Inhibition of prostanoid synthesis protects against neuronal damage induced by focal ischemia in rat brain.
Changes in prostanoids concentration and effects of the non-specific COX inhibitor indomethacin on prostanoids levels and extension of tissue damage were studied following focal ischemia induction in the fronto-parietal region of rat brain. Ischemia was induced in animals bearing a transcerebral microdialysis probe by injection of Rose Bengal, a photosensitive dye, followed by light activation. Prostanoid levels were determined in the dialysate using immunoenzymatic techniques. PGD2 levels rose significantly up to 237+/-22 pg/ml compared to a basal level measured before ischemia induction which was below the detection limit. TXB2 changes were smaller and had a different time course. Treatment with indomethacin abolished the ischemia-induced PGD2 release and reduced the extent of injury to the area by 43+/-3.7%. These results suggest that prostanoid release may play an important role in neurodegenerative processes and that cyclooxygenase inhibitors may contribute to protect against cerebral tissue damage.
Buccellati
C
C
Institute of Pharmacological Sciences, University of Milan, Italy.
Folco
G C
GC
Sala
A
A
Scelsi
R
R
Masoero
E
E
Poggi
P
P
Govoni
S
S
Favalli
L
L
Rozza
A
A
D000818:Animals; D001930:Brain Injuries / Q000473:pathology / Q000517:prevention & control; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009474:Neurons / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D011448:Prostaglandin Antagonists / Q000627:therapeutic use; D011453:Prostaglandins / Q000096:biosynthesis* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D011448:Prostaglandin Antagonists; D011453:Prostaglandins