Ferulic acid prevents cerebral ischemic injury-induced reduction of hippocalcin expression.

Abstract

Intracellular calcium overload is a critical pathophysiological factor in ischemic injury. Hippocalcin is a neuronal calcium sensor protein that buffers intracellular calcium levels and protects cells from apoptotic stimuli. Ferulic acid exerts a neuroprotective effect in cerebral ischemia through its anti-oxidant and anti-inflammation activity. This study investigated whether ferulic acid contributes to hippocalcin expression during cerebral ischemia and glutamate exposure-induced neuronal cell death. Rats were immediately treated with vehicle or ferulic acid (100 mg/kg, i.v.) after middle cerebral artery occlusion (MCAO). Brain tissues were collected 24 h after MCAO and followed by assessment of cerebral infarct. Ferulic acid reduced MCAO-induced infarct regions. A proteomics approach elucidated a decrease in hippocalcin in MCAO-operated animals, ferulic acid attenuates the injury-induced decrease in hippocalcin expression. Reverse transcription-polymerase chain reaction and Western blot analyses confirmed that ferulic acid prevents the injury-induced decrease in hippocalcin. In cultured HT22 hippocampal cells, glutamate exposure increased the intracellular Ca(2+) levels, whereas ferulic acid attenuated this increase. Moreover, ferulic acid attenuated the glutamate toxicity-induced decrease in hippocalcin expression. These findings can suggest the possibility that ferulic acid exerts a neuroprotective effect through modulating hippocalcine expression and regulating intracellular calcium levels.

• Authors: Phil-Ok Koh
• Journal: Synapse (New York, N.Y.) (Synapse) Vol. 67 Issue 7 Pg. 390-8 (Jul 2013) ISSN: 1098-2396 [Electronic] United States
• PMID: 23401261 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Wiley Periodicals, Inc.

Chemical References

• Coumaric Acids
• Neuroprotective Agents
• Hippocalcin
• Glutamic Acid
• ferulic acid
• Calcium

Topics

• Animals
• Apoptosis (drug effects)
• Calcium (metabolism)
• Coumaric Acids (pharmacology, therapeutic use)
• Down-Regulation
• Glutamic Acid (toxicity)
• Hippocalcin (genetics, metabolism)
• Hippocampus (cytology, metabolism)
• Infarction, Middle Cerebral Artery (drug therapy, metabolism, prevention & control)
• Male
• Neurons (drug effects, metabolism)
• Neuroprotective Agents (pharmacology, therapeutic use)
• Proteomics
• Rats
• Rats, Sprague-Dawley
• Transcription, Genetic (drug effects)