The brain protection mechanism of autophagy on the rabbits by hypothemia treatment after cardiopulmonary cerebral resuscitation
Abstract：Objective To investigate the protective role of hypothermia treatment for cardiopulmonary cerebral resuscitation and whether autophagy is involved in the protective mechanism . Methods Ninety-six male New Zealand rabbits were randomly divided into 4 groups:a sham group, a normothermic treatment group ( NT group ) , a post -arrest therapeutic hypothermia treatment group (PATH group) and an autophagy-suppressive LY294002 group(LY294002 group).Aside from a sham group of 6 rabbits, each group was divided into 3 sub -groups of 10 rabbits: 4, 6 or 24 hours after return of spontaneous circulation ( ROSC) .The NT group had only a right ventricular fibrillation for 4 minutes and was allowed to recover to ROSC .In the PATH group , the hypothermia intervention occurred immediately after ROSC.The target temperature was 34 ℃ and was maintained for 4 hours.In LY294002 group, an injection of LY294002 (1.4 mg/kg), which dissolves in dimethyl sulfoxide , into the rabbit's cerebral ventricle was made 20 minutes before ROSC occurred .The correct insertion location was determined by using a rabbit stereotaxic apparatus .Hypothermia intervention was also applied , occurring immediately after ROSC .The Western -blotting method is applied to determine the brain tissue Bcl-2, Caspase-9, Caspase-3 and LC3-Ⅱand Beclin-1 expression.Results For the NT group both 9 and 24 hours after ROSC all results significantly increased over the sham group ( P <0.05 ) , and within the NT group the 24 -hour subgroup was obviously increased over the 9 -hour subgroup(P<0.05).For the PATH group both 9 and 24 hours after ROSC Bcl -2, Caspase -9, Caspase-3 results decreased compared to the corresponding time point in the NT group (P<0.05), whereas the LC3-Ⅱand Beclin-1 results increased (P<0.05).For the LY294002 group both 9 and 24 hours after ROSC Bcl-2, Caspase-9, Caspase-3 results increased compared to the corresponding time point in the PATH group (P<0.05), whereas the LC3-Ⅱand Beclin-1 results decreased (P<0.05 ) .Conclusion Hypothermia treatment reduces brain edema after cardiopulmonary resuscitation by inhibiting apoptosis , the mechanism may be related to increased autophagy adjustment .
Keywords：Cardiopulmonary cerebral resuscitationHypothermia treatmentApoptosisAutophagy
Publication Date：2014-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：6( 1114-1118,1119 )