Resumen de 2-arakidonoilglizerolaren efektua nitxo neurogenikoetan jaiotza inguruko asfixiaren ostean

Gorane Beldarrain Gonzalez, Malein Pacho, Antonia de los Angeles Alvarez Diaz, Marc Chillida, Jon Ander Alart Lorenzo, María Moro, Miren Josune Canduela Perez, Enrique Hilario Rodríguez, Daniel Alonso Alconada

• euskara

  Entzefalopatia hipoxiko-iskemikoak (EHI), sarritan hipoxia-iskemiak (HI) eraginda, jaioberriengan kalte neurologikoa eragin dezake, bai eta heriotza ere. HIak energia-gutxiegitasuna, erreakzio kaltegarrien ur-jauzi metaboliko bat eta zelulen heriotza masiboa eragiten ditu, besteak beste. Hortaz, azken urteetan, zelulen galera hori konpentsatzeko mekanismoak bai eta zelulen heriotza murriztu dezaketen mekanismoak ere asko ikertu dira, hala nola lan honetan aztertutako 2-arakidonoilglizerola (2-AG). Ikerketen arabera, endokannabinoideek hantura, estres oxidatiboak eragindako kaltea eta glutamatoak eragindako eszitotoxikotasuna murriztu dezakete. Hori dela eta, gure lanean efektu horiek ikertu ziren egun ezagutzen diren bi nitxo neurogenikoetan: albo-bentrikuluetako bentrikulu azpiko gunean (Subventricular zone edo SVZ) eta hipokanpoko bihurgune horzduneko pikordun geruza azpiko gunean (Subgranular zone edo SGZ). Dirudienez, zelulen proliferazioa bultzatuz, HIak eragindako kaltea konpentsa liteke. Horretarako, nitxoen zelularitatea eta azalera neurtu genituen HIa pairatu eta gero eta 2-AGaren tratamendua jaso eta gero. Emaitzek erakutsi zuten kaltetutako animalietan hemisferio ipsilateraletako azalera aldatzen zela, SGZan murriztuz eta SVZan emendatuz. Gainera, HIak zelularitatea murriztu zuen SGZan, baina ez SVZan. 2-AGak, hala ere, morfologia eta zelularitatearen berrestea lortu zuen SGZan.

• English

  Hypoxic-ischemic encephalopathy (HIE), often caused by hypoxia-ischemia (HI), can lead to neurological damage in newborns, and often even to death. HI causes energy shortage, a waterfall of biochemical reactions and massive cell death, among others. Therefore, in recent years, the aim has been to develop mechanisms that compensate for that loss of cells, as well as mechanisms that promote lower cell death, such as 2-arachidonoylglycerol (2-AG). Several research has shown that endocannabinoids can reduce neuro-inflammation, minimize damage from oxidative stress and reduce glutamate-related excitotoxicity. Hence, we examined those effects on the two neurogenic niches known so far: the subventricular zone (SVZ) of the lateral brain ventricles and the subgranular zone of the dentate gyrus (SGZ). It is believed that by promoting cell proliferation, the damage caused by hypoxia-ischemia could be compensated, so the cellularity and area of these niches were measured after hypoxia-ischemia and after the application of 2-AG. The results showed that the area of the ipsilateral hemispheres changed in the affected animals, decreasing in SGZ and increasing in SVZ. In addition, HI reduced cellularity in SGZ, but not in SVZ. However, 2-AG helped to restore morphology and cellularity in SGZ.