The inflammatory response plays an important role in neuroprotection and regeneration after ischemic insult. The use of non-steroidal anti-inflammatory drugs has been a matter of debate as to whether they have beneficial or detrimental effects. In this context, the effects of the
anti-inflammatory agent meloxicam have been scarcely documented after
stroke, but its ability to inhibit both
cyclooxygenase isoforms (1 and 2) could be a promising strategy to modulate post-ischemic
inflammation. This study analyzed the effect of
meloxicam in a transient focal
cerebral ischemia model in rats, measuring its
neuroprotective effect after 48 hours and 7 days of reperfusion and the effects of the treatment on the
glial scar and regenerative events such as the generation of new progenitors in the subventricular zone and axonal sprouting at the edge of the damaged area. We show that
meloxicam's
neuroprotective effects remained after 7 days of reperfusion even if its administration was restricted to the two first days after
ischemia. Moreover,
meloxicam treatment modulated
glial scar reactivity, which matched with an increase in axonal sprouting. However, this treatment decreased the formation of neuronal progenitor cells. This study discusses the dual role of anti-inflammatory treatments after
stroke and encourages the careful analysis of both the neuroprotective and the regenerative effects in preclinical studies.