PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21557879-0	2012	Cerebroside-A provides potent neuroprotection after cerebral ischaemia through reducing glutamate release and Ca2+ influx of NMDA receptors.	cerebroside A	0-13	carbonic anhydrase 2	Rattus norvegicus	110-113
21557879-4	2012	We herein report that treatment with CS-A after 60-min middle cerebral artery occlusion dose-dependently reduced the cerebral infarction with at least a 6-h efficacious time-window, which was partially blocked by the BKCa channel blocker charybdotoxin (CTX).	cerebroside A	37-41	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	217-221
21557879-5	2012	Treatment with CS-A after 20 min global cerebral ischaemia (four-vessel occlusion) significantly attenuated the death of pyramidal cells in hippocampal CA1 area, which was also sensitive to CTX.	cerebroside A	15-19	carbonic anhydrase 1	Rattus norvegicus	152-155
21557879-6	2012	CS-A, by opening the BKCa channel, could prevent excessive glutamate release after oxygen-glucose deprivation (OGD).	cerebroside A	0-4	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	21-25
21557879-7	2012	In addition, CS-A could inhibit NMDAR Ca2+ influx, which did not require the activation of the BKCa channel.	cerebroside A	13-17	carbonic anhydrase 2	Rattus norvegicus	38-41
21557879-8	2012	Furthermore, CS-A blocked the OGD-induced NMDAR-dependent long-term potentiation in hippocampal CA1 region.	cerebroside A	13-17	carbonic anhydrase 1	Rattus norvegicus	96-99
21557879-9	2012	These findings indicate that treatment with CS-A after stroke exerts potent neuroprotection through prevention of excessive glutamate release and reduction of Ca2+ influx through NMDARs.	cerebroside A	44-48	carbonic anhydrase 2	Rattus norvegicus	159-162