Protective Effects Of GM₁on Cerebral Injury Induced By Cardiopulmonary Bypass Of Rats

Objective: To investigate the Protective effects of GM1on cerebral injury inducedby Cardiopulmonary Bypass of RatsMethods: Twenty-four adult male SD rats weighing350-450g were randomlydivided into3groups (n=8each). CPB model was not made in groupⅠ sham operationgroup(Sham group); group Ⅱ (CPBgroup) in which saline(1ml/kg) was administratedfor priming fliud; group Ⅲ(GMlgroup) in which GMl(20mg/kg) was administrated forpriming fliud. CPB was maintained for60min in CPB group and GMlgroup. Venousblood was collected at the end of CPB(T2)and3hours after the end of CPB(T4). Plasmalevels of tumor necrosis factor-α(TNF-α) was detected by enzyme-linkedimmunosorbent assay. Brain sample were collected at3h after CPB. Electronmicroscopy technique to observe ultrastructure of the cortex, neuron apoptosis werequantitatively examined with TUNEL method and NF-κB protein were detected byimmunohistochemistry, cortical NF-κB protein activity was detected by Western-blot.Results: There were no statistically difference between group CPB and groupGMlin mean arterial pressure, heart rate, PaO2, PaCO2or hematocrit during CPB.Compared with sham group, under the transmission electron microscope, thenuclear membrane of cerebral cortex neurons of group CPB is vague, within differentnuclear chromatin condensation or margination, and organelles have reduced orvacuolization; Local membrane of vascular endothelial cells is fuzzy and tight junctionsbetween cells is relatively loose. By contrast, ultrastructural changes in group GMlissignificantly reduced.Under the immunohistochemistry, which shows that the apoptosis of nerve cells inthe cerebral cortex were increased during CPB. Compared with group Sham, the nerveapoptotic cells were statistically increased (P<0.05) in group CPB and group GMl; compared with Group CPB, the apoptosis of nerve cells were statistically reduced inGroup GMl(P<0.05) cerebral cortex neurons.Compared with sham group, the level of plasma inflammatory mediator TNF-α ofgroup CPB and GMlincreased (P<0.05) at both time of T2and T4. Compared withgroup CPB, the level of plasma TNF-α of group GMldecreased at both time of T2andT4, and the difference at T2and T4had statistics significance (P<0.05).Under the immunohistochemistry and Western-blot, which shows that theexpression of NF-κB activity in the cerebral cortex were increased during CPB.Compared with group Sham, the expression of NF-κB protein was increased in groupCPB and group GMl; compared with Group CPB, the expression of NF-κB activity andthe ratio of NF-κB were statistically reduced in Group GMl(P<0.05) cerebral cortexneurons.Conclusion:1.There is a closely correlation between cerebral injury associated-CPB andneuronal apoptosis.2.Systemic inflammatory reaction factor activation may be one of the reasons thathave caused brain cortex nerve cell apoptosis.3.GM1could reduce inflammatory reaction factor expression by CardiopulmonaryBypass and slow neuronal with the role of apoptosis, also the function of cerebralprotection.