Although
dexamethasone is very effective for controlling peritumoral
cerebral edema, it is associated with distressing side effects that decrease the quality of life for many patients. One potential mechanism to explain the ability of
dexamethasone to repair blood-brain barrier dysfunction is through the inhibition of
cyclooxygenase-2 (COX-2). The purpose of this study was to determine in a rat
brain tumor model whether
SC-236, a selective
COX-2 inhibitor, is as effective as
dexamethasone. Twenty-nine adult male Fischer 344 rats were implanted with intracerebral 9L
gliosarcomas and divided into 3 treatment groups. One group (n = 9) served as controls, another (n = 9) was treated with
dexamethasone (3 mg/kg p.o. daily), and a third group (n = 11) received
SC-236 (3 mg/kg p.o. daily). A survival study was performed. The median survival in the control group was 16 days, compared with 23 days for the
dexamethasone group and 23 days for the
COX-2 inhibitor group. Kaplan-Meier analysis on pairwise group comparisons showed improved survival that was statistically significant for each treatment group compared with the control group (log-rank test P = 0.009 for
dexamethasone to control and P = 0.005 for COX-2 to control), and no significant difference in survival for the COX-2 compared with
dexamethasone (log-rank test P = 0.2). These results suggest that a selective
COX-2 inhibitor appears to be as effective as
dexamethasone in prolonging survival in a rat
brain tumor model.