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1.
The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.  相似文献   

2.
The change of the expression of Cyclins in neurons of rats after focal cerebral ischemia was investigated. Ischemia was induced by temporary middle cerebral artery occlusion (MCAO). The experimental rats induced by MCAO were sacrificed on 7th and 14th day after reperfusion. The brain was taken out at 7th and 14th day after injury, and the expression of Cyclin D1, E, A and B1 in neurons of cerebral cortex or hippocampal CA1 region was detected by immunofluorescence and confocal microscope. The results showed that after MCAO, in the ipsilateral CA1 subfield of hippocampus the expression of Cyclin D1, E, A and B1 in neurons was significantly gradually up-regulated at 7th and 14th day after reperfusion (P〈0.05) as compared with that in control group. In the ipsilateral cerebral cortex the expression of Cyclin D1 and B1 in neurons was notably gradually down-regulated at 7th and 14th day, and that of Cyclin E and A was significantly up-regulated at 14th day after reperfusion as compared with that in control group (all P〈0.05). It was concluded that there was a differential sensitivity among neurons from different brain regions to ischemic injury. But all of them re-enter into cell cycle after MCAO.  相似文献   

3.
OBJECTIVE:To investigate the effects of different frequencies of electro-acupuncture at Shuigou(GV 26) on the latent period and wave amplitude of motor evoked potentials(MEPs) in rats with focal cerebral infarction.METHODS:Fifty healthy male Wistar rats were randomly divided into five groups:controls,model,2 Hz Shuigou,50 Hz Shuigou and 100 Hz Shuigou.There were 10 rats in each group.Using a modification of a technique for middle cerebral artery occlusion,focal cerebral ischemic injury was induced in all rats except those in the control group.The rats in the control group received no treatment.After behavioral deficit had been evaluated using the Zausinger 6-point neurological function score,therats in the Shuigou groups underwent acupuncture and continuous wave stimulation at a frequency of 2 Hz,50 Hz or 100 Hz(intensity 1 mA) for 10 min twice daily for 3 days.The control and model groups underwent no intervention.Zausinger 6-point neurological function score and MEPs were measured 72 h after the start of treatment.RESULTS:The neurological function scores of the three Shuigou groups were significantly higher than those of the model group(P<0.05).There was no significant difference between sides in the latency and amplitude of MEPs in the model group(P> 0.05).The latency on the affected side in the model group was significantly longer than that in the control group(P<0.05) and the amplitude on affected side was significantly reduced(P<0.01).After 3 days of electro-acupuncture,the latency on the affected side in the 2 Hz Shuigou group was significantly shortened(P<0.05) and the amplitude was significantly increased(P<0.05) compared with the model group.CONCLUSION:Low frequency electro-acupuncture at Shuigou(GV 26) can promote recovery of motor function after focal cerebral ischemic injury in rats.  相似文献   

4.
Objective To study the protective effect of agrimony extracts from different extracting methods on cerebral ischemia-reperfusion injury in rats, in order to optimize the extraction scheme of agrimony. Methods Male rats were randomly assigned into seven groups: 1. Sham-operated group, 2. Untreated MCAO group (MCAO), 3. Petroleum ether extract of Agrimonia pilosa treated MCAO group (PEA), 4. Ethyl acetate extract of Agrimonia pilosa treated MCAO group (EAEA), 5. Ethanol extract of Agrimonia pilosatreated MCAO group (EEA), 6. Water extract of Agrimonia pilosatreated MCAO group (WEA), 7. Nimodipine treated MCAO group (NP). Intragastrical drug administration (i.g) was performed at 0 and 6 hours after MCAO. Neurological function tests were performed after reperfusion for 24 hours, then the brain was removed for the evaluations of the cerebral infarction volume (percentage of total brain volume) by immunohistochemistry, histological changes (hematoxylin-eosin staining), Na+/K+-ATPase, Ca2+-ATPase (modified method of Svoboda and Mosinger), mRNA expression of Tumor suppressor gene (P53) and hot shock protein (HSP70) (quantitative real-time PCR). Results The neurological function of MCAO group had significantly higher scores than the sham group (P<0.01). The WEA group showed a significantly lower neurological score than the MCAO group (P<0.05), indicating the protective effect of WEA on neurological deficits. The mean infarction volumes of WEA (13.5±6.6%,F=4.75,P<0.01), EEA (19.90±6.90%,F=5.23,P<0.01), PEA (20.40±5.30%, F=4.68, P<0.01) and EAEA (22.50±10.50%,F=6.25,P<0.05) group were all significantly smaller than that of MCAO group (29.40±6.50%). HE staining demonstrated that, compared to the treated groups, the infarcted cerebral tissue of MCAO group had more swelling neural cells, lighter stained nucleus, fewer and irregularly distributed neurons. The activity of Na+/K+-ATPase and Ca2+-ATPase reduced in the MCAO group (3.67±0.48 U/mg, 1.28±0.26 U/mg, respectively), and were significantly higher in WEA group (7.56±0.85 U/mg,F=12.65, P=0.010; 3.59±0.22 U/mg,F=8.32,P=0.041, respectively). The MCAO group showed significantly elevated P53 and HSP70 mRNA expressions compared to the sham group (P<0.01,P<0.05). P53 mRNA expressions in Agrimony extracts treated groups were significantly lower than that of the MCAO group (allP<0.01), with the WEA group showing the greatest difference from MCAO group. The HSP70 mRNA level of the treated groups were not significantly different from that of the MCAO group. Conclusions Treatmentusingwater extracts of agrimony can promote the best functional and metabolic recovery for rat model of cerebral ischemia-reperfusion injury, which maybe relate with the upregulation of energy metabolism in nerve cells after MCAO.  相似文献   

5.
Objective To investigate the effects of propofol,midazolam and thiopental sodium on outcomes and amino acid accumulation in focal cerebral ischemia-reperfusion in rats.Methods Male Spregue Dawley(SD)rats were scheduled to undergo 3-hour middle cerebral artery occlusion by intraluminal suture and 24-hour reperfusion.Neurologic outcomes were scored on a 0-5 grading scale.Infarct volume was shown with triphenyltetrazolium chloride staining and measured by an image analysis system.Concentrations of various amino acids(aspartate,glutamate,glycine,taurine,and gama-aminobutyric acid)were measured after 3 hours of reperfusion using high performance liquid chromatography,Propofol,midazolam and thiopental sodium were given intraperitoneally at the beginning of reperfusion.Results Both propofol and midazolam attenuated neurological deficits and reduced infarct and edema volumes.Propofol showed better neurological protection than midazolam while thiopental sodium did not exhibit any protective effect.Both propofol and midazolam decreased excitatory amino acids accumulation,while propofol increased gana-aminobutyric acid accumulation in ischemic areas in reperfusion. Conclusion Propofol and midazolan,but not thiopental sodium,may provide protective effects against repefrusion induced injury in rats subjected to focal cerebral ischemia.This neurological protection may be due to the acceleration of excitatory amino acids elimination in reperfusion.  相似文献   

6.
7.
Objective To investigate whether pretreatment with repeated electroacupuncture (EA)at th e Baihui acupoint could induce ischemic tolerance against transient focal cerebr al ischemic injury in rats. Methods Thirty male Sprague- Dawley (SD) rats were randomly divided into 3 groups (n=10 for each): the control group consisted of animals receiving no treatment, the is oflurane (ISO) group had animals that inhaled 1.5% isoflurane for 30 min a day for 5 days, and animals in the EA group received electroacupuncture at the Baihu i acupoint for 30 min a day for 5 days under 1.5% isoflurane anesthesia. Twent y- four hours after the last treatment, the middle cerebral artery was occluded with No. 3 nylon monofilament for 120 min. The neurological outcomes were evalu ated 24 h after reperfusion. The infarct volumes were then assessed using 2% tr iphenyltetrazolium chloride staining after the neurological outcome evaluation. Results The neurological deficit score (NDS) of the EA group [1 (0-2)] was lower tha n that of the ISO group [2 (1-3)] and the control group [2 (1-4)], P&lt;0. 05. The infarct volume of the EA group (38.3±25.4 mm(3)) was significantly smaller than that of the control group (220.5±66.0 mm(3)) and the ISO group (168.6±57.6 mm(3)) 24 h after reperfusion. Conclusion Electroacupuncture at the Baihui acupoint 30 min a day for 5 days significantly reduces neurological injury induced by transient middle cerebral artery occlusion.  相似文献   

8.
To study the effect of Buyang Huanwu Decoction (补阳还五汤BYHWD) on spinal ischemia-reperfusion injury and explore the possible mechanism involved. Method: 27 model rabbits with ischemia-reperfusion injury were randomly divided into a sham operation group, a model group and a BYHWD-pre-treated group. 24 and 48 hours after the ischemia-reperfusion injury, the motor functions of hind limbs were observed, the expressions of apoptosis-related proteins bcl-2 and Bax in the spinal tissue were investigated with the immunohistochemical methods and apoptosis of nervous cells with TUNEL straining; and the malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in the spinal cord were then determined. Results: BYHWD can improve significantly the motor function of hind limbs, increase SOD activity and decrease the level of MDA, up-regulate expression of Bcl-2 and down-regulated expression of Bax, and depress apoptosis of nervous ceils in the spinal cord caused by the ischemia reperfusion in the rabbits. Conclusion: BYHWD has a protective action on the spinal ischemia-reperfusion injury, and the mechanisms may be related to the decrease of lipid peroxidation and inhibition of apoptosis of nervous cells.  相似文献   

9.
In order to investigate the protective effects of the overexpression of bcl-xl gene on local cerebral infarction in the transgenic mice subject to permanent occlusion of middle cerebral artery, the models of bcl-xl transgenic mice were established and subjected to cerebral infarction by intraluminal occlusion of the middle cerebral artery. The infarct volume and the neurological scores were observed and comparison between the wild type mice and the transgenic mice was made. It was found that the infarct volume and the neurological scores in the transgenic mice were significantly decreased as compared with those in the wild type mice. It was suggested that the overexpression of bcl-xl gene in transgenic mice could reduce the infarct volume and improve the neurological function of the mice.  相似文献   

10.
The effect of transcranial magnetic stimulation (TMS) on the neurological functional recovery and expression of c-Fos and brain-derived neurotrophic factor (BDNF) of the cerebral cortex in rats with cerebral infarction was investigated. Cerebral infarction models were established by using left middle cerebral artery occlusion (MCAO) and were randomly divided into a model group (n=40) and a TMS group (n=40). TMS treatment (2 times per day, 30 pulses per time) with a frequency of 0.5 Hz and magnetic field intensity of 1.33 Tesla was carried out in TMS group after MCAO. Modified neurological severity score (NSS) were recorded before and 1, 7, 14, 21, and 28 day(s) after MCAO. The expression of c-Fos and BDNF was immunohistochemically detected 1, 7, 14, 21, and 28 day(s) after infarction respectively. Our results showed that a significant recovery of NSS (P〈0.05) was found in animals treated by TMS on day 7, 14, 21, and 28 as compared with the animals in the model group. The positive expression of c-Fos and BDNF was detected in the cortex surrounding the infarction areas, while the expression of c-Fos and BDNF increased significantly in TMS treatment group in comparison with those in model group 7, 14, 21, and 28 days (P〈0.05) and 7 14, 21 days (P〈0.01) after infarction, respectively. It is concluded that TMS has therapeutic effect on cerebral infarction and this may have something to do with TMS's ability to promote the expression of c-Fos and BDNF of the cerebral cortex in rats with cerebral infarction.  相似文献   

11.
目的 观察缺血后适应对大鼠缺血再灌注损伤时Bcl-2和GAP-43表达变化的影响.方法 50只成年健康雄性SD大鼠随机分为缺血2h再灌注组(n=25)、缺血4.5 h后适应组(n=25).线栓法制备大脑中动脉闭塞模型(MCAO),Lumila Belayev12分、Zea Longa5分和悬吊实验术后24 h进行神经功能评分,TTC法染色后测量脑梗死体积,免疫组织化学方法和Western Blot检测Bcl-2及GAP-43蛋白.结果 与缺血2h再灌注组相比,缺血4.5 h后适应组神经功能评分和脑梗死体积差异没有统计学意义(P>0.05).缺血4.5 h后适应组Nogo-A表达降低,GAP-43表达增加,差异有统计学意义(P<0.05).结论 缺血后适应能够改善神经功能损伤,减小脑梗死体积,增加GAP-43的表示以及减少Nogo-A的表达,对缺血的脑组织起保护作用.  相似文献   

12.
目的 探讨干细胞因子(stem cell factor,SCF)联合抗白细胞介素-17A抗体(anti-IL-17A)对小鼠脑缺血预后的影响.方法 通过线栓法对C57BL/6小鼠建立大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,60 min后取出线栓,恢复右侧大脑中动脉血流,建立脑缺血再灌注模型.小鼠脑缺血再灌注后分别给予腹腔注射生理盐水(normal saline,NS)、anti-IL-17A、SCF、anti-IL-17A+SCF.观察各组小鼠MCAO术后脑梗死体积、脑组织病理损伤和脑水肿程度、神经功能评分、神经细胞凋亡和炎症反应等变化.结果 与NS组相比,其余各治疗组脑梗死体积、脑组织病理损伤和脑水肿均显著减轻(P<0.05),神经功能评分得到明显改善(P<0.05),神经细胞凋亡减少(P<0.05),且anti-IL-17A+ SCF组显著优于anti-IL-17A组和SCF组(P<0.05).此外,anti-IL-17A还能明显减少脑组织IL-17A和IL-1 β的表达(P<0.05).结论 SCF联合anti-IL-17A能更好地改善脑缺血损伤和促进神经功能恢复.  相似文献   

13.
目的 探讨重组人粒细胞集落刺激因子(rhG-CSF)鼻腔给药对脑梗死大鼠的脑保护作用.方法 线栓法制备大鼠大脑中动脉阻塞模型,缺血2h再灌注,皮下及鼻腔给予 rhG-CSF(60 μg/kg).将动物分为正常组、假手术对照组、脑梗死组、脑梗死+皮下注射rhG-CSF组、脑梗死+经鼻生理盐水组、脑梗死+经鼻rhG-CSF组,每组6只.于术后3 d进行神经功能评分及FasL免疫荧光检测.结果 除正常组、假手术对照组外,其余各组动物均于术后出现不同程度的神经功能缺损,尤以脑梗死组、脑梗死+经鼻生理盐水组最为严重,神经功能评分最高[(10.20±1.85)分,(10.30±1.76)分],海马FasL阳性细胞数最多[(41.17±3.25)个,(41.00±2.76)个],差异无显著性( P >0.05),rhG-CSF皮下给药组大鼠神经功能评分降低[(5.67±1.32)分,P <0.01],海马FasL表达减少[(32.67±1.97)分,P <0.01],rhG-CSF经鼻给药组大鼠神经功能评分进一步降低[(4.00±0.93)分,P <0.05],海马FasL表达进一步减少[(19.50±1.05)个,P <0.01].结论 rhG-CSF经鼻给药能预防和修复脑梗死大鼠的神经功能缺损,通过抑制FasL表达发挥脑保护作用.  相似文献   

14.
目的:探讨泊洛沙姆188与银杏内酯B联合应用对小鼠脑缺血-再灌注损伤的保护作用。方法:以线栓造成小鼠脑组织缺血状态,线栓移除前5min经尾静脉单次注射泊洛沙姆188(0.4g/kg),银杏内酯B(20mg/kg)或两药的混合溶液,24小时后评价小鼠神经症状并测定脑梗死面积和脑含水量。另一批小鼠在静脉注射给药后再每天腹腔注射上述等效剂量药物,24天后统计各组存活状况,绘制生存曲线;采用爬杆试验、悬挂试验测试小鼠肢体运动功能。结果:生理盐水组小鼠脑梗死面积为35.49%±8.31%,P188组、GB组以及合用组的脑梗死面积分别减少为27.76%±6.41%,25.51%±5.81%和21.16%±8.67%,P188与GB合用组比药物单用组的脑梗死面积更小,差异有统计学意义(P<0.05)。生理盐水组小鼠24天后的生存率为38.89%,P188组,GB组以及合用组小鼠的生存率分别为50%,53.57%和69.21%。P188与GB合用组与药物单用组相比,生存期明显延长,差异均有统计学意义(P<0.05)。P188组、GB组以及药物合用组T/turn分别为6.22秒,6.56秒和5.25秒,T/floor分别为15.50秒,14.88秒和13.25秒,P188和GB合用组与药物单用组相比,T/turn和T/floor均显著缩短,差异均有统计学意义(P<0.05)。与泊洛沙姆188和银杏内酯B单用相比,联合用药能进一步降低脑梗死面积,延长生存期,增强小鼠肢体的运动功能。结论:泊洛沙姆188与银杏内酯B合用能够增强对小鼠脑缺血-再灌注损伤的保护作用。  相似文献   

15.
目的观察电针预处理对脑缺血再灌注大鼠皮质神经元TRPC6表达的影响,探讨其对神经元可能的保护机制。方法将SD大鼠随机分为假手术组、模型组和电针预处理组,每组8只。采用大脑中动脉栓塞法制备脑缺血再灌注模型。电针预处理组在造模前取"百会"和"大椎"穴给予电针刺激。造模后24h进行神经功能评分并急性分离大鼠皮质神经元,通过蛋白免疫印迹(western blot)检测神经元TRPC6和Caspase-3蛋白表达,钙影像检测细胞内相对钙离子浓度。结果与假手术组比较,模型组大鼠的神经功能评分明显增高(P0.05),大脑皮质神经细胞TRPC6和Caspase-3蛋白表达明显增高(P0.05),神经元内钙离子浓度升高(P0.01);与模型组比较,电针预处理组能明显改善脑缺血再灌注后大鼠的神经功能症状(P0.05),抑制大脑皮质神经细胞TRPC6和Caspase-3蛋白表达(P0.05),并降低细胞内钙离子浓度(P0.01)。结论电针预处理对脑缺血再灌注大鼠脑损伤有保护作用,其机制可能与TRPC6下调,减少细胞钙离子内流从而抑制神经凋亡。  相似文献   

16.
氯胺酮咪唑安定麻醉对大鼠局灶性脑缺血损伤的影响   总被引:1,自引:0,他引:1  
目的比较氯胺酮联合咪唑安定麻醉与单纯氯胺酮麻醉对局灶性脑缺血损伤的影响。方法30只SD大鼠在氯胺酮或氯胺酮-咪唑安定麻醉下制作永久性大脑中动脉阻塞模型。术后4h行神经病学评分、24h测量梗塞体积、72h进行TUNEL染色检测半暗带内的细胞凋亡。结果术后4h神经病学评分在氯胺酮-咪唑安定组和氯胺酮组间无显著性差异(1.74±0.52vs1.57±0.65,P>0.05),但氯胺酮-咪唑安定组大鼠的脑梗塞体积和半暗带内凋亡细胞密度明显低于氯胺酮组大鼠的相应参数(梗塞体积:24.1%±4.63%vs38.48%±4.18%;凋亡细胞密度:178±23个/mm2vs258±15个/mm2,P<0.05)。结论氯胺酮麻醉中联合应用咪唑安定对大鼠局灶性脑缺血损伤具有保护作用。  相似文献   

17.
目的 研究重组人可溶性血栓调节蛋白(ART-123)对小鼠脑缺血/ 再灌注损伤的影响。方法 BALB/c 小鼠行4 h 大脑中动脉闭塞(MCAO),再灌注时静脉注射Vehicle 或ART-123(1 或5 mg/kg)。再灌注24 h 后 评估小鼠脑梗死体积、运动协调、血浆高迁移率族蛋白(HMGB1)水平及出血量。结果 ART-123 可减少 MCAO 小鼠脑梗死体积,并呈剂量依赖性(F =4.843,P =0.038)。与Vehicle 组比较,ART-123(5 mg/kg)可 改善旋转试验中MCAO 小鼠运动协调(P =0.028);降低血浆HMGB1 水平(P =0.000)。此外,Vehicle 组和 ART-123 组小鼠出血量差异无统计学意义(P >0.05)。结论 ART-123 可能通过抑制HMGB1 改善小鼠脑 缺血/ 再灌注损伤。  相似文献   

18.
目的:研究远隔缺血预适应( remote ischemic preconditioning,RIPC)对大鼠脑缺血再灌注后诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的影响,以探讨 RIPC 保护脑缺血损伤的相关机制。方法应用线栓法制作大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,将21只健康雄性 SD 大鼠采用数字表法随机分为3组:假手术组(sham,n=7),MCAO 组(n=7),RIPC+MCAO 组(n =7)。在 MCAO 手术前连续3 d,进行远隔肢体缺血预适应处理(双侧股动脉夹闭10 min/放开10 min,每天3次)。在缺血2 h-再灌注24 h 后进行神经功能评分,TTC 染色检测脑梗死体积,采用 Western blotting 方法检测梗死侧脑组织的 iNOS 蛋白表达水平。结果1)在 MCAO 手术过程中,3组实验动物的生理指标均在正常范围内,且组间差异无统计学意义。与 sham 组相比,MCAO 组大鼠再灌注24 h 时神经功能缺损评分显著升高、脑梗死体积明显增大(P〈0.05)。而 RIPC+MCAO 组大鼠神经功能较 MCAO 组大鼠得到明显改善、脑梗死体积显著减少(P〈0.05)。2)再灌注24 h 时,与 sham 组相比,MCAO 组大鼠脑梗死侧 iNOS 蛋白表达显著增加(P〈0.05)。与 MCAO 组相比,RIPC+MCAO 组大鼠脑梗死侧 iNOS 蛋白表达显著降低(P〈0.05)。结论 RIPC 处理对大鼠脑缺血损伤具有保护作用,其机制与降低脑缺血大鼠脑内 iNOS 蛋白表达有关。  相似文献   

19.
目的 :探讨活血化瘀系列方 (活血汤、活血益气汤、活血养阴汤 )对大鼠脑缺血再灌注损伤的保护作用及其机制。方法 :采用大脑中动脉阻断法制备大鼠脑缺血再灌注模型 ,缺血 6 0 min,再灌注 3d。观察药物对脑缺血再灌注引起的神经功能缺损症状及病理损伤的影响 ,检测脑组织一氧化氮合酶 (NOS)、超氧化物歧化酶 (SOD)活性的变化和丙二醛 (MDA)含量的变化 ,免疫印迹分析 NMDA受体亚单位蛋白 NR1和内皮型 NOS(e NOS)的表达。结果 :活血化瘀系列方及尼莫地平能显著改善神经功能缺失症状 ,减小梗死体积和脑水肿面积 ,减少神经元损伤 (P<0 .0 5 ) ,组间没有显著性差异 ;活血化瘀系列方和尼莫地平不同程度降低脑组织内 NOS活性和 MDA含量 ,抑制NR1表达 ,增加 SOD的活性 ,但对 e NOS的表达均无明显影响。结论 :活血化瘀系列方对大鼠脑缺血再灌注损伤有保护作用 ,其机制可能与降低脑组织内 NOS活性 ,降低 NR1的表达 ,减少 MDA含量和增加 SOD活性有关。  相似文献   

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