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[Effects of sodium tanshinone B on the protein expression of NMDAR1 in rat hippocampal subfields following focal ischemia/reperfusion injury].

UNLABELLED
OBJECTIVE To observe the changing laws of the protein expression of N-methyl D-aspartate receptor (NMDAR) in rat hippocampal subfields following focal ischemia/reperfusion injury, and to study the effects of sodium tanshinone B (STB) on it, thus exploring the possible mechanism of STB for treating cerebral ischemia.


METHODS
The rat model of focal cerebral ischemia/reperfusion injury was established using middle cerebral artery occlusion (MCAO) by reversibly inserting a nylon thread. The Wistar rats were randomly divided into the sham-operation group, the I/R model group, and the low, middle, and high dose STB groups. The neural functional disturbance was scored referring to the 5-grade Zea Longa EL standard. The protein expression of NMDAR1 in the ischemic side was detected using immunohistochemical assay.


RESULTS
There was statistical difference in the scores of the neural functional disturbance in the middle and high dose STB groups when compared with the model group (P < 0.01). Results of the immunohistochemical assay showed the expression of NMDAR1 in CA1 region was obviously higher in the I/R model group, the low and middle dose STB groups than in the sham-operation group (P < 0.01). The expression of NMDAR1 in CA1 region was obviously lower in the high dose STB group than in the I/R model group (P < 0.01), the low (P < 0.01) and middle dose STB groups (P < 0.05). The expression of NMDAR1 in CA3 region was obviously higher in the low dose STB group and the I/R model group than in the sham-operation group, the middle and high dose STB groups (P < 0.01). The expression of NMDAR1 in CA3 region was obviously higher in the high and middle dose STB groups than in the sham-operation group (P < 0.05).


CONCLUSIONS
STB could promote the recovery of neural functions in cerebral ischemia/reperfusion injury rats. STB fought against cerebral ischemia/reperfusion injury by lowering excitable neurotransmitter glumatic acid and reducing the protein expression of NMDAR1.