Cargando…
Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β
OBJECTIVE: Tissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxida...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10549825/ https://www.ncbi.nlm.nih.gov/pubmed/37904689 http://dx.doi.org/10.1002/iid3.1030 |
_version_ | 1785115404557877248 |
---|---|
author | Zheng, Xiu‐fen Zhang, Xiang‐jian Dong, Li‐peng Zhao, Jing‐ru Zhang, Cong Chen, Rong |
author_facet | Zheng, Xiu‐fen Zhang, Xiang‐jian Dong, Li‐peng Zhao, Jing‐ru Zhang, Cong Chen, Rong |
author_sort | Zheng, Xiu‐fen |
collection | PubMed |
description | OBJECTIVE: Tissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxidant, anti‐inflammatory, antiproliferative, and neuroprotective effects. In the present study, we explored the neuroprotective effects and potential mechanisms of Sal B after I/R injury. METHODS: We induced cerebral ischemia in male CD‐1 mice through transient (60 min) middle cerebral artery occlusion (tMCAO), and then injected Sal B (30 mg/kg) intraperitoneally. Neurological deficits, infarct volumes, and brain edema were assessed at 24 and 72 h after tMCAO. We detected the expression of Toll‐like receptor 4 (TLR4), phosphorylated‐p38 mitogen‐activated protein kinase (P‐p38 MAPK), phosphorylated c‐Jun amino (N)‐terminal kinases (p‐JNK), nuclear factor‐κB (NF‐κB), and interleukin‐1β (IL‐1β) in the brain tissue. RESULTS: Compared with the tMCAO group, Sal B significantly improved neurological deficits, reduced infarct size, attenuated cerebral edema, and downregulated the expression of pro‐inflammatory mediators TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β in brain tissue after I/R injury. CONCLUSION: We found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties. |
format | Online Article Text |
id | pubmed-10549825 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-105498252023-10-05 Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β Zheng, Xiu‐fen Zhang, Xiang‐jian Dong, Li‐peng Zhao, Jing‐ru Zhang, Cong Chen, Rong Immun Inflamm Dis Original Articles OBJECTIVE: Tissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxidant, anti‐inflammatory, antiproliferative, and neuroprotective effects. In the present study, we explored the neuroprotective effects and potential mechanisms of Sal B after I/R injury. METHODS: We induced cerebral ischemia in male CD‐1 mice through transient (60 min) middle cerebral artery occlusion (tMCAO), and then injected Sal B (30 mg/kg) intraperitoneally. Neurological deficits, infarct volumes, and brain edema were assessed at 24 and 72 h after tMCAO. We detected the expression of Toll‐like receptor 4 (TLR4), phosphorylated‐p38 mitogen‐activated protein kinase (P‐p38 MAPK), phosphorylated c‐Jun amino (N)‐terminal kinases (p‐JNK), nuclear factor‐κB (NF‐κB), and interleukin‐1β (IL‐1β) in the brain tissue. RESULTS: Compared with the tMCAO group, Sal B significantly improved neurological deficits, reduced infarct size, attenuated cerebral edema, and downregulated the expression of pro‐inflammatory mediators TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β in brain tissue after I/R injury. CONCLUSION: We found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties. John Wiley and Sons Inc. 2023-10-04 /pmc/articles/PMC10549825/ /pubmed/37904689 http://dx.doi.org/10.1002/iid3.1030 Text en © 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Zheng, Xiu‐fen Zhang, Xiang‐jian Dong, Li‐peng Zhao, Jing‐ru Zhang, Cong Chen, Rong Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title | Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title_full | Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title_fullStr | Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title_full_unstemmed | Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title_short | Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β |
title_sort | neuroprotective mechanism of salvianolic acid b against cerebral ischemia–reperfusion injury in mice through downregulation of tlr4, p‐p38mapk, p‐jnk, nf‐κb, and il‐1β |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10549825/ https://www.ncbi.nlm.nih.gov/pubmed/37904689 http://dx.doi.org/10.1002/iid3.1030 |
work_keys_str_mv | AT zhengxiufen neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b AT zhangxiangjian neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b AT donglipeng neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b AT zhaojingru neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b AT zhangcong neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b AT chenrong neuroprotectivemechanismofsalvianolicacidbagainstcerebralischemiareperfusioninjuryinmicethroughdownregulationoftlr4pp38mapkpjnknfkbandil1b |