@entity1286 Reduces XXXX via Heat Shock Protein 90 in Rodents.

@entity1 @entity49801 @entity9096 @entity19515 @entity63 @entity25650 @entity5101 @entity5252 @entity1188 @entity1286 @entity741 @entity35 @entity583
UNASSIGNED: Opioids reduce injury from @entity741 -reperfusion in @entity1 . In experimental models, this mechanism involves @entity9096 inhibition. @entity19515 regulates mitochondrial protein import, with @entity9096 inhibition increasing @entity19515 mitochondrial content. Therefore, we determined whether @entity1286 -induced cardioprotection is mediated by @entity19515 and if the protective effect is downstream of @entity9096 inhibition. Male @entity35 , aged 8-10 weeks, were subjected to an in vivo @entity741 -reperfusion injury protocol involving 30 minutes of @entity63 followed by 2 hours of reperfusion. Hemodynamics were continually monitored and @entity583 size determined. @entity35 received @entity1286 (0.3   mg/kg), the @entity9096 inhibitor, @entity25650 (0.6   mg/kg), or saline, 10 minutes prior to @entity63 . Some @entity35 received selective @entity19515 inhibitors, @entity49801 (0.3   mg/kg), or @entity5101 ( @entity5252 , 0.6   mg/kg) alone or 5 minutes prior to @entity1286 or @entity25650 . @entity1286 reduced @entity583 size when compared to control (42    2% versus 60    1%). This protection was abolished by prior treatment of @entity49801 or @entity5252 (59    1%, 56    2%). @entity9096 inhibition also reduced @entity583 size (41    2%) with @entity19515 inhibition by @entity49801 or @entity5252 partially inhibiting @entity25650 -induced @entity1188 size reduction (54    3%, 47    1%, resp.). These data suggest that opioid-induced cardioprotection is mediated by @entity19515 . Part of this protection afforded by @entity19515 is downstream of @entity9096 , potentially via the HSP-TOM mitochondrial import pathway.
