Cargando…
Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation
Sepsis-induced cardiomyopathy (SIC) is an important manifestation of sepsis, and abnormal cardiac function affects the development of sepsis. Notoginsenoside R1 (NG-R1) is a unique bioactive component of Panax notoginseng with anti-inflammatory and antioxidant effects. However, the effects and possi...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9880176/ https://www.ncbi.nlm.nih.gov/pubmed/36713827 http://dx.doi.org/10.3389/fphar.2023.1101240 |
_version_ | 1784878849053425664 |
---|---|
author | Shao, Ruifei Li, Wei Chen, Rui Li, Kunlin Cao, Yu Chen, Guobing Jiang, Lihong |
author_facet | Shao, Ruifei Li, Wei Chen, Rui Li, Kunlin Cao, Yu Chen, Guobing Jiang, Lihong |
author_sort | Shao, Ruifei |
collection | PubMed |
description | Sepsis-induced cardiomyopathy (SIC) is an important manifestation of sepsis, and abnormal cardiac function affects the development of sepsis. Notoginsenoside R1 (NG-R1) is a unique bioactive component of Panax notoginseng with anti-inflammatory and antioxidant effects. However, the effects and possible mechanisms of NG-R1 on SIC are not clear. The purpose of this study was to identify the potential targets and regulatory mechanisms of the action of NG-R1 on SIC. To investigate the potential mechanism, we used network pharmacology, molecular docking, qRT-PCR, and immunofluorescence. The results showed that NG-R1 ameliorated myocardial fibrosis in septic mice. Validation of network pharmacology and molecular docking results revealed that NG-R1 reduced tumor necrosis factor-Alpha (TNF-α) expression in myocardial tissues and AC16 cardiomyocytes in mice, as well as inflammatory factor release in AC16 cells, so TNF-α may be a potential target of NG-R1 against SIC. The present study demonstrated that NG-R1 could protect against SIC and by regulating the expression of TNF-α inflammatory factors, providing a new idea for sepsis drug development. |
format | Online Article Text |
id | pubmed-9880176 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-98801762023-01-28 Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation Shao, Ruifei Li, Wei Chen, Rui Li, Kunlin Cao, Yu Chen, Guobing Jiang, Lihong Front Pharmacol Pharmacology Sepsis-induced cardiomyopathy (SIC) is an important manifestation of sepsis, and abnormal cardiac function affects the development of sepsis. Notoginsenoside R1 (NG-R1) is a unique bioactive component of Panax notoginseng with anti-inflammatory and antioxidant effects. However, the effects and possible mechanisms of NG-R1 on SIC are not clear. The purpose of this study was to identify the potential targets and regulatory mechanisms of the action of NG-R1 on SIC. To investigate the potential mechanism, we used network pharmacology, molecular docking, qRT-PCR, and immunofluorescence. The results showed that NG-R1 ameliorated myocardial fibrosis in septic mice. Validation of network pharmacology and molecular docking results revealed that NG-R1 reduced tumor necrosis factor-Alpha (TNF-α) expression in myocardial tissues and AC16 cardiomyocytes in mice, as well as inflammatory factor release in AC16 cells, so TNF-α may be a potential target of NG-R1 against SIC. The present study demonstrated that NG-R1 could protect against SIC and by regulating the expression of TNF-α inflammatory factors, providing a new idea for sepsis drug development. Frontiers Media S.A. 2023-01-13 /pmc/articles/PMC9880176/ /pubmed/36713827 http://dx.doi.org/10.3389/fphar.2023.1101240 Text en Copyright © 2023 Shao, Li, Chen, Li, Cao, Chen and Jiang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Pharmacology Shao, Ruifei Li, Wei Chen, Rui Li, Kunlin Cao, Yu Chen, Guobing Jiang, Lihong Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title | Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title_full | Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title_fullStr | Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title_full_unstemmed | Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title_short | Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
title_sort | exploring the molecular mechanism of notoginsenoside r1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9880176/ https://www.ncbi.nlm.nih.gov/pubmed/36713827 http://dx.doi.org/10.3389/fphar.2023.1101240 |
work_keys_str_mv | AT shaoruifei exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT liwei exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT chenrui exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT likunlin exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT caoyu exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT chenguobing exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation AT jianglihong exploringthemolecularmechanismofnotoginsenosider1insepsisinducedcardiomyopathybasedonnetworkpharmacologyandexperimentsvalidation |