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AIM: To determine direct protective effect of monosialoganglioside (GM1) on hippocampal slices after oxygen- glucose deprivation and reperfusion (OGD/RP), and investigate the influence on the expression of N-methyl-D- aspartate receptor subunit 1 (NMDAR1) in those hippocampal slices. METHODS: Injury of hippocampal slices and protective effects of GM1 were detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining, toluidine blue staining, and transmission electron microscopy of rat hippocampal slices. Expression of NMDAR1 was detected by Western blot. RESULTS: (1) GM1 at 1.0 μmol/L was the most effective concentration to preserve the TTC staining of the hippocampal slices after OGD/RP (P<0.05), and the next was GM1 at 10.0 μmol/L(P<0.05). (2) Toluidine blue staining and transmission electron microscopy showed GM1 protected the injuried hippocamal slices after OGD/RP. (3) GM1 downregulated the temporally high expression of NMDAR1 in the hippocampal slices immediately after a 25-min OGD and prevented the over low expression of NMDAR1 after a 30-min reperfusion. CONCLUSION: GM1 could protect injuried rat hippocampal slices after OGD/RP through stabilizing the expres- sion of NMDAR1.
AIM: To determine direct protective effect of monosialoganglioside (GM1) on hippocampal slices after oxygen-glucose deprivation and reperfusion (OGD / RP), and investigate the influence on the expression of N-methyl-D- aspartate receptor subunit 1 (NMDAR1) in METHODS: Injury of hippocampal slices and protective effects of GM1 were detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining, toluidine blue staining, and transmission electron microscopy of rat hippocampal slices. Expression of NMDAR1 was detected by Western blot. RESULTS: (1) GM1 at 1.0 μmol / L was the most effective concentration to preserve the TTC staining of the hippocampal slices after OGD / RP (P <0.05), and the next was GM1 at 10.0 μmol / L <0.05). (2) Toluidine blue staining and transmission electron microscopy showed GM1 protected the injuried hippocamal slices after OGD / RP. (3) GM1 downregulated the temporally high expression of NMDAR1 in the hippocampal slices immediately afte r a 25-min OGD and prevented the over low expression of NMDAR1 after a 30-min reperfusion. CONCLUSION: GM1 could protect injuried rat hippocampal slices after OGD / RP through stabilizing the expansions of NMDAR1.