The Experts below are selected from a list of 1050 Experts worldwide ranked by ideXlab platform
Miriam T. Levy - One of the best experts on this subject based on the ideXlab platform.
-
the pro fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride induced Experimental Liver Injury
Immunology and Cell Biology, 2017Co-Authors: Xin M. Wang, Lauren E. Holz, Sumaiya Chowdhury, Shaun Cordoba, Kathryn A. Evans, Margaret G. Gall, Ana Julia Vieira De Ribeiro, Yuan Zhou Zheng, Miriam T. LevyAbstract:Liver fibrosis is a progressive pathological process involving inflammation and extracellular matrix deposition. Dipeptidyl peptidase 4 (DPP4), also known as CD26, is a cell surface glycoprotein and serine protease. DPP4 binds to fibronectin, can inactivate specific chemokines, incretin hormone and neuropeptides, and influences cell adhesion and migration. Such properties suggest a pro-fibrotic role for this peptidase but this hypothesis needs in vivo examination. Experimental Liver Injury was induced with carbon tetrachloride (CCl4) in DPP4 gene knockout (gko) mice. DPP4 gko had less Liver fibrosis and inflammation and fewer B cell clusters than wild type mice in the fibrosis model. DPP4 inhibitor-treated mice also developed less Liver fibrosis. DNA microarray and PCR showed that many immunoglobulin (Ig) genes and some metabolism-associated transcripts were differentially expressed in the gko strain compared with wild type. CCl4-treated DPP4 gko Livers had more IgM+ and IgG+ intrahepatic lymphocytes, and fewer CD4+, IgD+ and CD21+ intrahepatic lymphocytes. These data suggest that DPP4 is pro-fibrotic in CCl4-induced Liver fibrosis and that the mechanisms of DPP4 pro-fibrotic action include energy metabolism, B cells, NK cells and CD4+ cells.
-
The pro‐fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride‐induced Experimental Liver Injury
Immunology and cell biology, 2016Co-Authors: Xin M. Wang, Lauren E. Holz, Sumaiya Chowdhury, Shaun Cordoba, Kathryn A. Evans, Margaret G. Gall, Ana Julia Vieira De Ribeiro, Yuan Zhou Zheng, Miriam T. LevyAbstract:The pro-fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride-induced Experimental Liver Injury
Bu-gao Zhou - One of the best experts on this subject based on the ideXlab platform.
-
Erzhi Pill® Protected Experimental Liver Injury Against Apoptosis via the PI3K/Akt/Raptor/Rictor Pathway
Frontiers in pharmacology, 2018Co-Authors: Hai-mei Zhao, Duan-yong Liu, Xin Wang, Yong Zou, Zhengyun Zuo, Xiao-yun Zhang, Bu-gao ZhouAbstract:Erzhi Pill (EZP) is one of the basic prescriptions for treating Liver diseases in traditional Chinese medicine. However, its mechanism of action is still undefined. The PI3K/AKT/Raptor/Rictor signaling pathway is closely related to apoptosis and plays a significant role in the pathogenesis of Liver disease. To define the mechanism of the hepatoprotective effect of EZP in the treatment of Liver disease, hepatic Injury induced by 2-acetylaminofluorene/partial hepatectomy was treated by EZP for 14 days. The therapeutic effect of EZP was confirmed by the decreased production of aspartate aminotransferase and alanine aminotransferase, recovery of pathological Liver Injury, followed by inhibition of pro-inflammatory cytokines and transforming growth factor-β1. Bromodeoxyuridine assay and TUNEL staining indicated that apoptosis was suppressed and the numbers of cells in S phase and G0/G1phase were decreased. The crucial proteins in the PI3K/AKT/Raptor/Rictor signaling pathway were deactivated in rats with Experimental Liver Injury treated by EZP. These results indicated that the hepatoprotective effect of EZP via inhibition of hepatocyte apoptosis was closely related to repression of the PI3K/Akt/Raptor/Rictor signaling pathway.
-
Effect of Puerarin Regulated mTOR Signaling Pathway in Experimental Liver Injury
Frontiers Media S.A., 2018Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Wen Zhou, Fu-chun Liu, Xue-ke Liu, Duan-yong LiuAbstract:It is known that excessive hepatocellular apoptosis is a typical characteristic of hepatic disease, and is regulated by the mammalian target of rapamycin (mTOR) signaling pathway. As the main active component of Kudzu (Pueraria lobata) roots, which is frequently used to treat hepatic diseases, Puerarin (Pue) has been reported to alleviate and protect against hepatic Injury. However, it is unclear whether Pue can inhibit mTOR signaling to prevent excessive apoptosis in the treatment of hepatic diseases. In the present study, Pue effectively ameliorated pathological Injury of the Liver, decreased serum enzyme (ALT, AST, γ-GT, AKP, DBIL, and TBIL) levels, regulated the balance between pro-inflammatory (TNF-α, IL-1β, IL-4, IL-6, and TGF-β1) and anti-inflammatory cytokines (IL-10), restored the cell cycle and inhibited hepatocellular apoptosis and caspase-3 expression in rats with Liver Injury induced by 2-AAF/PH. Pue inhibited p-mTOR, p-AKT and Raptor activity, and increased Rictor expression in the Liver tissues of rats with Experimental Liver Injury. These results indicated that Pue effectively regulated the activation of mTOR signaling pathway in the therapeutic and prophylactic process of Pue on Experimental Liver Injury
-
erzhi pill repairs Experimental Liver Injury via tsc mtor signaling pathway inhibiting excessive apoptosis
Evidence-based Complementary and Alternative Medicine, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
-
Erzhi Pill® Repairs Experimental Liver Injury via TSC/mTOR Signaling Pathway Inhibiting Excessive Apoptosis.
Evidence-based complementary and alternative medicine : eCAM, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
Xin M. Wang - One of the best experts on this subject based on the ideXlab platform.
-
the pro fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride induced Experimental Liver Injury
Immunology and Cell Biology, 2017Co-Authors: Xin M. Wang, Lauren E. Holz, Sumaiya Chowdhury, Shaun Cordoba, Kathryn A. Evans, Margaret G. Gall, Ana Julia Vieira De Ribeiro, Yuan Zhou Zheng, Miriam T. LevyAbstract:Liver fibrosis is a progressive pathological process involving inflammation and extracellular matrix deposition. Dipeptidyl peptidase 4 (DPP4), also known as CD26, is a cell surface glycoprotein and serine protease. DPP4 binds to fibronectin, can inactivate specific chemokines, incretin hormone and neuropeptides, and influences cell adhesion and migration. Such properties suggest a pro-fibrotic role for this peptidase but this hypothesis needs in vivo examination. Experimental Liver Injury was induced with carbon tetrachloride (CCl4) in DPP4 gene knockout (gko) mice. DPP4 gko had less Liver fibrosis and inflammation and fewer B cell clusters than wild type mice in the fibrosis model. DPP4 inhibitor-treated mice also developed less Liver fibrosis. DNA microarray and PCR showed that many immunoglobulin (Ig) genes and some metabolism-associated transcripts were differentially expressed in the gko strain compared with wild type. CCl4-treated DPP4 gko Livers had more IgM+ and IgG+ intrahepatic lymphocytes, and fewer CD4+, IgD+ and CD21+ intrahepatic lymphocytes. These data suggest that DPP4 is pro-fibrotic in CCl4-induced Liver fibrosis and that the mechanisms of DPP4 pro-fibrotic action include energy metabolism, B cells, NK cells and CD4+ cells.
-
The pro‐fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride‐induced Experimental Liver Injury
Immunology and cell biology, 2016Co-Authors: Xin M. Wang, Lauren E. Holz, Sumaiya Chowdhury, Shaun Cordoba, Kathryn A. Evans, Margaret G. Gall, Ana Julia Vieira De Ribeiro, Yuan Zhou Zheng, Miriam T. LevyAbstract:The pro-fibrotic role of dipeptidyl peptidase 4 in carbon tetrachloride-induced Experimental Liver Injury
Duan-yong Liu - One of the best experts on this subject based on the ideXlab platform.
-
Erzhi Pill® Protected Experimental Liver Injury Against Apoptosis via the PI3K/Akt/Raptor/Rictor Pathway
Frontiers in pharmacology, 2018Co-Authors: Hai-mei Zhao, Duan-yong Liu, Xin Wang, Yong Zou, Zhengyun Zuo, Xiao-yun Zhang, Bu-gao ZhouAbstract:Erzhi Pill (EZP) is one of the basic prescriptions for treating Liver diseases in traditional Chinese medicine. However, its mechanism of action is still undefined. The PI3K/AKT/Raptor/Rictor signaling pathway is closely related to apoptosis and plays a significant role in the pathogenesis of Liver disease. To define the mechanism of the hepatoprotective effect of EZP in the treatment of Liver disease, hepatic Injury induced by 2-acetylaminofluorene/partial hepatectomy was treated by EZP for 14 days. The therapeutic effect of EZP was confirmed by the decreased production of aspartate aminotransferase and alanine aminotransferase, recovery of pathological Liver Injury, followed by inhibition of pro-inflammatory cytokines and transforming growth factor-β1. Bromodeoxyuridine assay and TUNEL staining indicated that apoptosis was suppressed and the numbers of cells in S phase and G0/G1phase were decreased. The crucial proteins in the PI3K/AKT/Raptor/Rictor signaling pathway were deactivated in rats with Experimental Liver Injury treated by EZP. These results indicated that the hepatoprotective effect of EZP via inhibition of hepatocyte apoptosis was closely related to repression of the PI3K/Akt/Raptor/Rictor signaling pathway.
-
Effect of Puerarin Regulated mTOR Signaling Pathway in Experimental Liver Injury
Frontiers Media S.A., 2018Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Wen Zhou, Fu-chun Liu, Xue-ke Liu, Duan-yong LiuAbstract:It is known that excessive hepatocellular apoptosis is a typical characteristic of hepatic disease, and is regulated by the mammalian target of rapamycin (mTOR) signaling pathway. As the main active component of Kudzu (Pueraria lobata) roots, which is frequently used to treat hepatic diseases, Puerarin (Pue) has been reported to alleviate and protect against hepatic Injury. However, it is unclear whether Pue can inhibit mTOR signaling to prevent excessive apoptosis in the treatment of hepatic diseases. In the present study, Pue effectively ameliorated pathological Injury of the Liver, decreased serum enzyme (ALT, AST, γ-GT, AKP, DBIL, and TBIL) levels, regulated the balance between pro-inflammatory (TNF-α, IL-1β, IL-4, IL-6, and TGF-β1) and anti-inflammatory cytokines (IL-10), restored the cell cycle and inhibited hepatocellular apoptosis and caspase-3 expression in rats with Liver Injury induced by 2-AAF/PH. Pue inhibited p-mTOR, p-AKT and Raptor activity, and increased Rictor expression in the Liver tissues of rats with Experimental Liver Injury. These results indicated that Pue effectively regulated the activation of mTOR signaling pathway in the therapeutic and prophylactic process of Pue on Experimental Liver Injury
-
erzhi pill repairs Experimental Liver Injury via tsc mtor signaling pathway inhibiting excessive apoptosis
Evidence-based Complementary and Alternative Medicine, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
-
Erzhi Pill® Repairs Experimental Liver Injury via TSC/mTOR Signaling Pathway Inhibiting Excessive Apoptosis.
Evidence-based complementary and alternative medicine : eCAM, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
Hai-mei Zhao - One of the best experts on this subject based on the ideXlab platform.
-
Erzhi Pill® Protected Experimental Liver Injury Against Apoptosis via the PI3K/Akt/Raptor/Rictor Pathway
Frontiers in pharmacology, 2018Co-Authors: Hai-mei Zhao, Duan-yong Liu, Xin Wang, Yong Zou, Zhengyun Zuo, Xiao-yun Zhang, Bu-gao ZhouAbstract:Erzhi Pill (EZP) is one of the basic prescriptions for treating Liver diseases in traditional Chinese medicine. However, its mechanism of action is still undefined. The PI3K/AKT/Raptor/Rictor signaling pathway is closely related to apoptosis and plays a significant role in the pathogenesis of Liver disease. To define the mechanism of the hepatoprotective effect of EZP in the treatment of Liver disease, hepatic Injury induced by 2-acetylaminofluorene/partial hepatectomy was treated by EZP for 14 days. The therapeutic effect of EZP was confirmed by the decreased production of aspartate aminotransferase and alanine aminotransferase, recovery of pathological Liver Injury, followed by inhibition of pro-inflammatory cytokines and transforming growth factor-β1. Bromodeoxyuridine assay and TUNEL staining indicated that apoptosis was suppressed and the numbers of cells in S phase and G0/G1phase were decreased. The crucial proteins in the PI3K/AKT/Raptor/Rictor signaling pathway were deactivated in rats with Experimental Liver Injury treated by EZP. These results indicated that the hepatoprotective effect of EZP via inhibition of hepatocyte apoptosis was closely related to repression of the PI3K/Akt/Raptor/Rictor signaling pathway.
-
Effect of Puerarin Regulated mTOR Signaling Pathway in Experimental Liver Injury
Frontiers Media S.A., 2018Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Wen Zhou, Fu-chun Liu, Xue-ke Liu, Duan-yong LiuAbstract:It is known that excessive hepatocellular apoptosis is a typical characteristic of hepatic disease, and is regulated by the mammalian target of rapamycin (mTOR) signaling pathway. As the main active component of Kudzu (Pueraria lobata) roots, which is frequently used to treat hepatic diseases, Puerarin (Pue) has been reported to alleviate and protect against hepatic Injury. However, it is unclear whether Pue can inhibit mTOR signaling to prevent excessive apoptosis in the treatment of hepatic diseases. In the present study, Pue effectively ameliorated pathological Injury of the Liver, decreased serum enzyme (ALT, AST, γ-GT, AKP, DBIL, and TBIL) levels, regulated the balance between pro-inflammatory (TNF-α, IL-1β, IL-4, IL-6, and TGF-β1) and anti-inflammatory cytokines (IL-10), restored the cell cycle and inhibited hepatocellular apoptosis and caspase-3 expression in rats with Liver Injury induced by 2-AAF/PH. Pue inhibited p-mTOR, p-AKT and Raptor activity, and increased Rictor expression in the Liver tissues of rats with Experimental Liver Injury. These results indicated that Pue effectively regulated the activation of mTOR signaling pathway in the therapeutic and prophylactic process of Pue on Experimental Liver Injury
-
erzhi pill repairs Experimental Liver Injury via tsc mtor signaling pathway inhibiting excessive apoptosis
Evidence-based Complementary and Alternative Medicine, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
-
Erzhi Pill® Repairs Experimental Liver Injury via TSC/mTOR Signaling Pathway Inhibiting Excessive Apoptosis.
Evidence-based complementary and alternative medicine : eCAM, 2017Co-Authors: Bu-gao Zhou, Hai-mei Zhao, Xin Wang, Yong Zou, Haiyang Yue, Yi Liu, Zhengyun Zuo, Duan-yong LiuAbstract:The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the Liver Injury via observing TSC/mTOR signaling pathway activation. The Experimental Liver Injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced Liver Injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, Liver weight, and index of Liver weight were elevated. Microscopic examination showed that EZP restored pathological Liver Injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in Liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.
