ArticleAmerican journal of translational research2017
Salvianolic acid A attenuates early brain injury after subarachnoid hemorrhage in rats by regulating ERK/P38/Nrf2 signaling.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- A Systematic Review of Inflammatory Cytokine Changes Following Aneurysmal Subarachnoid Hemorrhage in Animal Models and Humans.Translational stroke research · 2022Pooled it
- Efficacy of Melatonin in Animal Models of Subarachnoid Hemorrhage: A Systematic Review and Stratified Meta-Analysis.Frontiers in neurology · 2021Pooled it
- Salvianolic acid A inhibits ferroptosis and protects against intracerebral hemorrhage.Scientific reports · 2024Article
- Targeting post-stroke neuroinflammation with Salvianolic acid A: molecular mechanisms and preclinical evidence.Frontiers in immunology · 2024Review
- Pharmacological Modulations of Nrf2 and Therapeutic Implications in Aneurysmal Subarachnoid Hemorrhage.Molecules (Basel, Switzerland) · 2023Review
- Association between HO‑1 gene promoter polymorphisms and diseases (Review).Molecular medicine reports · 2022Review
- Inflammation and immune cell abnormalities in intracranial aneurysm subarachnoid hemorrhage (SAH): Relevant signaling pathways and therapeutic strategies.Frontiers in immunology · 2022Review
- Activation of AMP-Activated Protein Kinase-Sirtuin 1 Pathway Contributes to Salvianolic Acid A-Induced Browning of White Adipose Tissue in High-Fat Diet Fed Male Mice.Frontiers in pharmacology · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Oxidative Stress at the Crossroads of Aging, Stroke and Depression.Aging and disease · 2020Review
- Inflammatory Pathways Following Subarachnoid Hemorrhage.Cellular and molecular neurobiology · 2020Review
- Activation of the AMPK-SIRT1 pathway contributes to protective effects of Salvianolic acid A against lipotoxicity in hepatocytes and NAFLD in mice.Frontiers in pharmacology · 2020Article
- Simultaneous Quantification and Pharmacokinetic Study of Nine Bioactive Components ofMolecules (Basel, Switzerland) · 2019Article
- Some pharmacokinetic parameters of salvianolic acid A following single-dose oral administration to rats.Pharmaceutical biology · 2018Article
- Molecular Pharmacology of Rosmarinic and Salvianolic Acids: Potential Seeds for Alzheimer's and Vascular Dementia Drugs.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and inflammation play an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The present study aimed to evaluate the effect of salvianolic acid A (SalA) on EBI after SAH via its antioxidative, anti-inflammatory, and anti-apoptotic effects. The intraperitoneal administration of SalA (10 and 50 mg/kg/day) significantly alleviated EBI (including neurobehavioral deficits, brain edema, blood-brain barrier permeability, and cortical neuron apoptosis) after SAH in rats. SalA treatment also reduced the post-SAH elevated levels of reactive oxygen species level and malondialdehyde. Further, SalA increased glutathione peroxidase enzymatic activity and the concentrations of glutathione and brain-derived neurotrophic factor in brain cortex, at 24 h after SAH. In addition, SalA also decreased the release of inflammation cytokines (i.e., TNF-α, IL-1β, IL-6, and IL-8) in SAH rats. Expressions of cell apoptosis-related proteins were also regulated by SalA treatment in SAH rats. Meanwhile, SalA also modulated Nrf2 signaling, and the phosphorylation of ERK and P38 MAPK signaling in SAH rats. These results indicated that the administration of SalA may ameliorate EBI and provide neuroprotection after SAH in rat models.
Indexed as
Identifiers
29312516PMC5752914W2997910214What OpenQuestion holds
Registered trials
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.