Effects of intensive training on the expressions of semaphorin 3A and neuropilin-1 after cerebral ischemia-reperfusion in rats
Qiang Wang, Peipei Wang, Meng Pingping, Shouwei Yue
Abstract
Qiang Wang, Peipei Wang, Meng Pingping, Shouwei Yue
Abstract
Objective To observe the effects of intensive training at different intensities on the expressions of semaphorin 3A ( Sema 3A) and its receptor neuropilin ( NP-1 ) and the cell apoptosis in cerebrum after cerebral ischemia-reperfusion in rats,and to investigate the possible mechanism of intensive training in recovery of motor function after cerebral ischemia-reperfusion in rats. Methods To establish animal model of cerebral ischemia-reperfusion in rats,the intraluminal thread method was applied to cause left middle cerebral artery occlusion (MCAO) for 2 h and before reperfusion.After cerebral ischemia-reperfusion model were established for 24 h,60 male model Wistar rats were randomly divided into training group 1 ( swimming for 5 min once a day),training group 2 ( swimming for 10 min once a day),training group 3 (swimming for 10 min twice a day) and control group (no training) ; another 15 rats assigned to the sham-operation group were subject to no MCAO and no training.Neurological function was evaluated by Garcia scores,and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was performed to dectect the cortical cell apoptosis.Expressions of neural growth inhibition factor Sema 3A and its receptor NP-1 were detected by immunohistochemistry. Results The neurological function in sham-operation group was normal.The differences of Garcia scores at different time points beween sham-operation group and control group were significant (P < 0.01 ).Garcia scores in all training groups,were significantly higher than those in controls at the 7th and 14th d after swimming training ( P < 0.01 ),especially in training group 3 the Garcia scores were ( 12.80 ± 0.45 ),( 15.20 ± 0.45 ),( 16.80 ± 0.45 ),respectively,at the 3rd,7th and 14th d after swimming training.The rates of positive cell of Sema 3A,NP-1 and TUNEL indexes in all training groups were lower than those in controls at the 3rd,7th and 14th d after swimming training (P < 0.01 ),especially in the training group 3.At the 3rd,7th and 14th d after swimming training in training group 3,the rates of TUNEL indexes positive apoptosis cells were ( 29.43 ± 1.38 ) %,( 22.30 ± 1.21 ) %,( 17.58 ± 1.70) %,respectively,the positive cell rates of Sema 3A were ( 19.64 ± 1.17) %,(9.73 ± 3.83)%,(8.24 ± 0.87)%,respectively,the positive cell rates of NP-1 were ( 33.95 ± 6.86) %,( 27.95 ± 1.29 ) %,( 18.90 ± 1.44 ) %,respectively,the reduction of positive cells expressions in training group 3 was significantly more obvious compared with other training groups (P < 0.01 or 0.05). Conclusions Rehabilitation training can reduce the expression of positive cell of Sema 3A,NP-1 and TUNEL indexes in rats after cerebral ischemia-reperfusion and can improve motor function recovery and facilitate neural plasticity.The more intensive the training,the better the effects. Key words: Cerebral ischemia-reperfusion ; Intensive training ; Senaphorin 3 A ; Neuropilin-1 ; Cell apoptosis
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Objective To observe the effects of intensive training at different intensities on the expressions of semaphorin 3A ( Sema 3A) and its receptor neuropilin ( NP-1 ) and the cell apoptosis in cerebrum after cerebral ischemia-reperfusion in rats,and to investigate the possible mechanism of intensive training in recovery of motor function after cerebral ischemia-reperfusion in rats. Methods To establish animal model of cerebral ischemia-reperfusion in rats,the intraluminal thread method was applied to cause left middle cerebral artery occlusion (MCAO) for 2 h and before reperfusion.After cerebral ischemia-reperfusion model were established for 24 h,60 male model Wistar rats were randomly divided into training group 1 ( swimming for 5 min once a day),training group 2 ( swimming for 10 min once a day),training group 3 (swimming for 10 min twice a day) and control group (no training) ; another 15 rats assigned to the sham-operation group were subject to no MCAO and no training.Neurological function was evaluated by Garcia scores,and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was performed to dectect the cortical cell apoptosis.Expressions of neural growth inhibition factor Sema 3A and its receptor NP-1 were detected by immunohistochemistry. Results The neurological function in sham-operation group was normal.The differences of Garcia scores at different time points beween sham-operation group and control group were significant (P < 0.01 ).Garcia scores in all training groups,were significantly higher than those in controls at the 7th and 14th d after swimming training ( P < 0.01 ),especially in training group 3 the Garcia scores were ( 12.80 ± 0.45 ),( 15.20 ± 0.45 ),( 16.80 ± 0.45 ),respectively,at the 3rd,7th and 14th d after swimming training.The rates of positive cell of Sema 3A,NP-1 and TUNEL indexes in all training groups were lower than those in controls at the 3rd,7th and 14th d after swimming training (P < 0.01 ),especially in the training group 3.At the 3rd,7th and 14th d after swimming training in training group 3,the rates of TUNEL indexes positive apoptosis cells were ( 29.43 ± 1.38 ) %,( 22.30 ± 1.21 ) %,( 17.58 ± 1.70) %,respectively,the positive cell rates of Sema 3A were ( 19.64 ± 1.17) %,(9.73 ± 3.83)%,(8.24 ± 0.87)%,respectively,the positive cell rates of NP-1 were ( 33.95 ± 6.86) %,( 27.95 ± 1.29 ) %,( 18.90 ± 1.44 ) %,respectively,the reduction of positive cells expressions in training group 3 was significantly more obvious compared with other training groups (P < 0.01 or 0.05). Conclusions Rehabilitation training can reduce the expression of positive cell of Sema 3A,NP-1 and TUNEL indexes in rats after cerebral ischemia-reperfusion and can improve motor function recovery and facilitate neural plasticity.The more intensive the training,the better the effects. Key words: Cerebral ischemia-reperfusion ; Intensive training ; Senaphorin 3 A ; Neuropilin-1 ; Cell apoptosis
Key concepts: Ischemia, TUNEL assay, Medicine, Isoflurane, Anesthesia, Neuroprotection, Infarction, Occlusion