Journal Article Research Support, Non-U.S. Gov't Ppublish 16 citations
PubMed: 37904689 DOI: 10.1002/iid3.1030
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.
Immun Inflamm Dis 11(10):e1030
Authors: Xiu-Fen Zheng, Xiang-Jian Zhang, Li-Peng Dong, Jing-Ru Zhao, Cong Zhang, Rong Chen
Affiliations
- Department of Neurology, the Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, PR China.
- Department of Pediatrics, Tangshan Central Hospital, Tangshan, Hebei, PR China.
- Department of Neurology, the Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, PR China. Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, Hebei, PR China. Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, Hebei, PR China.
- Department of Neurology, the Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, PR China. Department of Neurology, Hebei General Hospital, Shijiazhuang, Hebei, PR China.
- Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, Hebei, PR China.
- Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, Hebei, PR China.
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.
MeSH
P38 Mitogen-Activated Protein Kinases, Brain, Neuroprotection, Immunity, Cellular, Immune System Diseases, Reperfusion, Reperfusion Injury, Down-Regulation, Tissues, Ischemia, Edema
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