Affiliation:
1. Department of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Hebei PR China
2. Department of Pediatrics Tangshan Central Hospital Tangshan Hebei PR China
3. Hebei Collaborative Innovation Center for Cardio‐cerebrovascular Disease Shijiazhuang Hebei PR China
4. Hebei Key Laboratory of Vascular Homeostasis Shijiazhuang Hebei PR China
5. Department of Neurology Hebei General Hospital Shijiazhuang Hebei PR China
Abstract
AbstractObjectiveTissue 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.MethodsWe 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.ResultsCompared 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.ConclusionWe found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties.
Subject
Immunology,Immunology and Allergy
Cited by
1 articles.
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