ArticleInternational journal of molecular sciences2022
Leonurine Reduces Oxidative Stress and Provides Neuroprotection against Ischemic Injury via Modulating Oxidative and NO/NOS Pathway.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Effect of acupuncture on cognitive impairment induced by sleep deprivation in animal models: a preclinical systematic review and meta-analysis.Frontiers in aging neuroscience · 2025Pooled it
- The protective effects of ligustrazine on ischemic stroke: a systematic review and meta-analysis of preclinical evidence and possible mechanisms.Frontiers in pharmacology · 2024Pooled it
- Leonurine: A Multifaceted Bioactive Alkaloid-From Pharmacological Mechanisms to Clinical Translation: A Narrative Review.Health science reports · 2026Article
- Epigenetic regulation of post-stroke cognitive impairment by gut microbiota and their metabolites.Frontiers in cellular and infection microbiology · 2026Review
- Comprehensive review of leonurine: harnessing its therapeutic potential for chronic diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Research progress on molecular mechanism and future perspectives of leonurine.Frontiers of medicine · 2025Review
- Article
- Phytochemicals against Osteoarthritis by Inhibiting Apoptosis.Molecules (Basel, Switzerland) · 2024Review
- Article
- The Activation of GABAAntioxidants (Basel, Switzerland) · 2024Article
- Leonurine: a comprehensive review of pharmacokinetics, pharmacodynamics, and toxicology.Frontiers in pharmacology · 2024Review
- Article
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023Article
- A literature review: mechanisms of antitumor pharmacological action of leonurine alkaloid.Frontiers in pharmacology · 2023Review
- Oxidative stress in cerebrovascular disease and associated diseases.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Leonurine (Leo) has been found to have neuroprotective effects against cerebral ischemic injury. However, the exact molecular mechanism underlying its neuroprotective ability remains unclear. The aim of the present study was to investigate whether Leo could provide protection through the nitric oxide (NO)/nitric oxide synthase (NOS) pathway. We firstly explored the effects of NO/NOS signaling on oxidative stress and apoptosis in in vivo and in vitro models of cerebral ischemia. Further, we evaluated the protective effects of Leo against oxygen and glucose deprivation (OGD)-induced oxidative stress and apoptosis in PC12 cells. We found that the rats showed anxiety-like behavior, and the morphology and number of neurons were changed in a model of photochemically induced cerebral ischemia. Both in vivo and in vitro results show that the activity of superoxide dismutase (SOD) and glutathione (GSH) contents were decreased after ischemia, and reactive oxygen species (ROS) and malondialdehyde (MDA) levels were increased, indicating that cerebral ischemia induced oxidative stress and neuronal damage. Moreover, the contents of NO, total NOS, constitutive NOS (cNOS) and inducible NOS (iNOS) were increased after ischemia in rat and PC12 cells. Treatment with L-nitroarginine methyl ester (L-NAME), a nonselective NOS inhibitor, could reverse the change in NO/NOS expression and abolish these detrimental effects of ischemia. Leo treatment decreased ROS and MDA levels and increased the activity of SOD and GSH contents in PC12 cells exposed to OGD. Furthermore, Leo reduced NO/NOS production and cell apoptosis, decreased Bax expression and increased Bcl-2 levels in OGD-treated PC12 cells. All the data suggest that Leo protected against oxidative stress and neuronal apoptosis in cerebral ischemia by inhibiting the NO/NOS system. Our findings indicate that Leo could be a potential agent for the intervention of ischemic stroke and highlighted the NO/NOS-mediated oxidative stress signaling.
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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.