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Altered brain lipid composition in cyclooxygenase-2 knockout mouse.

Kaizong Ma¹, Robert Langenbach, Stanley I Rapoport

¹Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.

Journal of Lipid Research

|January 5, 2007

Summary

Absence of cyclooxygenase-2 (COX-2) significantly alters brain lipid composition, increasing phosphatidylserine while decreasing triacylglycerol and cholesterol. These lipid changes in COX-2 knockout mice may explain altered fatty acid metabolism and neuroprotection.

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Area of Science:

Neuroscience
Biochemistry
Lipidomics

Background:

Cyclooxygenase-2 (COX-2) is implicated in brain arachidonic acid metabolism.
COX-2 expression elevates in neuroinflammation and excitotoxicity models.
COX-2's role in brain lipid metabolism warrants investigation.

Purpose of the Study:

To investigate the impact of COX-2 absence on brain lipid composition.
To compare lipid profiles in COX-2 knockout (COX-2(-/-)) versus wild-type (COX-2(+/+)) mice.

Main Methods:

Lipid concentrations were quantified in high-energy microwaved brain tissue.
Gas chromatography-mass spectrometry (GC-MS) was utilized for lipid analysis.

Main Results:

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COX-2(-/-) mouse brains showed a 15% increase in phosphatidylserine (PtdSer).

Significant reductions were observed in triacylglycerol (37%), cholesterol (27%), and the cholesterol-to-phospholipid ratio (32%) in COX-2(-/-) mice.

Increased palmitic acid (16:0) in PtdSer and elevated unesterified arachidic acid (20:0) were noted.

Conclusions:

Lifetime absence of COX-2 profoundly alters brain lipid composition.
Observed lipid alterations may correlate with modified fatty acid kinetics and enhanced resistance to neuroinflammation and excitotoxicity in COX-2(-/-) mice.