ArticleMolecular and cellular biochemistry2011
Schisandrin B elicits a glutathione antioxidant response and protects against apoptosis via the redox-sensitive ERK/Nrf2 pathway in H9c2 cells.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Effects of schisandra extract on muscle atrophy: a systematic review and meta-analysis of preclinical studies.Frontiers in pharmacology · 2026Pooled it
- Schisandrin B confers multi-organ protection via regulation of mitochondrial homeostasis: mechanistic integration, organ-specific differences, and translational challenges-a review.Frontiers in pharmacology · 2026Review
- Wuweizisu B for cancer treatment from multitarget mechanisms to precision delivery strategies (Review).International journal of molecular medicine · 2025Review
- The promising antioxidant effects of lignans: Nrf2 activation comes into view.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Cyclosporine-induced kidney damage was halted by sitagliptin and hesperidin via increasing Nrf2 and suppressing TNF-α, NF-κB, and Bax.Scientific reports · 2024Article
- Lignans as Pharmacological Agents in Disorders Related to Oxidative Stress and Inflammation: Chemical Synthesis Approaches and Biological Activities.International journal of molecular sciences · 2022Review
- Schizandrin B attenuates hypoxia/reoxygenation injury in H9c2 cells by activating the AMPK/Nrf2 signaling pathway.Experimental and therapeutic medicine · 2021Article
- Schisandrin B protects against angiotensin II-induced endotheliocyte deficits by targeting Keap1 and activating Nrf2 pathway.Drug design, development and therapy · 2018Article
- Schisandrin B elicits the Keap1-Nrf2 defense system via carbene reactive metabolite which is less harmful to mice liver.Drug design, development and therapy · 2018Article
- Schizandrin B protects LPS-induced sepsis via TLR4/NF-κB/MyD88 signaling pathway.American journal of translational research · 2018Article
- Neuroprotection of a sesamin derivative, 1, 2-bis [(3-methoxyphenyl) methyl] ethane-1, 2-dicaroxylic acid (MMEDA) against ischemic and hypoxic neuronal injury.Iranian journal of basic medical sciences · 2017Article
- Review
- Article
- A Naturally-Derived Compound Schisandrin B Enhanced Light Sensation in the pde6c Zebrafish Model of Retinal Degeneration.PloS one · 2016Article
- Dibenzocyclooctadiene lignans from Schisandra spp. selectively inhibit the growth of the intracellular bacteria Chlamydia pneumoniae and Chlamydia trachomatis.The Journal of antibiotics · 2015Article
- Comparisons of ethanol extracts of chinese propolis (poplar type) and poplar gums based on the antioxidant activities and molecular mechanism.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Protective effect of a sesamin derivative, 3-bis (3-methoxybenzyl) butane-1, 4-diol on ischemic and hypoxic neuronal injury.Journal of biomedical science · 2014Article
- Cytochrome P-450-catalyzed reactive oxygen species production mediates the (-)schisandrin B-induced glutathione and heat shock responses in H9c2 cardiomyocytes.Indian journal of pharmacology · 2012Article
- Schisandrin B as a hormetic agent for preventing age-related neurodegenerative diseases.Oxidative medicine and cellular longevity · 2012Review
- Increased glutathione synthesis following Nrf2 activation by vanadyl sulfate in human chang liver cells.International journal of molecular sciences · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study investigated the signal transduction pathway involved in the cytoprotective action of (-)schisandrin B [(-)Sch B, a stereoisomer of Sch B]. Using H9c2 cells, the authors examined the effects of (-)Sch B on MAPK and Nrf2 activation, as well as the subsequent eliciting of glutathione response and protection against apoptosis. Pharmacological tools, such as cytochrome P-450 (CYP) inhibitor, antioxidant, MAPK inhibitor, and Nrf2 RNAi, were used to delineate the signaling pathway. (-)Sch B caused a time-dependent activation of MAPK in H9c2 cells, with the degree of ERK activation being much larger than that of p38 or JNK. The MAPK activation was followed by an increase in the level of nuclear Nrf2, an indirect measure of Nrf2 activation, and the eliciting of a glutathione antioxidant response. The activation of MAPK and Nrf2 seemed to involve oxidants generated from a CYP-catalyzed reaction with (-)Sch B. Both ERK inhibition by U0126 and Nrf2 suppression by Nrf2 RNAi transfection largely abolished the cytoprotection against hypoxia/reoxygenation-induced apoptosis in (-)Sch B-pretreated cells. (-)Sch B pretreatment potentiated the reoxygenation-induced ERK activation, whereas both p38 and JNK activations were suppressed. Under the condition of ERK inhibition, Sch B treatment did not protect against ischemia/reperfusion injury in an ex vivo rat heart model. The results indicate that (-)Sch B triggers a redox-sensitive ERK/Nrf2 signaling, which then elicits a cellular glutathione antioxidant response and protects against hypoxia/reoxygenation-induced apoptosis in H9c2 cells. The ERK-mediated signaling is also likely involved in the cardioprotection afforded by Sch B in vivo.
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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.