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Cinnamtannin B-1 regulates cell proliferation of spinal cord astrocytes and protects the cell from oxygen-glucose-serum deprivation/reoxygenation-induced apoptosis.

Abstract
Astrocytes are important for protecting neurons in the central nervous system. It has been reported that some antioxidants could protect astrocytes from ischemia/reperfusion-induced dysfunction. Cinnamtannin B-1 is a naturally occurring A-type proanthocyanidin that exhibits anti-oxidant properties. In this study, we investigated the effects of cinnamtannin B-1 on spinal cord astrocytes. Astrocytes were subjected to oxygen-glucose-serum deprivation for eight hours followed by reoxygenation with or without cinnamtannin B-1. We found that cinnamtannin B-1 protected astrocytes from oxygen-glucose-serum deprivation and reoxygenation-induced apoptosis. Concurrently, cinnamtannin B-1 promoted the proliferation of astrocytes whereas the extracellular regulated protein kinase (ERK) inhibitor reversed this effect. The results indicated that cinnamtannin B-1 protects astrocytes from oxygen-glucose-serum deprivation/reoxygenation-induced apoptosis by promoting astrocyte proliferation via an ERK pathway. Therefore, as an anti-oxidant, cinnamtannin B-1 might provide extra benefit for astrocyte protection during ischemia/reperfusion in the central nervous system.
AuthorsZhiyong Chi, Xueling Ma, Guofeng Cui, Mingchao Li, Fuchun Li
JournalInternational journal of molecular sciences (Int J Mol Sci) Vol. 14 Issue 8 Pg. 15827-37 (Jul 30 2013) ISSN: 1422-0067 [Electronic] Switzerland
PMID23903044 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antioxidants
  • Proanthocyanidins
  • Protein Kinase Inhibitors
  • cinnamtannin B-1
  • Extracellular Signal-Regulated MAP Kinases
Topics
  • Animals
  • Antioxidants (pharmacology)
  • Apoptosis (drug effects)
  • Astrocytes (cytology, drug effects)
  • Cell Proliferation (drug effects)
  • Cells, Cultured
  • Extracellular Signal-Regulated MAP Kinases (antagonists & inhibitors, metabolism)
  • Proanthocyanidins (pharmacology)
  • Protein Kinase Inhibitors (pharmacology)
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction (drug effects)
  • Spinal Cord (cytology)

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