ArticlePloS one2023
Notoginsenoside R1 attenuates brain injury in rats with traumatic brain injury: Possible mediation of apoptosis via ERK1/2 signaling pathway.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 10 citations in OpenAlex.
- The therapeutic role of ginseng in promoting hippocampal neurogenesis and ameliorating cognitive function following whole brain radiotherapy in rats.Metabolic brain disease · 2025Article
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- NGR1 reduces neuronal apoptosis through regulation of ITGA11 following subarachnoid hemorrhage.Molecular medicine reports · 2025Article
- Enhancing glymphatic transport through angiotensin II type 2 receptor activation promotes neurological recovery after traumatic brain injury.Theranostics · 2025Article
- The role of Panax notoginseng saponins in cerebrovascular neurological disorders: an overview of mechanisms and functions.Frontiers in pharmacology · 2025Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Traumatic brain injury (TBI) occurs worldwide and is associated with high mortality and disability rate. Apoptosis induced by TBI is one of the important causes of secondary injury after TBI. Notoginsenoside R1 (NGR1) is the main phytoestrogen extracted from Panax notoginseng. Many studies have shown that NGR1 has potent neuroprotective, anti-inflammatory, and anti-apoptotic properties and is effective in ischemia-reperfusion injury. Therefore, we investigated the potential neuroprotective effects of NGR1 after TBI and explored its molecular mechanism of action. A rat model of TBI was established using the controlled cortical impact (CCI) method. The expression levels of Bcl-2, Bax, caspase 3, and ERK1/2-related molecules in the downstream pathway were also detected by western blotting. The expression levels of pro-inflammatory cytokines were detected by real-time quantitative PCR. Nissl staining was used to clarify the morphological changes around the injury foci in rats after TBI. Fluoro-Jade B (FJB) and terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) fluorescence staining were used to detect the apoptosis of neural cells in each group of rats. The results showed that NGR1 administration reduced neurological deficits after TBI, as well as brain edema and brain tissue apoptosis. It also significantly inhibited the expression of pro-inflammatory cytokines. Furthermore, NGR1 decreased the expression levels of extracellular signal-regulated kinase (ERK) and p-RSK1, which are phosphorylated after trauma. This study suggests that NGR1 can improve neuronal apoptosis in brain injury by inhibiting the ERK signaling pathway. NGR1 is a potential novel neuroprotective agent for the treatment of secondary brain injury after TBI.
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