Bilateral common carotid artery common trunk with aberrant right subclavian artery combined with right subclavian steal syndrome: A case report

BACKGROUND We report a rare case of numbness in the right hand,finally diagnosed as bilateral common carotid artery common trunk with aberrant right subclavian artery combined with right subclavian steal syndrome and explain the cause of these diseases.CASE SUMMARY The patient was a 65-year-old woman.She complained of dizziness,numbness and weakness of the right hand for 6 mo.She was diagnosed with bilateral common carotid artery common trunk with aberrant right subclavian artery combined with right subclavian steal syndrome by ultrasound,enhanced computed tomography,computed tomography angiography and other examinations.Considering the surgical risks,the patient refused the aberrant right subclavian artery stent implantation and was discharged.We hypothesize that these two kinds of deformity and right subclavian steal syndrome may not occur by accident and result from multiple malformations.CONCLUSION Bilateral common carotid artery common trunk with aberrant right subclavian artery combined with right subclavian steal syndrome is rare.This case reminds interventional radiologists of the possibility of these abnormalities before surgery.

Mechanism underlying the protective effect of Kaixin Jieyu Fang on vascular depression following cerebral white matter damage

The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter damage by ligation of the bilateral common carotid arteries. Rats received daily intragastric administration of a suspension of Kaixin ]ieyu Fang powder. After 3, 7 and 21 days of treatment, the degree of white matter damage in the cerebral ischemia rat model was alleviated, Bcl-2 protein and mRNA expression in brain tissue increased, and Bax protein and mRNA expression decreased. These results indicate that Kaixin Jieyu Fang can alleviate cere- bral white matter damage, and the underlying mechanism is associated with regulation of Bcl-2/ Bax protein and mRNA expression, which is one of possible mechanism behind the protective effect of Kaixin Jieyu Fang against vascular depression.

Information entropy-based fitting of the disease trajectory of brain ischemia-induced vascular cognitive impairment

The present study investigated the disease trajectory of vascular cognitive impairment using the entropy of information in a neural network mathematical simulation based on the free radical and excitatory amino acids theories. Glutamate, malondialdehyde, and inducible nitric oxide synthase content was significantly elevated, but acetylcholine, catalase, superoxide dismutase, glutathione peroxidase and constitutive nitric oxide synthase content was significantly decreased in our vascular cognitive impairment model. The fitting curves for each factor were obtained using Matlab software. Nineteen, 30 and 49 days post ischemia were the main output time frames of the influence of these seven factors. Our results demonstrated that vascular cognitive impairment involves multiple factors. These factors include excitatory amino acid toxicity and nitric oxide toxicity. These toxicities disrupt the dynamic equilibrium of the production and removal of oxygen free radicals after cerebral ischemia, reducing the ability to clear oxygen free radicals and worsening brain injury.

川芎-天麻对血管性认知障碍大鼠学习记忆的改善作用研究

为探讨川芎-天麻提取物对血管性认知障碍(VCI)大鼠学习记忆的改善作用及机制。本研究采用两血管阻断法(Two-vessel occlusion,2-VO)复制VCI模型,造模成功后随即分为模型组、阳性药组、高剂量组、低剂量组和假手术组。假手术组、模型组灌服蒸馏水,阳性药组灌服0.45 mg/(kg·d)盐酸多奈哌齐,高、低剂量组分别以3 g/(kg·d)、1.5 g/(kg·d)灌服提取物,给药56 d后,水迷宫和社交行为检测各组大鼠行为学;ELISA法检测乙酰胆碱含量和乙酰胆碱脂酶活性。结果表明,与假手术组比较,模型组大鼠空间学习记忆能力、探索能力和社交能力下降;水迷宫试验结果显示,逃避潜伏期明显延长(P <0.01),穿越平台次数明显缩短(P <0.01);社交行为结果显示,接触时间和接触次数显著减少(P<0.05);脑内乙酰胆碱表达水平下调,乙酰胆碱酯酶活力值表达水平上调(P<0.05)。与模型组比较,高剂量组大鼠空间学习记忆能力、探索能力和社交能力明显改善,表现为逃避潜伏期明显缩短,穿越平台次数及在原平台停留时间均明显增加,社交接触时间和接触次数显著增加(P<0.05)。脑内乙酰胆碱表达水平上调和乙酰胆碱酯酶表达水平下调(P <0.05)。川芎-天麻提取物可干预大鼠脑内乙酰胆碱表达,改善VCI大鼠学习与记忆能力。

采用流式细胞分选术区分中枢神经系统内小胶质细胞和浸润巨噬细胞

目的建立通过流式细胞分选术区分中枢神经系统内小胶质细胞和浸润巨噬细胞的方法。方法用成年C57BL/6小鼠建立双侧颈总动脉狭窄模型,分别采用集落刺激因子1受体抑制剂PLX5622或氯膦酸盐脂质体处理。将分离、匀浆、重悬后的小鼠脑和脊髓组织进行Percoll密度梯度离心,得到单核细胞悬液。采用CD45、CD11b和淋巴细胞抗原6家族成员C(Ly6C)抗体进行流式分选,获得小胶质细胞(CD11b^(+)CD45^(low)Ly6C^(-)细胞)和浸润巨噬细胞(CD11b^(+)CD45^(high)Ly6C^(+)细胞),并验证PLX5622和氯膦酸盐脂质体2种给药范式获得的处理效果。结果通过CD45、CD11b和Ly6C抗体可以有效区分中枢神经系统中小胶质细胞和浸润巨噬细胞。与对照组比较,PLX5622处理后小胶质细胞数量减少(P=0.001),而氯膦酸盐脂质体处理后浸润巨噬细胞数量减少(P<0.001)。结论所建立的流式细胞分选方法可有效区分中枢神经系统中小胶质细胞和浸润巨噬细胞,PLX5622和氯膦酸盐脂质体2种给药范式可分别选择性清除中枢神经系统内的小胶质细胞和浸润巨噬细胞。

Possible mechanisms of lycopene amelioration of learning and memory impairment in rats with vascular dementia

Oxidative stress is involved in the pathogenesis of vascular dementia. Studies have shown that lycopene can significantly inhibit oxidative stress;therefore, we hypothesized that lycopene can reduce the level of oxidative stress in vascular dementia. A vascular dementia model was established by permanent bilateral ligation of common carotid arteries. The dosage groups were treated with lycopene(50, 100 and 200 mg/kg) every other day for 2 months. Rats without bilateral carotid artery ligation were prepared as a sham group. To test the ability of learning and memory, the Morris water maze was used to detect the average escape latency and the change of search strategy. Hematoxylin-eosin staining was used to observe changes of hippocampal neurons. The levels of oxidative stress factors, superoxide dismutase and malondialdehyde, were measured in the hippocampus by biochemical detection. The levels of reactive oxygen species in the hippocampus were observed by dihydroethidium staining. The distribution and expression of oxidative stress related protein, neuron-restrictive silencer factor, in hippocampal neurons were detected by immunofluorescence histochemistry and western blot assays. After 2 months of drug administration,(1) in the model group, the average escape latency was longer than that of the sham group, and the proportion of straight and tend tactics was lower than that of the sham group, and the hippocampal neurons were irregularly arranged and the cytoplasm was hyperchromatic.(2) The levels of reactive oxygen species and malondialdehyde in the hippocampus of the model group rats were increased, and the activity of superoxide dismutase was decreased.(3) Lycopene(50, 100 and 200 mg/kg) intervention improved the above changes, and the lycopene 100 mg/kg group showed the most significant improvement effect.(4) Neuron-restrictive silencer factor expression in the hippocampus was lower in the sham group and the lycopene 100 mg/kg group than in the model group.(5) The above data indicate that lycopene 100 mg/kg could protect against the learning-memory ability impairment of vascular dementia rats. The protective mechanism was achieved by inhibiting oxidative stress in the hippocampus. The experiment was approved by the Animal Ethics Committee of Fujian Medical University, China(approval No. 2014-025) in June 2014.

Xiao-Xu-Ming decoction extract regulates differentially expressed proteins in the hippocampus after chronic cerebral hypoperfusion

Xiao-Xu-Ming decoction has been widely used to treat stroke and sequelae of stroke. We have previously shown that the active fractions of Xiao-Xu-Ming decoction attenuate cerebral ischemic injury. However, the global protein profile and signaling conduction pathways regulated by Xiao-Xu-Ming decoction are still unclear. This study established a two-vessel occlusion rat model by bilateral common carotid artery occlusion. Rats were intragastrically administered 50 or 150 mg/kg Xiao-Xu-Ming decoction for 4 consecutive weeks. Learning and memory abilities were measured with Morris water maze. Motor ability was detected with prehensile test. Coordination ability was examined using the inclined screen test. Neuronal plasticity was observed by immunofluorescent staining. Differentially expressed proteins of rat hippocampus were analyzed by label-free quantitative proteomics. Real time-polymerase chain reaction and western blot assay were used to identify the changes in proteins. Results showed that Xiao-Xu-Ming decoction dramatically alleviated learning and memory deficits, and motor and coordination dysfunction, and increased the expression of microtubule-associated protein 2. Xiao-Xu-Ming decoction extract remarkably decreased 13 upregulated proteins and increased 39 downregulated proteins. The regulated proteins were mainly involved in oxidation reduction process, intracellular signaling cascade process, and protein catabolic process. The signaling pathways were mainly involved in ubiquitin mediated proteolysis and the phosphatidylinositol signaling system. Furthermore, there was an interaction among Rab2 a, Ptpn1, Ppm1 e, Cdk18, Gorasp2, Eps15, Capza2, Syngap1 and Mt-nd1. Protein analyses confirmed the changes in expression of MTND1. The current findings provide new insights into the molecular mechanisms of Xiao-Xu-Ming decoction extract's effects on chronic cerebral hypoperfusion.

Neuroprotective effects of kaempferol against 2VO-induced chronic cerebral ischemia in rats

OBJECTIVE To investigate the effects of kaempferol(KAE)on chronic cerebral ischemia in rats.METHODS Chronic cerebral ischemia was induced in rats by permanent occlusion of bilateral common carotid arteries(2VO).Then,the rats with chronic cerebral ischemia were randomly divied into three groups:model group,KAE 10 and 30 mg·kg-1group.Another group rats without occlusion of common carotid arteries were used as the sham-operation group.Memory behavior was investigated by Morris water maze test.Prehensile ability was investigated by prehensile traction test.The structure of hippocampus and cortex neurons was observed with Nissel staining.In addition,the SOD activity and MDA content in brain tissue were determined.The DJ-1protein level was determined by Western blotting.RESULTS KAE 10 and 30 mg·kg-1could significantly improve cognitive impairment and prehensile traction ability(P<0.01)induced by chronic cerebral ischemia in rats.The results of the pathological analysis also suggested that KAE could ameliorate the pathological damage induced by chronic cerebral ischemia.In addition,KAE 30 mg·kg-1significantly increased the activity of SOD(P<0.05),but had no effect on the content of MDA in rat brain tissue.Western-blotting confirmed that KAE 10 and30 mg·kg-1could increase the expression of anti-oxidation proteins DJ-1 in hippocampus(P<0.01).CONCLUSION KAE may attenuate the chronic cerebral ischemic injury in rats.

Curcumin alters expression of glial fibrillary acidic protein and nestin following chronic cerebral ischemia

Astrocytes can alter their appearance and become reactive following chronic cerebral ischemia. In the present study, a rat model of chronic cerebral ischemia was treated with 50 and 100 mg/kg curcumin. Results showed that pathological changes of neuronal injury in hippocampal CA1 area of rats induced by chronic cerebral ischemia were attenuated, as well as upregulated expression of glial fibriliary acidic protein and nestin, in a dose-dependent manner.

自发性高血压和持续低灌流模型大鼠记忆能力与脑组织病理学对比研究

目的采用自发性高血压大鼠(SHR)与持续双侧颈总动脉结扎(2-VO)Wistar大鼠制作血管性痴呆(VD)模型,通过观察大鼠记忆能力及脑组织病理学改变,探讨VD的可能机制。方法将10只自发性高血压大鼠作为高血压对照组(SHR对照组);30只Wistar大鼠随机分为Wistar手术组、Wistar假手术组及Wistar对照组,其中Wistar手术组实施双侧颈动脉结扎手术。采用Morris水迷宫观察大鼠的空间记忆能力,HE染色观察大鼠前额叶、颞叶、海马、丘脑等脑区神经细胞形态,固蓝(LFB)染色观察脑室周围白质改变,并计量神经纤维髓鞘脱失情况。结果8月龄Wistar手术组、SHR对照组大鼠记忆功能较Wistar假手术组、Wistar对照组明显下降(P<0.01),而Wistar手术组较SHR对照组又有所下降(P>0.01)。在各脑区及脑室周围白质区,Wistar手术组、SHR对照组与Wistar假手术组、Wistar对照组比较,前两组神经元和髓鞘脱失明显(P<0.05);在前额叶、海马、丘脑等脑区,Wistar手术组与SHR对照组比较,前者神经元脱失明显(P<0.05),而在颞叶区神经元及脑室周围白质区,两组脱失程度无统计学差异(P>0.05)。结论自发性高血压大鼠或Wistar大鼠接受双侧颈总动脉结扎均可制备理想的血管性痴呆模型。慢性持续低灌流及高血压均可导致神经元数量减少、髓鞘脱失,神经功能受损。与高血压比较,持续低灌流对神经组织及功能的损伤更重。实验条件下,血管性痴呆的发生与神经元数量减少、髓鞘脱失等原因有关。

慢性脑缺血痴呆大鼠神经细胞凋亡的研究

目的:探讨细胞凋亡在慢性脑缺血导致大鼠痴呆中的作用。方法:Wister大鼠100只,雌雄各半,体质量350～400g。结扎大鼠双侧颈总动脉制备慢性脑确血致痴呆大鼠(vasculardementia,VD)模型;应用脱氧尿嘧啶缺口末端标记法(TUNEL)染色、流式细胞术及琼脂糖凝胶电泳方法检测VD大鼠的脑神经细胞凋亡情况。结果:流式细胞术检查发现额叶、海马在双侧颈总动脉结扎1周时细胞凋亡率分别为8.18%,21.92%;纹状体区2周时细胞凋亡率最高为9.22%,均明显高于对照组的2.84%,3.72%,2.18%(P<0.01),以后均逐渐下降。脑缺血一两周时TUNEL染色及额叶、海马及尾状核神经细胞凋亡明显高于对照组,4周以后与对照组差别不明显。琼脂糖凝胶电泳未见典型的细胞凋亡“梯形条带”。结论:神经细胞凋亡在大鼠双侧颈总动脉结扎后早期明显,晚期无明显改变。

脑卒中后抑郁症动物模型的建立与评价

目的探讨脑卒中后抑郁(PSD)的大鼠模型建立的可行性和有效性。方法采用双侧颈总动脉永久性结扎后予以行为限制制作PSD大鼠模型,观察大鼠自发性行为改变,海马区单胺类神经递质的变化。结果模型组大鼠水平运动得分、垂直运动得分、清洁动作次数分别为(25.00±9.76)次/5min、(13.33±4.13)次/5min、(1.00±0.89)次/5min,与假手术组比较下降(P<0.01or0.05),海马区5-HT、5-HIAA、DA、NE水平分别为(0.39±0.11)μg/g、(1.01±0.78)μg/g、(0.44±0.15)μg/g、(0.35±0.18)μg/g,与假手术组比较下调(P<0.05)。盐酸氟西汀可以改善卒中后抑郁大鼠的行为及脑内5-HT水平。结论大鼠双侧颈总动脉永久性结扎结合行为限制,可为卒中后抑郁的实验及临床研究提供较为理想的动物模型。

参麻益智方对双侧颈动脉结扎大鼠海马认知功能的影响

目的观察参麻益智方对双侧颈动脉结扎大鼠行为学及星形胶质细胞和小胶质细胞的影响。方法将60只Wistar大鼠随机分为假手术组(Sham)、双侧颈动脉结扎组(2-VO)、多奈哌齐组(0.5 mg/kg)、中药低剂量组(3.3 mg/kg)、中药中剂量组(6.6 mg/kg)和中药高剂量组(16.5 mg/kg),每组10只。灌胃给药4周后进行水迷宫实验,并观察海马CA1区星形胶质细胞及小胶质细胞的形态改变。结果 2-VO组大鼠逃避潜伏期较Sham组明显延长(P<0.05),目标象限停留时间百分比明显下降(P<0.05);多奈哌齐组及中药高剂量组、中剂量组大鼠逃避潜伏期较2-VO组明显缩短(P<0.05),目标象限停留时间百分比显著延长(P<0.05)。2-VO组大鼠海马CA1区星形胶质细胞及小胶质细胞较Sham组增多,胞体增大。给药后,多奈哌齐组与中药高剂量组、中剂量组星形胶质细胞及小胶质细胞较2-VO组数量减少,胞体变小。结论参麻益智方可改善大鼠学习记忆能力,减轻双侧颈动脉硬化大鼠海马CA1区星形胶质细胞和小胶质细胞的增生和激活,从而改善大鼠认知功能。

山奈酚对慢性脑缺血大鼠学习记忆能力的影响及机制探讨

目的探讨山奈酚(kaempferol,KAE)对慢性脑缺血大鼠的作用及其机制。方法采用双侧颈总动脉永久性结扎(bilateral common carotid arteries occlusion,2VO)建立大鼠慢性脑缺血动物模型;Morris水迷宫、抓握实验检测大鼠行为学;尼氏染色及HE染色观察脑组织病理改变;比色法检测MDA含量和SOD活性;Western blot检测脑组织DJ-1蛋白表达水平。结果与2-VO模型组比较,KAE明显改善慢性脑缺血诱导的学习记忆障碍和抓握能力损伤。此外,KAE明显减轻2VO大鼠脑组织病理损伤,增高脑组织中SOD活性,提高海马和皮层中抗氧化蛋白DJ-1的表达水平。结论KAE明显改善慢性脑缺血诱导的大鼠认知功能障碍、四肢平衡能力障碍及病理损伤,其机制可能与提高体内抗氧化系统有关。

新生鼠半球性脑缺血的实验模型

结扎并低氧处理7日龄大鼠右侧颈总动脉制备半球性脑缺血损伤模型。动物损伤后5—10min。大部份出现短暂的自发性向右旋转。24小时后,右侧大脑半球出现典型的脑缺血病理特征,如脑水肿、脱氢酶活力受抑制。说明该侧半球脑缺血已经发生。本方法具有动物死亡率低,脑缺血发生率高,有明显的行为指征出现等优点。

双侧颈总动脉结扎致大鼠脑血流低灌注不同时程的神经功能障碍和病理学变化

目的比较大鼠双侧颈总动脉结扎后不同时程的神经功能障碍、脑组织大体病理/显微病理和血清学炎性指标的变化。方法将SPF级Wistar大鼠麻醉后,施行永久性双侧颈总动脉结扎术。造模成功的大鼠按随机数字表分为术后2周、4周和6周共3组,每组10只。同时设立假手术组,大鼠10只,操作方法同模型组,但只穿线不结扎。分别于术后2周、4周和6周对大鼠进行神经功能检测,然后腹主动脉取血,采用ELISA法检测血清白细胞介素6(interleukin-6,IL-6)、白细胞介素1β(interleukin-1β,IL-1β)和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)含量。采用脑组织TTC染色法评价脑缺血范围,HE染色后进行显微镜下脑组织形态学观察。结果与假手术组比较,双侧颈总动脉结扎后2周组、4周组和6周组大鼠的神经功能评分明显降低(P<0.05);与2周组比较,4周组和6周组大鼠的神经功能评分下降明显(P<0.05)。血清炎性指标检测发现,与假手术组比较,不同时程模型组大鼠的IL-6水平明显升高(P<0.05),其余两个指标的差异无统计学意义(P> 0.05)。大鼠脑组织病理学观察显示,与假手术组比较,双侧颈总动脉结扎后2周组、4周组和6周组大鼠的脑组织缺血范围随时程延长而增加,脑组织形态也都有不同程度的损伤和炎性浸润。结论大鼠双侧颈总动脉结扎后脑组织病理改变由缺血发展到梗死灶出现,并伴随神经功能障碍,随时程的延长而变化不同,应根据药物作用机制选择干预时机。

雌激素对慢性低灌注大鼠血脑屏障通透性的影响

目的检测大鼠永久性双侧颈总动脉结扎（pBCCAO）早期脑组织伊文思蓝（EB）的含量、大鼠海马和脉络丛ZO-1的表达变化，以及17β-雌二醇（E2）对其影响，旨在揭示血管性痴呆（VD）早期血脑屏障通透性的变化，并探索可能的防治措施。方法成年雌性大鼠去双侧卵巢，7d后制备pBCCAO模型，随机分为控制组，pBCCAO后6h、1d．3d、7d实验组，E2处理组和溶剂对照组，采用比色分析法及激光共聚焦显微镜技术检测脑组织EB含量，Western blot技术及共聚焦显微镜技术观察ZO-1蛋白水平。结果大鼠行pBCCAO后1d脑组织EB渗出量较sham组明显升高，于第3天达到高峰，术后7d明显下降，但仍高于sham组；共聚焦结果显示，pBCCAO后3d大鼠海马槽EB红色荧光较sham组和E2组明显增强；Western blot结果显示，pBCCAO后3d大鼠海马中ZO-1较sham组明显降低，但E2处理组与sham组相似，ZO-1水平明显高于溶剂对照组；共聚焦结果显示，pBCCAO后3d脉络丛ZO-1免疫反应较sham组和E2处理组明显降低。结论pBCCAO早期即可造成大鼠血脑屏障损伤，下调ZO-1的表达；E2可有效改善此病理变化。

双侧颈动脉前向灌注在急性A型主动脉夹层合并单侧颈总动脉闭塞外科治疗中的应用

目的在急性Stanford A型(A型)主动脉夹层合并单侧颈动脉闭塞患者手术治疗中,通过改进传统手术、体外循环插管等方式,实施患者术中双侧颈动脉前向血流灌注、行闭塞侧颈动脉人工血管置换,以探索减少此类高危患者神经系统并发症的有效措施。方法本队列回顾性分析2017年9月至2019年2月,于广东省人民医院同期行主动脉夹层矫治以及颈动脉人工血管置换的5例急性A型主动脉夹层合并单侧颈动脉闭塞患者的临床资料。本组患者均行Bentall或Wheat合并主动脉弓部血管岛状吻合、术中降主动脉直接植入、患侧颈总动脉灌注及人工血管置换术(两例为右、三例为左侧颈总动脉闭塞),体外循环均行右腋动脉、股动脉、病变闭塞侧颈总动脉远端(近端颈总动脉结扎、远端颈总动脉与人工血管端-端吻合后直接与体外循环一分支动脉灌注)插管,后行患侧颈总动脉人工血管近端与升主动脉人工血管吻合完成主动脉-患侧颈总动脉血运重建;术中持续行双侧脑灌注,降主动脉支架植入过程暂停经股动脉血流灌注,待支架释放、固定后于人工支架内植入隔离球囊恢复全身循环。分析此5例A型主动脉夹层合并单侧颈动脉闭塞的患者基本资料及临床数据。结果5例患者中4例为男性,年龄(52±12.4)岁,体质量(65.9±11.9)kg,发病至手术时间(9.6±7.1)d,体外循环时间(262.6±37.3)min,主动脉阻断时间(148.2±27.1)min,下半身停循环时间(19.2±10.2)min,术后呼吸机使用时间(82±56.1)h,术后重症监护病房停留时间(8.4±4.0)d,术后住院时间(不包括重症监护病房停留时间)(22.6±10.3)d;术后随访时间(17.6±7.4)个月。患者经计算机断层扫描复查显示血运重建良好,无神经系统及其他主要并发症发生。结论急性A型夹层合并单侧颈动脉闭塞患者外科治疗风险、神经系统并发症发生率高,经过早期针对闭塞颈总动脉行双侧脑灌注的体外循环和手术策略的改进,可以使神经系统并发症发生率降低,手术效果得到提高,是针对此类患者安全有效的外科干预策略。

智复欣防治血管性认知障碍的作用机理研究

目的:评价智复欣对血管性认知障碍大鼠的治疗作用并探讨其相关作用机制。方法:大鼠分2次结扎双侧颈总动脉(2-VO),造模后1个月,将动物随机分为假手术组、模型组、多奈哌齐阳性对照组及智复欣高、中、低剂量组。连续给药8 w,然后采用Morris水迷宫法测定其学习、记忆能力;取脑组织进行组织病理学检查并检测其中乙酰胆碱酯酶(ACh E)、乙酰胆碱(ACh)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平;同时还考察了药物对ACh E的直接作用和对过氧化氢损伤PC12细胞的作用。结果:智复欣能显著缩短脑缺血大鼠在定位航行实验中的潜伏期,增加其在空间探索实验中进入平台的次数,并能显著增加脑缺血大鼠脑组织的神经细胞数量,降低脑组织ACh E、MDA水平,升高ACh、SOD水平。较高浓度的智复欣在体外对电鳗乙酰胆碱酯酶有微弱的抑制作用。智复欣体外对过氧化氢引起的PC12细胞损伤具有良好的保护作用。结论:智复欣能改善血管性认知障碍大鼠的认知功能,其作用机制可能与通过抗氧化等作用减少脑组织在缺血、缺氧条件下神经元的丢失有关。

开心解郁方对慢性脑白质损害大鼠中枢神经系统免疫激活的抑制作用

目的:研究开心解郁方对慢性脑白质损害大鼠认知功能、局部脑血流(rCBF)、额叶脑组织中前炎症细胞因子和脂质过氧化的作用,为培元开郁法治疗血管性抑郁症提供科学依据。方法:双侧颈总动脉结扎(LBCCA)制备慢性脑白质损害模型,分别在术后3,7,21 d,采用水迷宫法测定认知功能,激光多普勒血流仪测定rCBF,液相芯片技术测定额叶组织白介素-6(IL-6)、白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)蛋白含量,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活力,硫代巴比妥酸法测定丙二醛(MDA)含量。结果:与假手术组比较,模型组大鼠术后3 d额叶IL-1β、IL-6显著升高(P<0.05或0.001),水迷宫逃避潜伏期显著延长(P<0.05),额叶和顶叶皮质rCBF显著降低(P<0.05);术后7 d额叶IL-1β显著升高(P<0.05);术后21 d额叶MDA含量显著升高(P<0.05)。与模型组比较,开心解郁方组大鼠术后3 d额叶IL-6含量显著降低(P<0.01);术后7 d额叶皮质rCBF显著升高(P<0.01);术后21 d额叶IL-1β和MDA含量显著降低(P<0.001或0.01)。开心解郁方对大鼠认知功能和额叶组织SOD活力无显著影响。结论:开心解郁方对慢性脑白质损害的作用可能与改善脑缺血、抑制中枢神经系统脂质过氧化和免疫过度激活引起的前炎症细胞因子异常升高有关。