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Objective To explore the optimal duration of long-term mild hypothermia(MHT)for traumatic brain injury(TBI)in rats,and observe its effect on intracranial pressure(ICP)and neurological function.Methods Forty-eight healthy adult male SD rats were divided into the normal temperature treatment(NT)group,the MHT4 h group,the MHT24 h group and the MHT48 h group by random number table method,with twelve rats in each group.The TBI model of rats was prepared by electronic controllable cortical injury device,and ICP monitoring probe was implanted.After modeling,the NT group was treated with normal temperature(37℃),and the other groups were treated with low temperature(33.0±1.0)℃for 4 h,24 h and 48 h,respectively.ICP was monitored and brain water content(BWC)was calculated after MHT treatment in each group.Blood-brain barrier permeability was determined by Evansland(EB)staining.The expression of 5-bromodeoxyuracil nucleoside(BrdU),neuronal nuclear antigen antibody(NeuN)and leukocyte differentiation antigen 86(CD86)positive cells were detected by immunofluorescence staining.The expressions of B-cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),inducable nitric oxide synthase(iNOS),interleukin(IL)-10 and arginase 1(Arg-1)were detected by Western blot assay.Results Compared with the NT group,levels of BWC,ICP,EB,and CD86 positive cells,Bax and iNOS expression levels were decreased in the MHT4 h group,the MHT24 h group and the MHT48 h group,and the number of BrdU positive cells and BrdU/NeuN double-labeled positive cells were increased in hippocampus.The expression levels of Bcl-2,IL-10 and Arg-1 were increased(P＜0.01).Compared with the MHT24 h group,levels of BWC,ICP and EB,and CD86 positive cells,Bax and iNOS expression were decreased,and the number of BrdU positive cells and BrdU/NeuN double-labeled positive cells were increased in the MHT48 h group,while levels of Bcl-2,IL-10 and Arg-1 expression were increased(P＜0.01).Conclusion Long-term MHT can promote the proliferation and differentiation of neurons,inhibit apoptosis and reduce inflammation by suppressing ICP rebound,further promoting neuroprotection after TBI.
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Objective @#To investigate the neurobehavioral effects of long term mild hypothermia (MHT) combined with compound porcine cerebroside and ganglioside inj ection (CPCGI) after traumatic brain inj ury (TBI) in rats and its mechanism. @*Methods @#36 healthy adult male SD rats were randomly divided into model group , MHT group , CPCGI group and MHT + CPCGI group . The TBI model was prepared using an electronically controlled cortical in j ury device . The rats in model group received an intraperitoneal inj ection of an equal amount of normal saline (NS , 2 ml/kg) and were treated at room temperature (37 ℃) for 48 hours . The rats in MHT group received an intraper itoneal inj ection of an equal amount of NS and were treated at a slightly low temperature (33.0 ±1 0) ℃ for 48 hours . The rats in CPCGI group received an intraperitoneal inj ection of an equal amount of CPCGI (0.6 ml/kg) and were treated at room temperature for 48 hours . The rats in MHT + CPCGI group received an intraperitoneal injection of an equal amount of CPCGI and were treated at a slightly low temperature for 48 hours. The sensorimotor function of rats was evaluated by modified Neurological Severity Score ( mNSS) . The motor and spatial memory a bilities of rats were detected by Morris water maze test , and the motor function of rats was evaluated by beam walk ing test (BWT) and inclined grid climbing test. The number of neurons in hippocampus was ob served by Nissl stai ning and immunofluorescence was used to detect the expression of doublecortin (DCX) and neuronal nuclear anti gen antibody (NeuN) . Western blot was used to ob serve the protein expression of B cell lymphoma-2 ( Bcl-2) , Bcl 2 associated X protein ( Bax ) and cysteine proteinase-3 ( Caspase-3) . @*Results @#Compared with MHT group and CPCGI group , MHT + CPCGI group had a lower mNNS score, shorter escape latency , higher times across the platform and the percentage of time in the target quadrant , higher BWT score and larger climbing angle , increased numbers of neurons , DCX and NeuN positive cells , increased Bcl-2 expression and decreased expression of Bax and Caspase-3 . (P < 0.05) . @*Conclusion @#Long-term mild hypothermia combined with CPCGI can effectively improve the neurological deficits of TBI rats by promoting nerve regeneration and inhibiting cell apoptosis , and provide potential strategies and basis for the clinical treatment of TBI .
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Objective To explore the effects of delayed mild hypothermia (MHT) in different time windows on the expressions of Bcl-2, Bax and Caspase-3 in brain tissue of model rats with traumatic brain injury (TBI). Methods Thirty-six clean adult male SD rats were randomly divided into NT group (normal temperature), MHT 15 min group, MHT 2 h group and MHT 4 h group. TBI rat model was established by electronical controlled cortical injury device. The rats in the NT group were treated with normothermia (37℃) and the rats in the three hypothermia groups were implemented with low temperature (33.0±1.0)℃at 15 min, 2 h and 4 h for 6 h respectively after establishment of TBI model. The modified neurological senerity scores (mNSS), morphological changes in hippocampal CA1 areas, immunohistochemical staining and Western blot assay for Bcl-2, Bax and Caspase-3 were compared 3 days after TBI between the four groups. Results The neurological behavioral deficits were found in each group. Compared with the NT group, the mNSS were decreased in the three hypothermia groups (P<0.01). The results of HE staining showed that the structure of neurons was regular and arranged neatly, and the number of neurons decreased with alleviated nuclear fragmentation and dissolution in hypothermia groups. Compared with the NT group, the expression of Bcl-2 was upregulated, and the expressions of Bax and Caspase-3 were downregulated in three hypothermia groups (P<0.05). The above experimental results were superior in MHT15 min group to MHT 2 h group, and the therapeutic effect in MHT 2 h group was similar to MHT 4 h group. Conclusion The proper delayed mild hypothermia treatment could inhibit neuronal apoptosis and alleviate brain damage.
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Objective To analyse the efficacy of microvascular decompression for hemifacial spasm (HFS) caused by vertebral basilar artery compression. Methods A total of 141 patients with HFS treated by microvascular decompression in our hospital were collected in this study. The improvement of the symptoms after operation was compared between patients with HFS caused by vertebral basilar artery compression (28 cases) and patients with HFS caused by non-vertebral basilar artery compression (113 cases). Results There was no significant difference in the effective rate between the two groups of HFS (96.43%vs. 98.23%,P=0.49) with mean following-up 13.81 ± 1.57 months. And there was no significant difference in the delayed cure rate after surgery between two groups (37.04%vs. 20.72%,χ2=1.38, P>0.05). Conclusion Microvascular decompression is a safe and effective method for the treatment of HFS caused by compressed vertebral basilar artery.