Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium
Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmit...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhao, Yan [verfasserIn] |
|---|
| Format: |
Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2015 |
|---|
| Rechteinformationen: |
Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. |
|---|
| Übergeordnetes Werk: |
Enthalten in: Journal of ethnopharmacology - Shannon : Elsevier Science Ireland, 1979, 169(2015), Seite 210-218 |
|---|---|
| Übergeordnetes Werk: |
volume:169 ; year:2015 ; pages:210-218 |
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| DOI / URN: |
10.1016/j.jep.2015.04.030 |
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| 520 | |a Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. | ||
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10.1016/j.jep.2015.04.030 doi PQ20160617 (DE-627)OLC196801523X (DE-599)GBVOLC196801523X (PRQ)c1253-88382d71303efb93001e6c4741efe522db2f4e7de3e6704a0910f5d472aa797c0 (KEY)0090648420150000169000000210astragalosideivandcycloastragenolareequallyeffecti DE-627 ger DE-627 rakwb eng 610 390 DNB PHARM fid 44.40 bkl 73.61 bkl 73.00 bkl Zhao, Yan verfasserin aut Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. Li, Qiang oth Zhao, Wenjun oth Li, Jia oth Sun, Yan oth Liu, Kang oth Liu, Baolin oth Zhang, Ning oth Enthalten in Journal of ethnopharmacology Shannon : Elsevier Science Ireland, 1979 169(2015), Seite 210-218 (DE-627)129330159 (DE-600)134511-4 (DE-576)014584301 0378-8741 nnns volume:169 year:2015 pages:210-218 http://dx.doi.org/10.1016/j.jep.2015.04.030 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25922268 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-PHARM SSG-OLC-PHA SSG-OLC-ETH SSG-OPC-PHA GBV_ILN_20 GBV_ILN_4012 44.40 AVZ 73.61 AVZ 73.00 AVZ AR 169 2015 210-218 |
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10.1016/j.jep.2015.04.030 doi PQ20160617 (DE-627)OLC196801523X (DE-599)GBVOLC196801523X (PRQ)c1253-88382d71303efb93001e6c4741efe522db2f4e7de3e6704a0910f5d472aa797c0 (KEY)0090648420150000169000000210astragalosideivandcycloastragenolareequallyeffecti DE-627 ger DE-627 rakwb eng 610 390 DNB PHARM fid 44.40 bkl 73.61 bkl 73.00 bkl Zhao, Yan verfasserin aut Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. Li, Qiang oth Zhao, Wenjun oth Li, Jia oth Sun, Yan oth Liu, Kang oth Liu, Baolin oth Zhang, Ning oth Enthalten in Journal of ethnopharmacology Shannon : Elsevier Science Ireland, 1979 169(2015), Seite 210-218 (DE-627)129330159 (DE-600)134511-4 (DE-576)014584301 0378-8741 nnns volume:169 year:2015 pages:210-218 http://dx.doi.org/10.1016/j.jep.2015.04.030 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25922268 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-PHARM SSG-OLC-PHA SSG-OLC-ETH SSG-OPC-PHA GBV_ILN_20 GBV_ILN_4012 44.40 AVZ 73.61 AVZ 73.00 AVZ AR 169 2015 210-218 |
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10.1016/j.jep.2015.04.030 doi PQ20160617 (DE-627)OLC196801523X (DE-599)GBVOLC196801523X (PRQ)c1253-88382d71303efb93001e6c4741efe522db2f4e7de3e6704a0910f5d472aa797c0 (KEY)0090648420150000169000000210astragalosideivandcycloastragenolareequallyeffecti DE-627 ger DE-627 rakwb eng 610 390 DNB PHARM fid 44.40 bkl 73.61 bkl 73.00 bkl Zhao, Yan verfasserin aut Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. Li, Qiang oth Zhao, Wenjun oth Li, Jia oth Sun, Yan oth Liu, Kang oth Liu, Baolin oth Zhang, Ning oth Enthalten in Journal of ethnopharmacology Shannon : Elsevier Science Ireland, 1979 169(2015), Seite 210-218 (DE-627)129330159 (DE-600)134511-4 (DE-576)014584301 0378-8741 nnns volume:169 year:2015 pages:210-218 http://dx.doi.org/10.1016/j.jep.2015.04.030 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25922268 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-PHARM SSG-OLC-PHA SSG-OLC-ETH SSG-OPC-PHA GBV_ILN_20 GBV_ILN_4012 44.40 AVZ 73.61 AVZ 73.00 AVZ AR 169 2015 210-218 |
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10.1016/j.jep.2015.04.030 doi PQ20160617 (DE-627)OLC196801523X (DE-599)GBVOLC196801523X (PRQ)c1253-88382d71303efb93001e6c4741efe522db2f4e7de3e6704a0910f5d472aa797c0 (KEY)0090648420150000169000000210astragalosideivandcycloastragenolareequallyeffecti DE-627 ger DE-627 rakwb eng 610 390 DNB PHARM fid 44.40 bkl 73.61 bkl 73.00 bkl Zhao, Yan verfasserin aut Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. Li, Qiang oth Zhao, Wenjun oth Li, Jia oth Sun, Yan oth Liu, Kang oth Liu, Baolin oth Zhang, Ning oth Enthalten in Journal of ethnopharmacology Shannon : Elsevier Science Ireland, 1979 169(2015), Seite 210-218 (DE-627)129330159 (DE-600)134511-4 (DE-576)014584301 0378-8741 nnns volume:169 year:2015 pages:210-218 http://dx.doi.org/10.1016/j.jep.2015.04.030 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25922268 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-PHARM SSG-OLC-PHA SSG-OLC-ETH SSG-OPC-PHA GBV_ILN_20 GBV_ILN_4012 44.40 AVZ 73.61 AVZ 73.00 AVZ AR 169 2015 210-218 |
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10.1016/j.jep.2015.04.030 doi PQ20160617 (DE-627)OLC196801523X (DE-599)GBVOLC196801523X (PRQ)c1253-88382d71303efb93001e6c4741efe522db2f4e7de3e6704a0910f5d472aa797c0 (KEY)0090648420150000169000000210astragalosideivandcycloastragenolareequallyeffecti DE-627 ger DE-627 rakwb eng 610 390 DNB PHARM fid 44.40 bkl 73.61 bkl 73.00 bkl Zhao, Yan verfasserin aut Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. Li, Qiang oth Zhao, Wenjun oth Li, Jia oth Sun, Yan oth Liu, Kang oth Liu, Baolin oth Zhang, Ning oth Enthalten in Journal of ethnopharmacology Shannon : Elsevier Science Ireland, 1979 169(2015), Seite 210-218 (DE-627)129330159 (DE-600)134511-4 (DE-576)014584301 0378-8741 nnns volume:169 year:2015 pages:210-218 http://dx.doi.org/10.1016/j.jep.2015.04.030 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25922268 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-PHARM SSG-OLC-PHA SSG-OLC-ETH SSG-OPC-PHA GBV_ILN_20 GBV_ILN_4012 44.40 AVZ 73.61 AVZ 73.00 AVZ AR 169 2015 210-218 |
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astragaloside iv and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated txnip/nlrp3 inflammasome activation in the endothelium |
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Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium |
| abstract |
Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. |
| abstractGer |
Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. |
| abstract_unstemmed |
Astragaloside IV and cycloastragenol are present together in Astragalus membranaceus Moench (Fabaceae) and this study aims to simultaneously investigate their regulation of endothelial homeostasis in the setting of endoplasmic reticulum stress (ER stress). We stimulated endothelial cells with palmitate (PA 100μM) to evoked ROS-associated ER stress and observed the effects of astragaloside IV and cycloastragenol on thioredoxin-interacting protein (TXNIP) expression, NLRP3 inflammasome activation and mitochondrion-dependent apoptosis. Astragaloside IV and cycloastragenol inhibited ROS generation and attenuated ER stress inducer IRE1α phosphorylation, indicating the inhibition of ROS-associated ER stress. In response to ER stress, TXNIP expression increased, accompanied with NLRP3 induction and increased IL-1β and IL-6 production, but these alternations were reversed by treatment with astragaloside IV and cycloastragenol, demonstrating the inhibitory effects of astragaloside IV and cycloastragenol on TXNIP/NLRP3 inflammasome activation. Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis. |
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| title_short |
Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium |
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http://dx.doi.org/10.1016/j.jep.2015.04.030 http://www.ncbi.nlm.nih.gov/pubmed/25922268 |
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Inflammasome activation led to mitochondrial cell death in endothelial cells, whereas astragaloside IV and cycloastragenol restored the loss of the mitochondrial membrane potential with inhibition of caspase-3 activity, and thereby protected cells from ER stress-induced apoptosis. Astragaloside IV and cycloastragenol enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished their beneficial effects, indicative of the potential role of AMPK in their regulation. Astragaloside IV and cycloastragenol suppressed ROS-associated ER stress and then inhibited TXNIP/NLRP3 inflammasome activation with regulation of AMPK activity, and thereby ameliorated endothelial dysfunction by inhibiting inflammation and reducing cell apoptosis. Simultaneous investigations further showed that astragaloside IV and cycloastragenol were equally effective in regulation of endothelial homeostasis.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Qiang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhao, Wenjun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Jia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sun, Yan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Kang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Baolin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Ning</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of ethnopharmacology</subfield><subfield code="d">Shannon : Elsevier Science Ireland, 1979</subfield><subfield code="g">169(2015), Seite 210-218</subfield><subfield code="w">(DE-627)129330159</subfield><subfield code="w">(DE-600)134511-4</subfield><subfield code="w">(DE-576)014584301</subfield><subfield code="x">0378-8741</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:169</subfield><subfield code="g">year:2015</subfield><subfield code="g">pages:210-218</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1016/j.jep.2015.04.030</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/25922268</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-PHARM</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-ETH</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.40</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">73.61</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">73.00</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">169</subfield><subfield code="j">2015</subfield><subfield code="h">210-218</subfield></datafield></record></collection>
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