Effects of nimodipine on glutamate transporter expression of SAH model rats

Abstract

Objective To investigate the effects of Nimodipine on the expression of glutamate transporter in the brain stem of subarachnoid hemorrhage (SAH) rats. Methods Fifty-four Wistar rats were randomly divided into control group (n=6), SAH group (n=24) and SAH-Nimodipine group (n=24). SAH model was established by injecting blood twice. The level of glutamate transporter (EAATs) mRNA and the maximal blood flow velocity of basilar artery in rats were detected by injection of Nimodipine. Results The Vba of SAH group was significantly higher than that of control group at 1, 7 and 14 d (P<0.05). The Vba of SAH-Nimodipine group was significantly higher than that of control group at 1 and 7 d (P<0.05). The Vba of 1, 7 and 14 d were significantly lower than those of the control group (P<0.05). EAAT-1/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) of SAH group was significantly lower than that of control group at 1 d (P<0.05), and 21 d significantly higher than that of control group (P<0.05). The EAAT-1/GAPDH of SAH-Nimodipine group was significantly higher than that of the control group at 4 time points (P<0.05); the 1, 7 and 14 d were significantly higher than SAH group (P<0.05). The EAAT-2/GAPDH of SAH group was significantly lower than that of the control group at 1 and 7 d (P<0.05), and the EAAT-2/GAPDH of SAH group was significantly higher than that of SAH group at 14 d and 21 d after SAH-Nimodipine treatment (P<0.05). The EAAT-3/GAPDH of SAH group was significantly lower than that of the control group at 1 and 7 d (P<0.05). The EAAT-3/GAPDH of SAH group was significantly higher than that of SAH group at 1 and 7 d after SAH-nimodipine treatment(P<0.05). Conclusion Nimodipine can effectively increase the expression of EAATs, thereby relieving cerebral vasospasm, treatment of SAH. Key words: Nimodipine; Subarachnoid hemorrhage; Excitatory amino acid transporters