ArticleImmunity, inflammation and disease2023
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.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The potential value of traditional Chinese medicine monomers in cerebral ischemia-reperfusion injury: a network meta-analysis based on animal model.BMC complementary medicine and therapies · 2025Pooled it
- A Study on the Effects of Intranasally Administered Liquid Crystalline Nanoparticles Loaded with Salvianolic Acid B in Vascular Dementia.Molecular neurobiology · 2026Article
- Electroacupuncture ameliorates learning and memory impairment by inhibiting inflammation and promoting synaptic plasticity via inhibition of the NF-KB/NLRP3 signaling pathway in cerebral ischemic rats.Histology and histopathology · 2026Article
- Application of hyperbaric oxygen therapy in the treatment of spinal cord injury: insights from preclinical to clinical evidence.Medical gas research · 2026Review
- PCSK9-Mediated Inflammation in Foam Cell Formation and Exploring the Biologically Active Compounds Derived From Natural Resources.Advances in pharmacological and pharmaceutical sciences · 2026Review
- The "habitat-phytochemistry-pharmacological effect" nexus: a multidimensional review of ethnomedicinalFrontiers in pharmacology · 2026Review
- Exploring neuroprotective effects of Chuanzhitongluo capsule on an alzheimer's disease rat model.Metabolic brain disease · 2025Article
- Neuroprotective Effect of Rosuvastatin Calcium Combined with Hyperbaric Oxygen Mediated p38MAPK Pathway in Rats with Leukoaraiosis.Cell biochemistry and biophysics · 2025Article
- Influence and molecular mechanism of cinnamaldehyde against ventricular arrhythmia via the TAK1-p38MAPK-NLRP3 pathway.Heart and vessels · 2025Article
- Salvianolic Acid B Attenuates Ferroptosis in Acute Kidney Injury by Targeting PRDX5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Preclinical and experimental evidence of salvianolic acid B in the treatment of neurological diseases.Frontiers in pharmacology · 2025Review
- Novel Multi-Antioxidant Approach for Ischemic Stroke Therapy Targeting the Role of Oxidative Stress.Biomedicines · 2024Review
- Exosomes-Mediated Signaling Pathway: A New Direction for Treatment of Organ Ischemia-Reperfusion Injury.Biomedicines · 2024Review
- Role of salvianolic acid B in the treatment of acute ischemic stroke: a systematic review and meta-analysis of animal models.Frontiers in pharmacology · 2024Review
- 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 · 2023Article
- Bupropion Showed Neuroprotective Impacts Against Cerebral Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Inflammation.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTissue 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.