ArticleDrug design, development and therapy2018
Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial pathway.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Sinomenine Hydrochloride Impedes Memory Impairments via Nrf2/HO-1-Mediated Inhibition of Oxidative Stress, Neuroinflammation and Apoptosis in Mice Brain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Protective effect of sinomenine against CCl4-induced acute liver injury through regulation of mitochondrial biogenesis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- COIMMR: a computational framework to reveal the contribution of herbal ingredients against human cancer via immune microenvironment and metabolic reprogramming.Briefings in bioinformatics · 2023Article
- Saffron extract and crocin exert anti-inflammatory and anti-oxidative effects in a repetitive mild traumatic brain injury mouse model.Scientific reports · 2022Article
- Potential therapeutic effects and pharmacological evidence of sinomenine in central nervous system disorders.Frontiers in pharmacology · 2022Review
- Sinomenine ameliorates cardiac hypertrophy by activating Nrf2/ARE signaling pathway.Bioengineered · 2021Article
- Novel Synthetic and Natural Therapies for Traumatic Brain Injury.Current neuropharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSinomenine (SIN) has been shown to have protective effects against brain damage following traumatic brain injury (TBI). However, the mechanisms and its role in these effects remain unclear. This study was conducted to investigate the potential mechanisms of the protective effects of SIN.
methodsThe weight-drop model of TBI in Institute of Cancer Research (ICR) mice were treated with SIN or a vehicle via intraperitoneal administration 30 min after TBI. All mice were euthanized 24 h after TBI and after neurological scoring, a series of tests were performed, including brain water content and neuronal cell death in the cerebral cortex.
resultsThe level of cytochrome
conclusionSIN protected neuronal cells by protecting them against apoptosis via mechanisms that involve the mitochondria following TBI.
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Registered trials
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