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
Abstract 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 a...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2023-10-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.1030 |
| _version_ | 1797641988616486912 |
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| author | Xiu‐fen Zheng Xiang‐jian Zhang Li‐peng Dong Jing‐ru Zhao Cong Zhang Rong Chen |
| author_facet | Xiu‐fen Zheng Xiang‐jian Zhang Li‐peng Dong Jing‐ru Zhao Cong Zhang Rong Chen |
| author_sort | Xiu‐fen Zheng |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-03-11T13:53:40Z |
| format | Article |
| id | doaj.art-dacf395ecadf4500a04b3aac1695a06f |
| institution | Directory Open Access Journal |
| issn | 2050-4527 |
| language | English |
| last_indexed | 2024-03-11T13:53:40Z |
| publishDate | 2023-10-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj.art-dacf395ecadf4500a04b3aac1695a06f2023-11-02T07:56:18ZengWileyImmunity, Inflammation and Disease2050-45272023-10-011110n/an/a10.1002/iid3.1030Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1βXiu‐fen Zheng0Xiang‐jian Zhang1Li‐peng Dong2Jing‐ru Zhao3Cong Zhang4Rong Chen5Department of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaDepartment of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaDepartment of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaDepartment of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaDepartment of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaDepartment of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR ChinaAbstract 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.https://doi.org/10.1002/iid3.1030cerebral ischemia–reperfusioninflammationneuroprotectionsalvianolic acid B |
| spellingShingle | Xiu‐fen Zheng Xiang‐jian Zhang Li‐peng Dong Jing‐ru Zhao Cong Zhang Rong Chen 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 Immunity, Inflammation and Disease cerebral ischemia–reperfusion inflammation neuroprotection salvianolic acid B |
| 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 | cerebral ischemia–reperfusion inflammation neuroprotection salvianolic acid B |
| url | https://doi.org/10.1002/iid3.1030 |
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