针刺对脑出血大鼠C-Jun氯基末端激酶通路的影响

目的探讨针刺百会透曲鬓穴对实验性脑出血大鼠C-Jun氯基末端激酶（JNK）信号转导通路的影响。方法选取健康雄性Wistar大鼠192只，随机分为模型组、模型十针刺组（简称针刺组）、模型＋抑制剂组（简称抑制剂组）三组，每组60只，制备脑出血模型。另设空白组12只大鼠。针刺组针刺患侧百会透曲鬓穴，运用Western blot的检测方法，观察不同时相点针刺百会透曲鬓穴对脑出血大鼠血肿周围脑组织中P-JNK蛋白表达的影响。结果各造模组大鼠血肿周围脑组织的p-JNK阳性表达至2d时达高峰，7d时有所下降。在相同时相点，针刺组大鼠p-JNK表达均明显低于模型组（q=12．06，P〈0．01）；抑制剂组p-JNK表达也均明显低于模型组（q=10．85，P〈0．01）；针刺组与抑制剂组比较差异无统计学意义（q=1．21 P〉0．05）。结论针刺百会透曲鬓穴能够阻断JNK通路，抑制p-JNK蛋白的表达，从而抑制细胞凋亡、保护神经元细胞。     

针刺对脑出血大鼠继发性神经损伤保护机制的研究

目的 探讨针刺对脑出血大鼠继发性神经损伤保护作用的机制.方法 选取健康雄性Wistar大鼠160只,先随机分为:模型对照组(简称模型组),模型+针刺组(简称针刺组),模型+脑复康组(简称脑复康组),每组50只大鼠,每组又分为术后6 h、1 d,2 d,3 d,7 d 5个时相点,每个时相点10只大鼠,制备脑出血模型;另设10只正常大鼠作为空白对照组(简称正常组).针刺组针刺患侧百会透曲鬓穴.观察各组大鼠血肿周围脑组织神经生长因子(NGF)的表达.结果 针刺组大鼠血肿周围脑组织NGF的表达随不同时相点的变化而逐渐增加,至7 d时达高峰,与模型组比较差异有统计学意义(P＜0.01).结论 针刺能够促进脑出血大鼠血肿周围脑组织NGF的表达.     

针刺对脑出血大鼠细胞外信号调节蛋白激酶通路影响的研究

目的：探讨针刺百会透曲鬓穴对脑出血大鼠细胞外信号调节蛋白激酶（ ERK）信号转导通路的影响。方法选取健康雄性Wistar大鼠192只,随机分为空白组、模型组、模型＋针刺组（简称针刺组）、激动剂组四组。空白组12只大鼠,模型组、针刺组、激动剂组各60只大鼠,制备脑出血模型。针刺组针刺患侧百会透曲鬓穴,运用Western blot的检测方法,观察不同时相点针刺百会透曲鬓穴对脑出血大鼠血肿周围脑组织p-ERK蛋白表达的影响。结果各造模组大鼠血肿周围脑组织的p-ERK阳性细胞表达至7 d时达高峰。在1d、2d、3d、7d,针刺组大鼠p-ERK表达[（0．19±0．04）、（0．23±0．07）、（0．24±0．05）、（0．25±0．06）]均明显高于模型组[（0．10±0．04）、（0．17±0．02）、（0．09±0．05）、（0．10±0．06）,q＝11．45,均P＜0．01];激动剂组p-ERK表达[（0.20±0．05）、（0．24±0．06）、（0．25±0．09）、（0．26±0．09）]也均明显高于模型组[（0．10±0．04）、（0．17±0．02）、（0.09±0．05）、（0．10±0．06）,q＝10．07,均P＜0．01];针刺组与激动剂组比较差异无统计学意义（P＞0．05）。结论针刺百会透曲鬓穴能够激活ERK通路,增加p-ERK蛋白的表达,起到保护神经元细胞的作用。     

大鼠脑出血周边组织MMP-2、MMP-9的动态表达及其与脑水肿关系的研究

目的:研究大鼠脑出血周边组织MMP-2、MMP-9的动态表达及其与脑水肿形成的关系。方法:1Wistar大鼠60只,随机分为对照组和脑出血组,均分为(6h、24h、48h、72h、120h)5个时间点。2测定出血周边脑组织含水量、EB含量以及MMP-2/9蛋白表达。结果:1脑出血周边组织EB含量在24h迅速增高,48h达到高峰,显著高于对照组。2大鼠脑出血6h后含水量明显增高,72h达高峰,在6～120h内脑组织含水量与EB含量呈正相关。3对照组有极少量MMP-2阳性细胞表达;出血组中6h达高峰,各时点均显著高于对照组。4MMP-9在对照组极少量表达;出血组48h达高峰,在6～120h其表达与脑含水量和EB含量均呈正相关。结论:大鼠脑出血后MMP-2/9的释放与激活,是脑出血后早中期脑水肿形成的主要因素,导致BBB通透性增加而形成血管源性脑水肿。     

藻蓝蛋白对大鼠脑缺血再灌注后MMP-2和MMP-9表达的影响

目的探讨藻蓝蛋白对大鼠局灶性脑缺血再灌注后基质金属蛋白酶-2和9（MMP-2和MMP-9）表达的影响。方法应用线栓法建立大鼠左侧大脑中动脉阻塞再灌注（MCAO／R）模型，应用藻蓝蛋白进行干预，干湿重法测定脑组织含水量（BWC），比色法测定脑组织伊文斯蓝（EB）含量，免疫组化技术检测脑组织MMP-2和MMP-9的表达。结果脑缺血再灌注6h BWC和EB含量增加，至2d达高峰，应用藻蓝蛋白后均明显减少。对照组脑缺血再灌注24h脑组织MMP-2阳性细胞即开始出现，3～7d阳性细胞数达高峰，14d仍高于假手术组。藻蓝蛋白组MMP-2阳性细胞的变化趋势与对照组相似，但同一时间点明显低于对照组。对照组缺血侧脑组织MMP-9阳性细胞于再灌注后6h开始出现，12h明显增高，至2d达高峰，3d开始减少，至14d时恢复至假手术组水平。藻蓝蛋白组MMP-9阳性细胞变化趋势与对照组相似，同一时间点相比明显低于对照组。结论藻蓝蛋白可能通过下调MMP-2和MMP-9的表达而减轻脑水肿，对脑缺血再灌注损伤具有保护作用。     

大鼠脑出血后MMP-2、MMP-9的表达与神经元凋亡关系的实验研究

目的 探讨脑出血后基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)的表达和血肿周围神经细胞凋亡发生情况之间的关系,以明确MMP-2、MMP-9对脑出血后神经细胞发生凋亡的贡献作用.方法 80只雄性Wistar大鼠按照出血后的时闻分成对照组和出血后6 h、12 h、1 d、2 d、3 d、6 d和10 d组,分别应用免疫组化和流式细胞仪方法检测血肿周围脑组织MMP-2、MMP-9的表达和神经细胞凋亡率,同时检测脑组织的含水量并进行脑出血动物的神经缺损评分,并统计这些指标的相关性.结果 MMP-9,细胞凋亡率,神经功能缺损评分和脑组织含水量的动态变化均一致,脑出血后6 h开始升高,2 d达到高蜂,10 d与对照组差异仍有统计学意义(P<0.05).而MMP-2则是脑出血后1 d开始升高,6 d达到高峰,10 d后开始下降,与细胞凋亡率,神经功能缺损评分和脑组织含水量无明显相关性.结论 神经细胞凋亡和脑组织含水量直接与神经功能缺损相关,而MMP-9的高表达则促进神经细胞的凋亡,脑组织含水量的增加.     

他莫昔芬对高血压脑出血模型大鼠早期脑损伤的神经保护作用研究

目的:研究他莫昔芬对高血压脑出血模型大鼠早期脑损伤的神经保护作用。方法:取大鼠随机分为假手术组、模型组和高、中、低剂量实验(他莫昔芬10、5、2.5 mg/kg)组,每组48只,除假手术组外其余各组大鼠建立高血压脑出血模型,建模后分别腹腔注射相应药物,每24 h给药1次。考察给药后4、8、12、24、72 h和7 d时各组大鼠血肿周围脑组织中Fas相关死亡域蛋白(FADD)的阳性细胞数、凋亡细胞数、脑水肿情况以及脑组织形态学变化情况。结果:与假手术组比较,其余各组大鼠不同时间的脑组织中FADD阳性细胞数、凋亡细胞数、脑水肿比例均明显增加(P<0.05);与模型组比较,低剂量实验组大鼠的FADD阳性细胞数(给药后24、72 h)、凋亡细胞数(给药后24、72 h和7 d)和脑组织含水量(给药后72 h)均明显减少(P<0.05),中、高剂量实验组大鼠的FADD阳性细胞数(给药后8、12、24、72 h)、凋亡细胞数(给药后12、24、72 h和7 d)和脑组织含水量(给药后12、24、72 h和7 d)均明显减少(P<0.05),各剂量实验组大鼠血肿周围组织水肿范围变小、程度减轻,炎症细胞的浸润减轻,固缩细胞减少,肿胀细胞增多,细胞周围间隙变小,且均呈剂量依赖性。结论:他莫昔芬能够呈剂量依赖性地抑制高血压脑出血模型大鼠的FADD阳性细胞表达,减少脑组织细胞的凋亡,同时减轻脑出血后的脑水肿,发挥显著的神经保护作用。     

MMP-9和咬合蛋白在弥漫性脑损伤大鼠皮层的表达变化及与脑水肿的关系

目的：观察弥漫性脑损伤大鼠脑水肿及损伤区皮层MMP-9和咬合蛋白表达的变化。方法成年健康SD雄性大鼠160只,按随机数字表法分为对照组（ n ＝60）和模型组（ n ＝100）。应用Marmarou’s法建立弥漫性脑损伤大鼠模型。2组分别于术后3、12、24、72、144 h行干湿重法检测2组大鼠脑组织含水量变化,行免疫组化和Western blot检测损伤区周围皮层MMP-9和咬合蛋白表达水平。对各结果进行相关性分析。结果与对照组比较,模型组各时间点大鼠脑组织含水量明显增加,脑组织损伤区周围皮层MMP-9表达明显增高（ P ＜0．05）,咬合蛋白表达明显降低（ P ＜0．05）。脑组织含水量变化与MMP-9表达变化呈正相关（ P ＜0．05）,脑组织含水量变化与咬合蛋白表达变化呈负相关（ P ＜0．05）,MMP-9蛋白表达变化与咬合蛋白表达变化呈负相关（ P ＜0．05）。结论弥漫性脑损伤发生后损伤区皮层MMP-9蛋白表达明显增加,咬合蛋白表达明显降低,脑水肿形成。 MMP-9表达的增加,导致了咬合蛋白破坏,脑水肿形成。     

尼莫地平对早期脑出血大鼠AQP4mRNA、MMP-9mRNA表达的影响

目的：探讨尼莫地平对早期脑出血周边组织AQP4mRNA、MMP-9mRNA表达及由脑出血引起的继发性脑水肿与AQP4、MMP-9的关系。方法：制做脑出血大鼠模型,分为假手术组,脑出血组及尼莫地平组,分别观察6h、1d、3d、5d、7d等5个时间点出血周边脑组织含水量、AQP4mRNA、MMP-9mRNA。结果：（1）脑出血组3d含水量达到高峰,第7天明显下降,但仍高于正常水平;尼莫地平组3d含水量达高峰,但低于脑出血组。（2）脑出血组AQP4mRNA、MMP-9mRNA的表达逐渐升高,3d达到高峰,7d明显下降,5个时间点明显高于假手术组。（3）尼莫地平组大鼠脑水肿程度、AQP4mRNA、MMP-9mRNA表达逐渐升高,3d达到高峰,明显低于脑出血组。（4）脑出血的水肿程度与AQP4mRNA、MMP-9mRNA呈正相关。结论：（1）AQP4、MMP-9参与了出血性脑水肿损伤的过程。（2）尼莫地平可以抑制AQP4、MMP-9的表达,进而减轻脑水肿的程度。     

阿加曲班对脑出血模型大鼠脑损伤的改善作用

目的:研究阿加曲班对脑出血模型大鼠脑损伤的改善作用。方法:取50只SD大鼠随机均分为正常对照(等量生理盐水)组、模型(等量生理盐水)组和阿加曲班低、中、高剂量(0.75、1.5、3 mg/kg)组,除正常对照组外其余各组大鼠复制脑出血模型。复制模型30 min后各组大鼠ip给予相应药物,每天1次,连续给药3 d。处死大鼠,检测各组大鼠脑组织中肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)含量,半胱氨酸天冬氨酸蛋白水解酶3(Caspase-3)活性,Bcl-2、Bax、基质金属蛋白酶2(MMP-2)、MMP-9蛋白表达和核转录因子κB(NF-κB)p65、IκBα的磷酸化水平。结果:与正常对照组比较,模型组大鼠脑组织中TNF-α、IL-1β含量增加,Caspase-3活性和MMP-2、MMP-9、Bax蛋白表达增强,Bcl-2蛋白表达减弱,NF-κB p65、IκBα磷酸化水平升高,差异均具有统计学意义(P<0.01)。与模型组比较,阿加曲班低、中、高剂量组大鼠脑组织中TNF-α、IL-1β含量减少,Caspase-3活性和MMP-2、MMP-9、Bax蛋白表达减弱,Bcl-2蛋白表达增强,NF-κB p65、IκBα磷酸化水平降低,差异均具有统计学意义(P<0.01或P<0.05),且与剂量呈正相关。结论:阿加曲班呈剂量依赖性地抑制脑出血模型大鼠炎症因子分泌及脑组织细胞凋亡,其作用可能与NF-κB信号通路有关。     

Changes in brain orexin levels in a rat model of depression induced by neonatal administration of clomipramine

Depression is associated with a deficiency of serotonergic neurons that have been found to suppress orexinergic neurons, which in turn activate these neurons in a feedback loop. This evidence suggests that orexins may be involved in the pathology of depression. Long Evans rats were treated with clomipramine (CLI) and saline (SAL) from postnatal days 8 through 21. One set of rats from both groups was sacrificed at 35 days of age for quantification of orexins in multiple brain regions. At 3-4 months of age a second set of rats was tested for immobility in a forced swim procedure, a common test for depressive signs in rats, and a third set was sacrificed for the quantification of orexins. Compared with the control rats, adult rats with neonatal CLI treatment had (1) increased forced swim immobility and (2) increased orexins A and B in the hypothalamus. However, both orexins A and B levels were decreased in multiple brain regions in the juvenile CLI rats compared with same-age controls. We concluded that although orexin levels were decreased in juvenile CLI rats, adult CLI rats with features of depression had significantly higher levels of hypothalamic orexins compared with adult controls. These results imply that orexins are likely to be involved in the pathological regulation of depression.     

Effects of naftidrofuryl oxalate on microsphere embolism-induced decrease in regional blood flow of rat brain.

1. The purpose of the present study was to determine whether naftidrofuryl oxalate (naftidrofuryl), a vasodilator, is capable of improving brain regional blood flow of animals in sustained ischaemia. 2. Cerebral ischaemia was induced by injecting 900 microspheres (48 microns in diameter) into the right internal carotid artery of rats. Cerebral blood flow of brain regions was measured by a hydrogen clearance method on the 3rd, 7th and 28th days after the onset of ischaemia. Ischaemic animals were treated with naftidrofuryl, 15 mg kg-1 day-1 i.p., from the first to 28th day. 3. Microsphere-embolism caused a sustained decrease in cortical and striatal blood flow over a period of 28 days, whereas hippocampal blood flow was decreased on the 3rd day but not on the 7th or 28th day. On the 3rd day, the striatal and hippocampal but not cortical blood flow of naftidrofuryl-treated, microsphere-embolized rats was higher than untreated rats. On the 7th and 28th days, the cortical and striatal blood flow of the treated and untreated animals did not differ. 4. Brain slices from microsphere-embolized rats contained areas, which were not stained with triphenyltetrazolium chloride (TTC), to a similar degree on the 3rd, 7th and 28th days, indicating the genesis of cerebral infarction. TTC-unstained areas of microsphere-embolized rats that had received naftidrofuryl treatment were smaller than those of untreated rats on the 3rd and 7th days, but not on the 28th day.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in 3H-spiperone, 3H-WB 4101 and 3H-dihydroalprenolol bindings to brain membranes produced by postnatal pretreatment with chlorpromazine in adult rats

In order to elucidate possible mechanisms of the learning deficit produced by postnatal pretreatment with chlorpromazine (CPZ), changes in catecholamine receptors in the rat brain were investigated. Male neonates of Wistar strain rats were given s.c. 2 mg/kg/day of CPZ for 7 successive days from days 6 to 12 after birth. Effect of the postnatal pretreatment with CPZ on saturation constants for specific bindings of 3H-spiperone, 3H-WB 4101 and 3H-dihydroalprenolol, respectively, in 8 brain regions was investigated at 60 days after birth. Significant decreases in Bmax values of 3H-WB 4101 binding sites in the cortex, thalamus, hypothalamus, mid brain and medulla oblongata/pons and decreases in Kd values of the binding sites in thalamus, hypothalamus and mid brain were observed in CPZ-pretreated rats when compared with corresponding Bmax and Kd values obtained in saline-pretreated rats. Furthermore, significant decreases in both Bmax and Kd values of 3H-DHA binding sites in the thalamus were detected in CPZ-pretreated rats when compared with those obtained in saline-pretreated rats. However, no alterations in 3H-spiperone binding sites in all brain regions were found between CPZ- and saline-pretreated rats. These results suggest that the learning deficit observed in CPZ-pretreated rats may be produced by a functional disorder of catecholaminergic, in particular alpha 1-noradrenergic neurons in the brain.     

Protective effect of Calendula officinalis Linn. flowers against 3-nitropropionic acid induced experimental Huntington’s disease in rats

Abstract

Oxidative stress (OS) and nitric oxide mechanisms have been recently proposed in 3-nitropropionic acid (3-NP)-induced neurotoxicity. The compounds, having antioxidant, anti-inflammatory and estrogenic effects, have been suggested for neuroprotection in different experimental models. Calendula officinalis Linn. flower extract (COE) is known for its potent antioxidant, anti-inflammatory, estrogenic and neuroprotective activities. Hence, the present study was designed to evaluate the neuroprotective effect of COE on 3-NP-induced neurotoxicity in rats by observing behavioral changes, OS and striatal damage in rat brain. Adult female Wistar rats were pretreated with vehicle or COE (100 and 200?mg/kg) for 7 days, followed by cotreatment with 3-NP (15?mg/kg, intraperitoneally) for the next 7 days. At the end of the treatment schedule, rats were evaluated for alterations in sensory motor functions and short-term memory. Animals were sacrificed and brain homogenates were used for the estimation of lipid peroxidation (LPO), glutathione, total thiols, glutathione S-transferase, catalase and nitrite. A set of brain slices was used for the evaluation of neuronal damage in the striatal region of the brain. 3-NP caused significant alterations in animal behavior, oxidative defense system evidenced by raised levels of LPO and nitrite concentration, and depletion of antioxidant levels. It also produced a loss of neuronal cells in the striatal region. Treatment with COE significantly attenuated behavioral alterations, oxidative damage and striatal neuronal loss in 3-NP-treated animals. The present study shows that COE is protective against 3-NP-induced neurotoxicity in rats. The antioxidant, anti-inflammatory and estrogenic properties of COE may be responsible for its neuroprotective action.     

Effects of delayed treatment with nafronyl oxalate on microsphere embolism-induced changes in monoamine levels of rat brain regions.

1. The present study was undertaken to examine the effects of delayed treatment with nafronyl oxalate (nafronyl), a cerebral vasodilator, on monoamine neurotransmitters of brain regions in the microsphere-embolized rat. 2. Microsphere embolism was induced by injecting 900 microspheres with a diameter of 48 microns into the right internal carotid artery of rats. Microsphere-embolized rats were treated with nafronyl, 15 mg kg-1, i.p., twice daily from the first to the 5th day. Levels of monoamines and their metabolites in the cerebral cortex, striatum, and hippocampus were measured on days 3 and 5 after the operation by a high-performance liquid chromatograph with electrochemical detection. In vivo tyrosine or tryptophan hydroxylation was estimated by measurement of the accumulation of 3, 4-dihydroxyphenylalanine or 5-hydroxy-1-tryptophan after administration of 3-hydroxybenzylhydrazine dihydrochloride, an inhibitor of aromatic L-amino acid decarboxylase. 3. Microsphere embolism induced decreases in dopamine, noradrenaline and 5-hydroxytryptamine in three brain regions of the right hemisphere on days 3 and 5. In the left hemisphere, the monoamines were reduced, but to a lesser degree than in the right hemisphere. On days 3 and 5, the decrease in the monoamines of the right hemisphere was attenuated by nafronyl treatment except for noradrenaline on day 3. The decrease in the monoamines levels in the left hemisphere was almost completely prevented by nafronyl treatment. 4. On day 3 after microsphere embolism, in vivo tyrosine and tryptophan hydroxylation was lower than the pre-embolic value in all three brain regions. Treatment of the embolized rats with nafronyl significantly attenuated the decrease in in vivo tyrosine and tryptophan hydroxylation in the ipsilateral hemisphere, but not hippocampal tryptophan hydroxylation. 5. The results suggested that treatment with nafronyl improves or attenuates changes in monoamine neurotransmitter metabolism of the brain regions impaired by microsphere embolism. The mechanisms underlying this effect may be attributed to preservation of the ability to synthesize monoamines when the brain is ischaemic or oligaemic.     

Effects of lithium on alterations of pharmacokinetics of imipramine and on the related changes of monoamines in rat brain

Rats were given chronically i.p. imipramine (20 mg/kg), LiCl (1 mg/kg) or both drugs to examine the effects of lithium (Li) on the alterations of imipramine pharmacokinetics in the whole brain and on the imipramine-related changes of norepinephrine (NE) and serotonin (5-HT) levels in the brain. When rats were given Li for 3 days, followed by a single injection of imipramine, the concentrations of desipramine in the brain and serum were higher than those in the vehicle-treated rat, although the imipramine concentrations in both tissues did not differ in Li- and in vehicle-treated rats. In rats receiving both drugs for 10 days, the steady state levels of imipramine and desipramine in the brain were the same as those in the vehicle-treated rats but the steady state level of desipramine was reached earlier with Li treatments presumably because of the enhanced demethylation of imipramine. Consequently, the desipramine-dependent alterations of NE and 3-methoxy-4-hydroxyphenylglycol levels in the brain appeared to be induced earlier and more markedly when Li was given simultaneously. As the 5-hydroxyindole acetic acid (5-HIAA) levels were elevated in the brains of Li-treated rats and reduced in brains of imipramine-treated rats as compared with the level in vehicle-treated rats, the 5-HIAA level in rats receiving both drugs was equivalent to that in vehicle-treated rats.     

三水胶囊对脑出血模型大鼠的治疗作用

目的 观察三水胶囊对大鼠急性脑出血后脑水肿的防治作用.方法 将大鼠随机分为假手术组、模型组、安宫牛黄丸组、三水胶囊(高、中、低剂量分别为30、15、7.5 g·kg-1)组.于术前3d至术后8d给药.用脑内注射自身股动脉血建立大鼠急性脑出血模型,分别采用行为学评分法和干湿质量法,比较各组大鼠的行为学得分和脑组织的含水量.结果 从第1天开始至实验结束,模型组大鼠的行为学得分均非常显著地高于假手术组;与模型组比较,第1天、第4天,各给药组大鼠的行为学得分无显著差异;与模型组比较,术后第8天,高、中剂量三水胶囊组大鼠的行为学得分非常显著地降低,低剂量组的显著降低.与假手术组比较,模型组大鼠的脑系数和脑组织中的含水量均非常显著地升高;与模型组比较,高、中剂量三水胶囊组大鼠的脑系数和脑组织中的含水量显著地降低,低剂量组的差异不明显.结论 三水胶囊对脑出血水肿有较好的防治作用.     

脂肪间充质干细胞分泌组对颅脑创伤后 大鼠脑水肿的影响

摘要：目的 探讨脂肪间充质干细胞分泌组（ASC-ST）对大鼠颅脑创伤（TBI）后继发脑水肿的影响及其潜在机 制。方法 将 70 只 SD 大鼠随机分为 Sham 组（n=18）、TBI 组（n=26）和 TBI+ST 组（n=26）。应用电子颅脑损伤仪 （eCCI）建立TBI大鼠模型,Sham组只开骨窗;TBI组经尾静脉注射0.3 mL生理盐水,TBI+ST组经尾静脉注射0.2 mL ASC-ST 和 0.1 mL 生理盐水,连续注射 7 d。在 TBI 后 3、7、14 和 21 d 对 TBI 和 TBI+ST 组 8 只大鼠行神经功能评分 （mNSS）;每组选取6只大鼠在TBI后3、7和14 d行头颅核磁（MRI）测量表观弥散系数（ADC）;采用干湿比重法测量脑 水含量并提取损伤周围脑组织总RNA,采用实时定量多聚酶链反应（qRT-PCR）检测肿瘤坏死因子（TNF）-α、白细胞 介素（IL）-1β和IL-6的mRNA 表达水平。结果 TBI 后14、21 d时,TBI+ST 组mNSS 评分均低于TBI 组（P＜0.05）。 TBI后3 d,TBI组和TBI+ST组损伤周围皮层（IC）和损伤对侧皮层（CC）的ADC值均高于Sham组（P＜0.05）;TBI后7 d,TBI+ST组IC和损伤侧海马（IH）的ADC值均低于TBI组（P＜0.05）;TBI后14 d,TBI+ST组IC和CC的ADC值均低于 TBI组（P＜0.05）。TBI后3 d和7 d,TBI+ST组大鼠脑组织水含量与TBI组差异无统计学意义（P＞0.05）;TBI后14 d, TBI+ST组大鼠脑组织水含量低于TBI组（P＜0.05）。TBI后3 d,Sham组大鼠损伤周围脑组织中IL-6表达显著低于 TBI组和TBI+ST组,TBI+ST组TNF-α表达显著低于Sham组和TBI组,TBI组高于Sham组;TBI+ST组与TBI组IL-1β 表达均低于Sham组（均P＜0.05）。TBI后7 d,TBI+ST组与Sham组IL-6表达均低于TBI组,TBI+ST组低于Sham组; TBI组TNF-α表达高于Sham组;TBI组IL-1β表达高于其余两组,Sham组高于TBI+ST组（均P＜0.05）。TBI后14 d, TBI+ST组与Sham组IL-6表达均低于TBI组;TBI+ST组TNF-α表达仍低于其他组;TBI组IL-1β表达仍高于其余两组 （均P＜0.05）。结论 ASC-ST可通过减少TBI后炎症反应和炎性因子表达,显著改善大鼠TBI后脑水肿状况和神经 功能预后,是一种具有较高临床推广价值的生物治疗药物。     

发育期大鼠高热惊厥脑损伤CO变化及Znpp对其影响

目的:研究锌原卟啉对大鼠高热惊厥脑损伤CO变化的影响及作用机制.方法:21日龄Wistar大鼠,随机分为对照组、高热未惊厥组、FC组及Znpp治疗组.采用热水浴诱导FC大鼠动物模型和Znpp治疗模型.用分光光度计检测各组大鼠脑组织匀浆和血浆CO含量,用HE染色观察大鼠海马神经元形态学改变.结果:FC组血浆CO含量明显升高,与对照组、高热未惊厥组及Znpp治疗组比较,有显著性差异(P＜0.01),Znpp治疗组血浆CO含量升高与高热未惊厥组比较,亦有显著性差异(P＜0.05);FC组脑组织匀浆CO含量增高,与对照组、高热未惊厥组及Znpp治疗组比较有显著性差异(P＜0.01),Znpp治疗组脑组织匀浆CO含量升高,与对照组、高热未惊厥组比较有显著性差异(P＜0.01),高热未惊厥组与对照组比较差异无显著性(P＞0.05);结论:FC能够引起脑损伤且CO水平增高, Znpp能够使CO水平下降,对脑损伤有保护作用.