Research Article

Effects of MK-801 concentration on cell proliferation in rats with focal cerebral ischemia-reperfusion

Published: October 21, 2015
Genet. Mol. Res. 14 (4) : 12841-12847 DOI: https://doi.org/10.4238/2015.October.21.3
Cite this Article:
Y.K. Gui, L.L. Su, X.L. Niu, P. Zeng, R.R. Fang, H.X. Lv, P. Zhang (2015). Effects of MK-801 concentration on cell proliferation in rats with focal cerebral ischemia-reperfusion. Genet. Mol. Res. 14(4): 12841-12847. https://doi.org/10.4238/2015.October.21.3
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Abstract

We explored the relationship between MK-801 concentration and neural stem cell proliferation in rats with focal cerebral ischemia-reperfusion (FCIR). A total of 60 male Sprague Dawley rats were randomized into control (six rats), sham-operation (six rats), operation (12 rats), and MK-801 groups. The MK-801 group comprised 36 rats that were subjected to different doses of MK-801 (0.2, 0.4, 0.6, 0.8, 1.0, and 1.2 mg/kg). Suture occlusion was used to establish an ischemia reperfusion model of middle cerebral artery occlusion (MCAO); 30 min before establishing the FCIR model, the MK-801 group rats were intraperitoneally injected with different doses of MK-801, while the sham-operation and control groups were injected with normal saline. Seven days after model establishment, bromodeoxyuridine-positive cerebral cortex cells adjacent to the focus of infarction were labeled for immunohistochemistry. MK-801 at a concentration of 0.4 mg/kg prevented endogenous neural stem cell proliferation, and this inhibitory effect was strengthened with increasing MK-801 concentration, especially at concentrations greater than 0.8 mg/kg. MK-801 inhibits endogenous neural stem cell proliferation in rats with FCIR, and the inhibitory effect is strengthened with increasing MK-801 concentration.

We explored the relationship between MK-801 concentration and neural stem cell proliferation in rats with focal cerebral ischemia-reperfusion (FCIR). A total of 60 male Sprague Dawley rats were randomized into control (six rats), sham-operation (six rats), operation (12 rats), and MK-801 groups. The MK-801 group comprised 36 rats that were subjected to different doses of MK-801 (0.2, 0.4, 0.6, 0.8, 1.0, and 1.2 mg/kg). Suture occlusion was used to establish an ischemia reperfusion model of middle cerebral artery occlusion (MCAO); 30 min before establishing the FCIR model, the MK-801 group rats were intraperitoneally injected with different doses of MK-801, while the sham-operation and control groups were injected with normal saline. Seven days after model establishment, bromodeoxyuridine-positive cerebral cortex cells adjacent to the focus of infarction were labeled for immunohistochemistry. MK-801 at a concentration of 0.4 mg/kg prevented endogenous neural stem cell proliferation, and this inhibitory effect was strengthened with increasing MK-801 concentration, especially at concentrations greater than 0.8 mg/kg. MK-801 inhibits endogenous neural stem cell proliferation in rats with FCIR, and the inhibitory effect is strengthened with increasing MK-801 concentration.