Indomethacin treatment reduces microglia activation and increases numbers of neuroblasts in the subventricular zone and ischaemic striatum after focal ischaemia

Journal of biosciences

CELICE C SOUZA¹  MICHELLE C DA SILVA¹  ROSANA S LOPES¹  WALACE GOMES-LEAL1¹  ARTHUR O SAMPAIO¹  MARCELO M CARDOSO¹  MARCO AURELIOM FREIRE¹  RAFAEL RODRIGUES LIMA¹  ELANE MAGNO N FERREIRA¹  MARIO SANTOS BARBOSA Jr¹ 

[1] Laboratory of Experimental Neuroprotection and Neuroregeneration, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém, Brazil$$

关键词: Indomethacin;    inflammation;    microglia;    neuroblasts;    striatum;    stroke;   

DOI  :  

来源: Indian Academy of Sciences

【 摘 要 】

Neuroblasts from the subventricular zone (SVZ) migrate to striatum following stroke, but most of them die inthe ischaemic milieu and this can be related to exacerbated microglial activation. Here, we explored theeffects of the non-steroidal anti-inflammatory indomethacin on microglial activation, neuronal preservation andneuroblast migration following experimental striatal stroke in adult rats. Animals were submitted toendothelin-1 (ET-1)-induced focal striatal ischaemia and were treated with indomethacin or sterile saline(i.p.) for 7 days, being perfused after 8 or 14 days. Immunohistochemistry was performed to assess neuronalloss (anti-NeuN), microglial activation (anti-Iba1, ED1) and migrating neuroblasts (anti-DCX) by countingNeuN, ED1 and DCX-positive cells in the ischaemic striatum or SVZ. Indomethacin treatment reducedmicroglia activation and the number of ED1^{+} cells in both 8 and 14 days post injury as compared withcontrols. There was an increase in the number of DCX^{+} cells in both SVZ and striatum at the same survivaltimes. Moreover, there was a decrease in the number of NeuN^{+} cells in indomethacin-treated animals ascompared with the control group at 8 days but not after 14 days post injury. Our results suggest thatindomethacin treatment modulates microglia activation, contributing to increased neuroblast proliferation inthe SVZ and migration to the ischaemic striatum following stroke.

【 授权许可】

Unknown