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Brain Phospholipase A 2 Is Activated After Experimental Closed Head Injury in the Rat
Author(s) -
Shohami E.,
Shapira Y.,
Yadid G.,
Reisfeld N.,
Yedgar S.
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb08550.x
Subject(s) - chemistry , phospholipase a2 , endocrinology , medicine , anatomy , biochemistry , enzyme
Head injury was induced in rats by a weight drop device, falling over the left hemisphere. The rats were killed at 15 min, 4 h, and 24 h after injury. Cortical slices were taken from the injured zone, from the corresponding region of the contralateral hemisphere, and from the frontal lobe of both hemispheres. These cortical slices were incubated in the presence of a fluorescent phospholipid analogue, l‐acyl‐2‐( N ‐4‐nitrobenzo‐2‐oxa‐I,3‐diazole)aminocaproylphos‐phatidylcholine (C 6 ‐NBD‐PC) which is a substrate for phospholipase A 2 (PLA 2 ) in intact cells. The interaction of this substrate with cells produces only one fluorescent product, the fatty acid C 6 ‐NBD‐FA, released from the 2‐position of C 6 ‐NBD‐PC. Thus, the level of C 6 ‐NBD‐FA produced is a direct measure of PLA 2 activity. Fifteen minutes after trauma, a 75% increase of PLA 2 activity was found in the injured zone. At 4 h, the frontal lobe of the contused, left hemisphere had elevated PLA 2 activity, as well as the injured zone (92 and 81%, respectively). At 24 h, PLA 2 activity at the site of injury was 245% of sham. In the right, noninjured zone, no significant changes in PLA 2 activity were noticed during the entire time course of the experiment. Prostaglandin E 2 (PGE 2 ) was extracted from the same cortical slices as those used for PLA 2 activity measurement. A significant correlation (Pearson coefficient test, correlation coefficient = 0.469, p < 0.05, n = 21) was found between the elevation of PLA 2 activity and PGE 2 levels measured in the injured hemisphere, at 4 and 24 h. The elevation of PGE 2 production induced by the trauma was abolished when the rats were pretreated with dextran 70,000, which has been previously shown to inhibit PLA 2 activity. The results of this study support the hypothesis that activation of brain PLA 2 is involved in the increased cerebral production of eicosanoids induced by trauma.