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Apigenin inhibits the production of NO and PGE2 in microglia and inhibits neuronal cell death in a middle cerebral artery occlusion-induced focal ischemia mice model.

Abstract
Flavonoids have been intensively studied on their pharmacological activities such as anti-cancer, anti-oxidant and anti-inflammation. However, little is known about their neuroprotective effects. Recent studies suggest that inflammation mediated by microglia may play a role in neurodegenerative diseases. In this study, we evaluated the anti-inflammatory effect of various flavonoid compounds by using BV-2, a murine microglia cell line. Of the compounds that were evaluated, apigenin inhibited the production of nitric oxide and prostaglandin E(2) by suppressing the expression of inducible nitric oxide synthase and cyclooxygenase-2 protein, respectively. Moreover, apigenin suppressed p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) phosphorylation without affecting the activity of extracellular signal-regulated kinase (ERK). Apigenin was also found to protect neuronal cells from injury in middle cerebral artery occlusion.
AuthorsSang Keun Ha, Pyeongjae Lee, Jeong A Park, Hye Rim Oh, Sang Yeon Lee, Ji-Ho Park, Eunjoo H Lee, Jong Hoon Ryu, Kang Ro Lee, Sun Yeou Kim
JournalNeurochemistry international (Neurochem Int) 2008 Mar-Apr Vol. 52 Issue 4-5 Pg. 878-86 ISSN: 0197-0186 [Print] England
PMID18037535 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Flavonoids
  • Lipopolysaccharides
  • Neuroprotective Agents
  • Nitric Oxide
  • Apigenin
  • Nitric Oxide Synthase Type II
  • Mitogen-Activated Protein Kinases
  • Dinoprostone
Topics
  • Animals
  • Apigenin (pharmacology)
  • Blotting, Western
  • Brain Ischemia (pathology)
  • Cell Death (drug effects)
  • Cell Line
  • Dinoprostone (biosynthesis)
  • Flavonoids (pharmacology)
  • Immunohistochemistry
  • Infarction, Middle Cerebral Artery (pathology, prevention & control)
  • Lipopolysaccharides (antagonists & inhibitors, toxicity)
  • Male
  • Mice
  • Mice, Inbred ICR
  • Microglia (drug effects, metabolism)
  • Mitogen-Activated Protein Kinases (biosynthesis)
  • Neurons (drug effects, pathology)
  • Neuroprotective Agents (pharmacology)
  • Nitric Oxide (biosynthesis)
  • Nitric Oxide Synthase Type II (metabolism)

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