ArticleInternational journal of molecular sciences2014
Ginsenoside Rd attenuates mitochondrial permeability transition and cytochrome C release in isolated spinal cord mitochondria: involvement of kinase-mediated pathways.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Research progress on the role of ginsenoside Rd in central nervous system diseases.African health sciences · 2024Review
- Rapidly Inhibiting the Inflammatory Cytokine Storms and Restoring Cellular Homeostasis to Alleviate Sepsis by Blocking Pyroptosis and Mitochondrial Apoptosis Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Target engagement of ginsenosides in mild cognitive impairment using mass spectrometry-based drug affinity responsive target stability.Journal of ginseng research · 2022Article
- Insights into Recent Studies on Biotransformation and Pharmacological Activities of Ginsenoside Rd.Biomolecules · 2022Review
- Pharmacological effects of natural medicine ginsenosides against Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Mechanisms of ginsenosides exert neuroprotective effects on spinal cord injury: A promising traditional Chinese medicine.Frontiers in neuroscience · 2022Review
- Biotransformation, Pharmacokinetics, and Pharmacological Activities of Ginsenoside Rd Against Multiple Diseases.Frontiers in pharmacology · 2022Review
- Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives.Journal of ginseng research · 2021Review
- CGA ameliorates cognitive decline by regulating the PI3K/AKT signaling pathway and neurotransmitter systems in rats with multi-infarct dementia.Experimental and therapeutic medicine · 2020Article
- Red Ginseng Inhibits Tau Aggregation and Promotes Tau DissociationOxidative medicine and cellular longevity · 2020Article
- Red Ginseng Attenuates Aβ-Induced Mitochondrial Dysfunction and Aβ-mediated Pathology in an Animal Model of Alzheimer's Disease.International journal of molecular sciences · 2019Article
- COX6B1 relieves hypoxia/reoxygenation injury of neonatal rat cardiomyocytes by regulating mitochondrial function.Biotechnology letters · 2019Article
- Mitochondrial permeability transition pore: a potential drug target for neurodegeneration.Drug discovery today · 2018Review
- Ethnopharmacological Approaches for Dementia Therapy and Significance of Natural Products and Herbal Drugs.Frontiers in aging neuroscience · 2018Review
- Ginsenoside-Rd Promotes Neurite Outgrowth of PC12 Cells through MAPK/ERK- and PI3K/AKT-Dependent Pathways.International journal of molecular sciences · 2016Article
- Effects of ascorbic acid on α-l-arabinofuranosidase and α-l-arabinopyranosidase activities fromJournal of the Korean Society for Applied Biological ChemistryArticle
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, has multifunctional activity via different mechanisms and neuroprotective effects that are exerted probably via its antioxidant or free radical scavenger action. However, the effects of Rd on spinal cord mitochondrial dysfunction and underlying mechanisms are still obscure. In this study, we sought to investigate the in vitro effects of Rd on mitochondrial integrity and redox balance in isolated spinal cord mitochondria. We verified that Ca2+ dissipated the membrane potential, provoked mitochondrial swelling and decreased NAD(P)H matrix content, which were all attenuated by Rd pretreatment in a dose-dependent manner. In contrast, Rd was not able to inhibit Ca2+ induced mitochondrial hydrogen peroxide generation. The results of Western blot showed that Rd significantly increased the expression of p-Akt and p-ERK, but had no effects on phosphorylation of PKC and p38. In addition, Rd treatment significantly attenuated Ca2+ induced cytochrome c release, which was partly reversed by antagonists of Akt and ERK, but not p-38 inhibitor. The effects of bisindolylmaleimide, a PKC inhibitor, on Rd-induced inhibition of cytochrome c release seem to be at the level of its own detrimental activity on mitochondrial function. Furthermore, we also found that pretreatment with Rd in vivo (10 and 50 mg/kg) protected spinal cord mitochondria against Ca2+ induced mitochondrial membrane potential dissipation and cytochrome c release. It is concluded that Rd regulate mitochondrial permeability transition pore formation and cytochrome c release through protein kinases dependent mechanism involving activation of intramitochondrial Akt and ERK pathways.
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