-hua Wang, Jing Tao Liu, Jingrong Cui
    Abstract:

    beta-Escin, the major active compound in extracts of the horse chestnut Aesculus hippocastanum seed, has shown clinically significant activity in chronic venous insufficiency (CVI). Our previous studies had shown that beta-Escin sodium inhibited angiogenesis in chick chorioallantoic membrane (CAM) and in aortic disk assay. In this study, we explored the direct effect of beta-Escin sodium on proliferation, migration and apoptosis in human umbilical vein endothelial cells (HUVECs) and ECV304 cells. Sulforhodamine B (SRB) assay showed that beta-Escin sodium (10, 20, 40 microg/ml) inhibited endothelial cells (ECs) proliferation dose-dependently. beta-Escin sodium also induced ECs apoptosis at 40 microg/ml. Cell migration was evaluated by an improved wound assay: barren spot assay. And the direct effect on cell motility excluding influence of cell proliferation was examined by High Content Screening (HCS, Cellomics) assay. The data indicated that beta-Escin sodium suppressed ECs migration and cell motility. Western blot results suggested that beta-Escin sodium acts on ECs possibly by increasing expression of thrombospondin-1 (TSP-1), and decreasing expression of PKC-alpha and activation of p44/42 mitogen-activated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK). Our findings give the evidence that beta-Escin sodium might have potential anti-angiogenic activity via its direct effects on ECs.

  • Effect of beta-Escin sodium on endothelial cells proliferation, migration and apoptosis.
    Vascular pharmacology, 2008
    Co-Authors: Xu-hua Wang, Jing Tao Liu, Jingrong Cui
    Abstract:

    beta-Escin, the major active compound in extracts of the horse chestnut Aesculus hippocastanum seed, has shown clinically significant activity in chronic venous insufficiency (CVI). Our previous studies had shown that beta-Escin sodium inhibited angiogenesis in chick chorioallantoic membrane (CAM) and in aortic disk assay. In this study, we explored the direct effect of beta-Escin sodium on proliferation, migration and apoptosis in human umbilical vein endothelial cells (HUVECs) and ECV304 cells. Sulforhodamine B (SRB) assay showed that beta-Escin sodium (10, 20, 40 microg/ml) inhibited endothelial cells (ECs) proliferation dose-dependently. beta-Escin sodium also induced ECs apoptosis at 40 microg/ml. Cell migration was evaluated by an improved wound assay: barren spot assay. And the direct effect on cell motility excluding influence of cell proliferation was examined by High Content Screening (HCS, Cellomics) assay. The data indicated that beta-Escin sodium suppressed ECs migration and cell motility. Western blot results suggested that beta-Escin sodium acts on ECs possibly by increasing expression of thrombospondin-1 (TSP-1), and decreasing expression of PKC-alpha and activation of p44/42 mitogen-activated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK). Our findings give the evidence that beta-Escin sodium might have potential anti-angiogenic activity via its direct effects on ECs.

Tian Wang - One of the best experts on this subject based on the ideXlab platform.

  • Escin ameliorates the impairments of neurological function and blood brain barrier by inhibiting systemic inflammation in intracerebral hemorrhagic mice.
    Experimental neurology, 2020
    Co-Authors: Yu-xin Ding, Leiming Zhang, Sijin Duan, Gao-wa Eerduna, Rong-xia Liu, Tian Wang
    Abstract:

    Abstract This study aims to investigate whether Escin ameliorates the impairments of neurological function by ameliorating systemic inflammation instead of targeting the brain directly in intracerebral hemorrhage (ICH) mice. It showed that Escin did not cross the blood brain barrier (BBB). Compared with the ICH group, the Garcia test scores in the Escin groups were significantly increased. Brain water contents and Evans blue extravasation of the right basal ganglia in the ICH group were augmented, and significantly reduced by Escin. Escin abated the increases of monocyte counts and serum IL-1β levels induced by ICH. IL-1β administration reversed the effect of Escin on Garcia test scores, the brain water contents, and the Evans blue extravasation. Escin ameliorated the increasing levels of RhoA, ROCK1, nuclear NF-κB and the decreasing expression of IκBα, cytosolic NF-κB, occludin, claudin-5 in the ICH group. IL-1β administration blocked not only Escin-mediated increases of IκBα, cytosolic NF-κB, occludin, and claudin-5, but also Escin-caused decreases of RhoA, ROCK1, and nuclear NF-κB. The results indicate that Escin improves neurological outcomes and the BBB function in ICH mice, which is associated with attenuating ICH-induced peripheral system inflammation, and therefore, inhibiting IL-1β/RhoA/NF-κB signaling pathway in BBB, at least in part. These findings suggest that it may be useful to ameliorate brain injury by inhibiting systemic inflammation instead of aiming to target the brain directly after ICH.

  • network pharmacology based research on the combination mechanism between Escin and low dose glucocorticoids in anti rheumatoid arthritis
    Frontiers in Pharmacology, 2019
    Co-Authors: Leiming Zhang, Tian Wang, Yanan Huang, Meiling Wang, Xinlin Wang, Yanfang Wang, Yanfei Hao, Baofeng Fan, Zhuye Gao
    Abstract:

    Rheumatoid arthritis (RA) is characterized by chronic progressive symmetrical synovitis and destruction of multiple joints. Glucocorticoids (GCs) are widely used in the treatment of RA. However, their adverse effects can be serious. Escin, which is isolated from Aesculus hippocastanum L., has been reported to have anti-inflammatory effects. We investigated the anti-RA effect of Escin combined with low dose GCs (dexamethasone, Dex) and the underlying mechanism. Adjuvant-induced rheumatoid arthritis rats and lipopolysaccharides (LPS)-injured RAW 264.7 cells were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. The results showed that Escin combined with low-dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α levels, reduced paw swelling, and ameliorated the joint pathology and immune organ pathology. Gene chip results revealed that Nr3c1 (GR) expression was significantly altered, and that GR was activated by Escin and low dose Dex in vivo and in vitro. Additionally, Escin combined with low dose Dex also significantly increased GR mRNA expression. However, when GR expression was suppressed by its specific inhibitor, the anti-RA effect of Escin combined with low-dose Dex was abolished. The data in this study demonstrated that Escin combined with Dex reduced the dose of Dex, and exerted significant anti-RA effects, which could also reduce the adverse effects of Dex. This combination might result from GR activation. This study might provide a new combination of drugs for the treatment of RA.

  • Network Pharmacology Based Research on the Combination Mechanism Between Escin and Low Dose Glucocorticoids in Anti-rheumatoid Arthritis
    Frontiers Media S.A., 2019
    Co-Authors: Leiming Zhang, Yanan Huang, Meiling Wang, Xinlin Wang, Yanfang Wang, Yanfei Hao, Tian Wang
    Abstract:

    Rheumatoid arthritis (RA) is characterized by chronic progressive symmetrical synovitis and destruction of multiple joints. Glucocorticoids (GCs) are widely used in the treatment of RA. However, their adverse effects can be serious. Escin, which is isolated from Aesculus hippocastanum L., has been reported to have anti-inflammatory effects. We investigated the anti-RA effect of Escin combined with low dose GCs (dexamethasone, Dex) and the underlying mechanism. Adjuvant-induced RA rats and lipopolysaccharides (LPS)-injured RAW264.7 cells were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. The results showed that Escin combined with low-dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α levels, reduced paw swelling, and ameliorated the joint pathology and immune organ pathology. Gene chip results revealed that Nr3c1 (GR) expression was significantly altered, and that GR was activated by Escin and low dose Dex in vivo and in vitro. Additionally, Escin combined with low dose Dex also significantly increased GR mRNA expression. However, when GR expression was suppressed by its specific inhibitor, the anti-RA effect of Escin combined with low-dose Dex was abolished. The data in this study demonstrated that Escin combined with Dex reduced the dose of Dex, and exerted significant anti-RA effects, which could also reduce the adverse effects of Dex. This combination might result from GR activation. This study might provide a new combination of drugs for the treatment of RA

  • Research Article Oral Administration of Escin Inhibits Acute Inflammation and Reduces Intestinal Mucosal Injury in Animal Models
    2016
    Co-Authors: Leiming Zhang, Jianqiao Zhang, Sijin Duan, Tian Wang
    Abstract:

    which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Thepresent study aimed to investigate the effects of oral administration of Escin on acute inflammation and intestinalmucosal injury in animal models. The effects of Escin on carrageenan-induced paw edema in a rat model of acute inflammation, cecal ligation and puncture (CLP) induced intestinal mucosal injury in a mouse model, were observed. It was shown that oral administration of Escin inhibits carrageenan-induced paw edema and decreases the production of prostaglandin E2 (PGE2) and cyclooxygenase- (COX-) 2. In CLP model, low dose of Escin ameliorates endotoxin induced liver injury and intestinal mucosal injury and increases the expression of tight junction protein claudin-5 in mice.These findings suggest that Escin effectively inhibits acute inflammation and reduces intestinal mucosal injury in animal models. 1

  • Oral Administration of Escin Inhibits Acute Inflammation and Reduces Intestinal Mucosal Injury in Animal Models
    Evidence-based complementary and alternative medicine : eCAM, 2015
    Co-Authors: Leiming Zhang, Jianqiao Zhang, Sijin Duan, Tian Wang
    Abstract:

    The present study aimed to investigate the effects of oral administration of Escin on acute inflammation and intestinal mucosal injury in animal models. The effects of Escin on carrageenan-induced paw edema in a rat model of acute inflammation, cecal ligation and puncture (CLP) induced intestinal mucosal injury in a mouse model, were observed. It was shown that oral administration of Escin inhibits carrageenan-induced paw edema and decreases the production of prostaglandin E2 (PGE2) and cyclooxygenase- (COX-) 2. In CLP model, low dose of Escin ameliorates endotoxin induced liver injury and intestinal mucosal injury and increases the expression of tight junction protein claudin-5 in mice. These findings suggest that Escin effectively inhibits acute inflammation and reduces intestinal mucosal injury in animal models.

Jing Tao Liu - One of the best experts on this subject based on the ideXlab platform.

  • β Escin sodium inhibits inducible nitric oxide synthase expression via downregulation of the jak stat pathway in a549 cells
    Molecular Carcinogenesis, 2011
    Co-Authors: Jing Tao Liu, Fu Xiang Ran, Jingrong Cui
    Abstract:

    β-Escin, a triterpene saponin, is one of the major active compounds extracted from horse chestnut (Aesculus hippocastanum) seed. Previous work has found that β-Escin sodium has antiinflammatory and antitumor effects. In the present study, we investigated its effect on cell proliferation and inducible nitric-oxide synthase (iNOS) expression in human lung carcinoma A549 cells. β-Escin sodium (5-40 µg/mL) inhibited cytokine mixture (CM)-induced nitric oxide (NO) production in A549 cells by reducing the expression of iNOS. β-Escin sodium suppressed phosphorylation and nuclear translocation of STAT1 (Tyr701) and STAT3 (Tyr705) induced by CM but did not affect the activation of c-Jun and NF-κB. β-Escin sodium inhibited the activation of protein tyrosine kinase JAK2. Pervanadate treatment reversed the β-Escin sodium-induced downregulation of STAT3 and STAT1. β-Escin sodium treatment enhanced an activating phosphorylation of the phosphatase SHP2. Small interfering RNA-mediated knockdown of SHP2 inhibited β-Escin sodium-induced phospho-STAT dephosphorylation. Moreover β-Escin sodium reduced the activation of p38 MAPK. Finally, β-Escin sodium inhibited the proliferation of A549 cells, did not change the cell membrane's permeability, nuclear morphology and size and the mitochondria's transmembrane potential of A549 cells. Taken together, these results demonstrate that β-Escin sodium could downregulate iNOS expression through inhibiting JAK/STAT signaling and p38 MAPK activation in A549 cells. β-Escin sodium has a marked antiproliferative effect on A549 cells at least in part by inhibiting the JAK/STAT signaling pathway, but not by a cytotoxic effect. β-Escin sodium would be useful as a chemopreventive agent or a therapeutic against inflammatory-associated tumor. © 2011 Wiley Periodicals, Inc.

  • β-Escin sodium inhibits inducible nitric oxide synthase expression via downregulation of the JAK/STAT pathway in A549 cells.
    Molecular carcinogenesis, 2011
    Co-Authors: Jing Tao Liu, Fu Xiang Ran, Jingrong Cui
    Abstract:

    β-Escin, a triterpene saponin, is one of the major active compounds extracted from horse chestnut (Aesculus hippocastanum) seed. Previous work has found that β-Escin sodium has antiinflammatory and antitumor effects. In the present study, we investigated its effect on cell proliferation and inducible nitric-oxide synthase (iNOS) expression in human lung carcinoma A549 cells. β-Escin sodium (5-40 µg/mL) inhibited cytokine mixture (CM)-induced nitric oxide (NO) production in A549 cells by reducing the expression of iNOS. β-Escin sodium suppressed phosphorylation and nuclear translocation of STAT1 (Tyr701) and STAT3 (Tyr705) induced by CM but did not affect the activation of c-Jun and NF-κB. β-Escin sodium inhibited the activation of protein tyrosine kinase JAK2. Pervanadate treatment reversed the β-Escin sodium-induced downregulation of STAT3 and STAT1. β-Escin sodium treatment enhanced an activating phosphorylation of the phosphatase SHP2. Small interfering RNA-mediated knockdown of SHP2 inhibited β-Escin sodium-induced phospho-STAT dephosphorylation. Moreover β-Escin sodium reduced the activation of p38 MAPK. Finally, β-Escin sodium inhibited the proliferation of A549 cells, did not change the cell membrane's permeability, nuclear morphology and size and the mitochondria's transmembrane potential of A549 cells. Taken together, these results demonstrate that β-Escin sodium could downregulate iNOS expression through inhibiting JAK/STAT signaling and p38 MAPK activation in A549 cells. β-Escin sodium has a marked antiproliferative effect on A549 cells at least in part by inhibiting the JAK/STAT signaling pathway, but not by a cytotoxic effect. β-Escin sodium would be useful as a chemopreventive agent or a therapeutic against inflammatory-associated tumor. © 2011 Wiley Periodicals, Inc.

  • Effect of β-Escin sodium on endothelial cells proliferation, migration and apoptosis
    Vascular Pharmacology, 2008
    Co-Authors: Xu-hua Wang, Jing Tao Liu, Jingrong Cui
    Abstract:

    beta-Escin, the major active compound in extracts of the horse chestnut Aesculus hippocastanum seed, has shown clinically significant activity in chronic venous insufficiency (CVI). Our previous studies had shown that beta-Escin sodium inhibited angiogenesis in chick chorioallantoic membrane (CAM) and in aortic disk assay. In this study, we explored the direct effect of beta-Escin sodium on proliferation, migration and apoptosis in human umbilical vein endothelial cells (HUVECs) and ECV304 cells. Sulforhodamine B (SRB) assay showed that beta-Escin sodium (10, 20, 40 microg/ml) inhibited endothelial cells (ECs) proliferation dose-dependently. beta-Escin sodium also induced ECs apoptosis at 40 microg/ml. Cell migration was evaluated by an improved wound assay: barren spot assay. And the direct effect on cell motility excluding influence of cell proliferation was examined by High Content Screening (HCS, Cellomics) assay. The data indicated that beta-Escin sodium suppressed ECs migration and cell motility. Western blot results suggested that beta-Escin sodium acts on ECs possibly by increasing expression of thrombospondin-1 (TSP-1), and decreasing expression of PKC-alpha and activation of p44/42 mitogen-activated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK). Our findings give the evidence that beta-Escin sodium might have potential anti-angiogenic activity via its direct effects on ECs.

  • Effect of beta-Escin sodium on endothelial cells proliferation, migration and apoptosis.
    Vascular pharmacology, 2008
    Co-Authors: Xu-hua Wang, Jing Tao Liu, Jingrong Cui
    Abstract:

    beta-Escin, the major active compound in extracts of the horse chestnut Aesculus hippocastanum seed, has shown clinically significant activity in chronic venous insufficiency (CVI). Our previous studies had shown that beta-Escin sodium inhibited angiogenesis in chick chorioallantoic membrane (CAM) and in aortic disk assay. In this study, we explored the direct effect of beta-Escin sodium on proliferation, migration and apoptosis in human umbilical vein endothelial cells (HUVECs) and ECV304 cells. Sulforhodamine B (SRB) assay showed that beta-Escin sodium (10, 20, 40 microg/ml) inhibited endothelial cells (ECs) proliferation dose-dependently. beta-Escin sodium also induced ECs apoptosis at 40 microg/ml. Cell migration was evaluated by an improved wound assay: barren spot assay. And the direct effect on cell motility excluding influence of cell proliferation was examined by High Content Screening (HCS, Cellomics) assay. The data indicated that beta-Escin sodium suppressed ECs migration and cell motility. Western blot results suggested that beta-Escin sodium acts on ECs possibly by increasing expression of thrombospondin-1 (TSP-1), and decreasing expression of PKC-alpha and activation of p44/42 mitogen-activated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK). Our findings give the evidence that beta-Escin sodium might have potential anti-angiogenic activity via its direct effects on ECs.

Na Jiang - One of the best experts on this subject based on the ideXlab platform.

  • anti inflammatory effects of Escin are correlated with the glucocorticoid receptor nf κb signaling pathway but not the cox pgf2α signaling pathway
    Experimental and Therapeutic Medicine, 2013
    Co-Authors: Hongsheng Wang, Leiming Zhang, Na Jiang, Zhenhua Wang, Yating Chong
    Abstract:

    In China, Escin has been widely used in the clinic as a potent anti-inflammatory drug. Previous studies have indicated that Escin exerts its anti-inflammatory effect by enhancing the release of glucocorticoids (GCs) and prostaglandin-F2α (PGF2α), and this has been documented in the drug description. However, our previous studies demonstrated that Escin did not increase the secretion of GCs, but instead elevated the protein expression of the GC receptor (GR), which may have repressed nuclear factor (NF)-κB-mediated gene expression. The aim of this study was to determine the functions of NF-κB and PGF2α with regard to the anti-inflammatory effect of Escin. We investigated the anti-inflammatory effects of dexamethasone, diclofenac and Escin against carrageenan-induced paw edema in rats, and observed that Escin exerted a GC-like anti-inflammatory effect. In addition, we studied the role of PGF2α in the anti-inflammatory effect exerted by Escin in an acetic acid-induced capillary permeability model in mice. The results revealed that the coadministration of Escin and diclofenac, a potent prostaglandin-synthesis inhibitor, did not affect the anti-inflammatory effect of Escin. Furthermore, we investigated the function of NF-κB with regard to the anti-inflammatory effect exerted by Escin in lipopolysaccharide (LPS)-treated mice, and demonstrated that Escin significantly inhibited the expression of NF-κB. These results suggest that Escin has a GC-like anti-inflammatory effect, and that its mechanisms may be correlated with the GC receptor/NF-κB signaling pathway, but not the COX/PGF2α signaling pathway.

  • Anti-inflammatory effects of Escin are correlated with the glucocorticoid receptor/NF-κB signaling pathway, but not the COX/PGF2α signaling pathway.
    Experimental and therapeutic medicine, 2013
    Co-Authors: Hongsheng Wang, Leiming Zhang, Na Jiang, Zhenhua Wang, Yating Chong
    Abstract:

    In China, Escin has been widely used in the clinic as a potent anti-inflammatory drug. Previous studies have indicated that Escin exerts its anti-inflammatory effect by enhancing the release of glucocorticoids (GCs) and prostaglandin-F2α (PGF2α), and this has been documented in the drug description. However, our previous studies demonstrated that Escin did not increase the secretion of GCs, but instead elevated the protein expression of the GC receptor (GR), which may have repressed nuclear factor (NF)-κB-mediated gene expression. The aim of this study was to determine the functions of NF-κB and PGF2α with regard to the anti-inflammatory effect of Escin. We investigated the anti-inflammatory effects of dexamethasone, diclofenac and Escin against carrageenan-induced paw edema in rats, and observed that Escin exerted a GC-like anti-inflammatory effect. In addition, we studied the role of PGF2α in the anti-inflammatory effect exerted by Escin in an acetic acid-induced capillary permeability model in mice. The results revealed that the coadministration of Escin and diclofenac, a potent prostaglandin-synthesis inhibitor, did not affect the anti-inflammatory effect of Escin. Furthermore, we investigated the function of NF-κB with regard to the anti-inflammatory effect exerted by Escin in lipopolysaccharide (LPS)-treated mice, and demonstrated that Escin significantly inhibited the expression of NF-κB. These results suggest that Escin has a GC-like anti-inflammatory effect, and that its mechanisms may be correlated with the GC receptor/NF-κB signaling pathway, but not the COX/PGF2α signaling pathway.

  • Potent anti-inflammatory agent Escin does not affect the healing of tibia fracture and abdominal wound in an animal model
    Experimental and therapeutic medicine, 2012
    Co-Authors: Leiming Zhang, Tian Wang, Na Jiang, Hongsheng Wang, Feiyan Liu, Yating Chong
    Abstract:

    Escin, a potent anti-inflammatory and anti-edematous agent, has been widely used clinically in preventing inflammatory edema after trauma, such as fracture and surgery. The aim of this study was to investigate whether Escin has an inhibitory effect on fracture healing, and whether Escin has an inhibitory effect on wound healing after surgery. Male New Zealand white rabbits underwent tibial mid-diaphyseal osteotomy, and were administered Escin once per day for 10 days. At weeks 2, 4 and 6, bone fracture healing and bone mineral density were measured. The histologic examination of callus, osteocalcin, alkaline phosphatase, calcium and phosphate in the serum were also assayed. In another experiment, the rats underwent midline laparotomy, and received Escin once prior to or after the operation. Six days later, the abdominal incision wounds were excised for measuring hydroxyproline levels. The results showed that there were no significant differences in fracture healing between the model and rabbits administered Escin, and Escin did not affect the hydroxyproline levels in the abdominal incision wounds of the rats. These findings suggest that Escin has no inhibitory effect on fracture and wound healing in animal models.

  • protective effect of aEscin from the seeds of aesculus hippocastanum on liver injury induced by endotoxin in mice
    Phytomedicine, 2011
    Co-Authors: Na Jiang, Yuan Du, Chong Li, Leiming Zhang, Tian Wang, Fenghua Fu
    Abstract:

    Abstract To investigate the effect and underlying mechanism of aEscin on acute liver injury induced by endotoxin, liver injury was established by injecting lipopolysaccharide (LPS) in mice. Animals were assigned to seven groups: the control group and groups treated with LPS (40 mg/kg), aEscin (3.6 mg/kg), LPS plus dexamethasone (4 mg/kg) and LPS plus aEscin (0.9, 1.8 or 3.6 mg/kg). Hepatic histopathological changes were examined under a light microscope. Activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were determined. Levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), nitric oxide (NO) and antioxidative parameters in liver homogenate were measured. Glucocorticoid receptor (GR), 11 beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and 11 beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) expressions in liver were determined by western blotting. Treatment with Escin could inhibit immigration of inflammatory cells, alleviate the degree of necrosis, and decrease serum ALT and AST activities. AEscin also down-regulated levels of inflammation mediators (TNF-α, IL-1β and NO) and 11β-HSD2 expression in liver, up-regulated GR expression, enhanced endogenous antioxidative capacity, but have no obvious effect on 11β-HSD1 expression in liver. The findings suggest aEscin has protective effects on endotoxin-induced liver injury, and the underlying mechanisms were associated with its anti-inflammatory effects, up-regulating GR expression, down-regulating 11β-HSD2 experssion, and antixoidation.

  • The potent anti-inflammatory agent Escin does not increase corticosterone secretion and immune cell apoptosis in mice.
    Fitoterapia, 2011
    Co-Authors: Leiming Zhang, Tian Wang, Hongsheng Wang, Huaying Fan, Na Jiang
    Abstract:

    Escin exerts potent glucocorticoid-like anti-inflammatory effects. The aim of this study was to investigate whether the anti-inflammatory effect of Escin is through the up-regulation of glucocorticoids and if Escin induces pathological changes in immune organs. Mice were administrated with Escin intravenously for 7 days before observing the relevant parameters. The results showed that Escin exhibits a potent anti-inflammatory effect, but does not increase corticosterone secretion in mice, and does not increase immune cell apoptosis in the spleen and thymus of mice. These findings suggest that the anti-inflammatory effect of Escin is not dependent on the release of corticosterone.