Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Pharmaceutical Sciences |
Texto Completo: | https://www.revistas.usp.br/bjps/article/view/205310 |
Resumo: | Ligustrazine is widely used for the treatment of cardiovascular diseases in traditional Chinese medication. It has been reported that Ligustrazine decreases the concentration of intracellular calcium ions (Ca2+); however, the underlying mechanism remains unknown. In the present study, the effect of Ligustrazine on adenosine diphosphate (ADP)-induced platelet aggregation was evaluated using a turbidimetric approach. The changes in concentration of intracellular Ca2+ stimulated by ADP was measured using fluo-4, a fluorescent Ca2+ indicator dye. The mRNA expression of stromal interaction molecule l (STIM1) and Orai1, calcium sensor, was determined using real-time PCR. In addition, the protein expression of STIM1, Orai1, and serum/glucocorticoid-regulated protein kinase 1 (SGK1) was determined using Western blot analysis. The data demonstrated that Ligustrazine significantly suppressed platelet aggregation in a dose-dependent manner and reduced the concentration of intracellular Ca2+ triggered by ADP. Our data showed that Ligustrazine treatment inhibited the expression of STIM1 and Orai1 induced by ADP at both mRNA and protein levels, and suppressed the protein expression of SGK1. Taken together, our data indicated that Ligustrazine suppressed platelet aggregation by partly inhibiting the activities of calcium sensors, thereby suggesting that Ligustrazine may be a promising candidate for the treatment of platelet aggregation. |
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Brazilian Journal of Pharmaceutical Sciences |
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Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensorsCa2 release-activated Ca2 channel Intracellular calcium concentrationOrai1Platelet activationStromal interaction molecule l (STIM1)Serum/glucocorticoid-regulated protein kinase 1 (SGK1)Ligustrazine is widely used for the treatment of cardiovascular diseases in traditional Chinese medication. It has been reported that Ligustrazine decreases the concentration of intracellular calcium ions (Ca2+); however, the underlying mechanism remains unknown. In the present study, the effect of Ligustrazine on adenosine diphosphate (ADP)-induced platelet aggregation was evaluated using a turbidimetric approach. The changes in concentration of intracellular Ca2+ stimulated by ADP was measured using fluo-4, a fluorescent Ca2+ indicator dye. The mRNA expression of stromal interaction molecule l (STIM1) and Orai1, calcium sensor, was determined using real-time PCR. In addition, the protein expression of STIM1, Orai1, and serum/glucocorticoid-regulated protein kinase 1 (SGK1) was determined using Western blot analysis. The data demonstrated that Ligustrazine significantly suppressed platelet aggregation in a dose-dependent manner and reduced the concentration of intracellular Ca2+ triggered by ADP. Our data showed that Ligustrazine treatment inhibited the expression of STIM1 and Orai1 induced by ADP at both mRNA and protein levels, and suppressed the protein expression of SGK1. Taken together, our data indicated that Ligustrazine suppressed platelet aggregation by partly inhibiting the activities of calcium sensors, thereby suggesting that Ligustrazine may be a promising candidate for the treatment of platelet aggregation.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas2022-12-23info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/bjps/article/view/20531010.1590/s2175-97902022e20101 Brazilian Journal of Pharmaceutical Sciences; Vol. 58 (2022)Brazilian Journal of Pharmaceutical Sciences; v. 58 (2022)Brazilian Journal of Pharmaceutical Sciences; Vol. 58 (2022)2175-97901984-8250reponame:Brazilian Journal of Pharmaceutical Sciencesinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/bjps/article/view/205310/194917Copyright (c) 2022 Brazilian Journal of Pharmaceutical Scienceshttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccess Gao, ShuiboLei, ZhenWu, Hong2023-06-07T14:08:36Zoai:revistas.usp.br:article/205310Revistahttps://www.revistas.usp.br/bjps/indexPUBhttps://old.scielo.br/oai/scielo-oai.phpbjps@usp.br||elizabeth.igne@gmail.com2175-97901984-8250opendoar:2023-06-07T14:08:36Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
title |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
spellingShingle |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors Gao, Shuibo Ca2 release-activated Ca2 channel Intracellular calcium concentration Orai1 Platelet activation Stromal interaction molecule l (STIM1) Serum/glucocorticoid-regulated protein kinase 1 (SGK1) |
title_short |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
title_full |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
title_fullStr |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
title_full_unstemmed |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
title_sort |
Ligustrazine suppresses platelet aggregation through inhibiting the activities of calcium sensors |
author |
Gao, Shuibo |
author_facet |
Gao, Shuibo Lei, Zhen Wu, Hong |
author_role |
author |
author2 |
Lei, Zhen Wu, Hong |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Gao, Shuibo Lei, Zhen Wu, Hong |
dc.subject.por.fl_str_mv |
Ca2 release-activated Ca2 channel Intracellular calcium concentration Orai1 Platelet activation Stromal interaction molecule l (STIM1) Serum/glucocorticoid-regulated protein kinase 1 (SGK1) |
topic |
Ca2 release-activated Ca2 channel Intracellular calcium concentration Orai1 Platelet activation Stromal interaction molecule l (STIM1) Serum/glucocorticoid-regulated protein kinase 1 (SGK1) |
description |
Ligustrazine is widely used for the treatment of cardiovascular diseases in traditional Chinese medication. It has been reported that Ligustrazine decreases the concentration of intracellular calcium ions (Ca2+); however, the underlying mechanism remains unknown. In the present study, the effect of Ligustrazine on adenosine diphosphate (ADP)-induced platelet aggregation was evaluated using a turbidimetric approach. The changes in concentration of intracellular Ca2+ stimulated by ADP was measured using fluo-4, a fluorescent Ca2+ indicator dye. The mRNA expression of stromal interaction molecule l (STIM1) and Orai1, calcium sensor, was determined using real-time PCR. In addition, the protein expression of STIM1, Orai1, and serum/glucocorticoid-regulated protein kinase 1 (SGK1) was determined using Western blot analysis. The data demonstrated that Ligustrazine significantly suppressed platelet aggregation in a dose-dependent manner and reduced the concentration of intracellular Ca2+ triggered by ADP. Our data showed that Ligustrazine treatment inhibited the expression of STIM1 and Orai1 induced by ADP at both mRNA and protein levels, and suppressed the protein expression of SGK1. Taken together, our data indicated that Ligustrazine suppressed platelet aggregation by partly inhibiting the activities of calcium sensors, thereby suggesting that Ligustrazine may be a promising candidate for the treatment of platelet aggregation. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-12-23 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://www.revistas.usp.br/bjps/article/view/205310 10.1590/s2175-97902022e20101 |
url |
https://www.revistas.usp.br/bjps/article/view/205310 |
identifier_str_mv |
10.1590/s2175-97902022e20101 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/bjps/article/view/205310/194917 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2022 Brazilian Journal of Pharmaceutical Sciences https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Copyright (c) 2022 Brazilian Journal of Pharmaceutical Sciences https://creativecommons.org/licenses/by/4.0 |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
dc.source.none.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences; Vol. 58 (2022) Brazilian Journal of Pharmaceutical Sciences; v. 58 (2022) Brazilian Journal of Pharmaceutical Sciences; Vol. 58 (2022) 2175-9790 1984-8250 reponame:Brazilian Journal of Pharmaceutical Sciences instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Brazilian Journal of Pharmaceutical Sciences |
collection |
Brazilian Journal of Pharmaceutical Sciences |
repository.name.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
bjps@usp.br||elizabeth.igne@gmail.com |
_version_ |
1800222916594368512 |