首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 234 毫秒
1.
BACKGROUND: The stellate ganglion block (SGB) plays a protective role in focal cerebral ischemia/reperfusion injury. The human SGB can be simulated by transection of the cervical sympathetic trunk (TCST) in rats. OBJECTIVE: To observe the effects of TCST on inducible nitric oxide synthase (iNOS) levels and cerebral infarct volume in the hippocampus of rats with cerebral ischemia/reperfusion injury, and to analyze the mechanism of action. DESIGN, TIME AND SETTING: A completely randomized, controlled, neuropathological experiment was performed at the Institute of Neurological Disease, Taihe Hospital, Yunyang Medical College between March and September 2006. MATERIALS: A total of 93 Wistar rats, aged 1718 weeks, of either gender, were used for this study. 2, 3, 5-triphenyl tetrazolium chloride was purchased from Changsha Hongyuan Biological Reagent Company China. Rabbit iNOS antibody and goat anti-rabbit IgG antibody were the products of Wuhan Boster Biological Reagent Co., Ltd., China. METHODS: Ten rats were randomly selected for the sham-operated group. Cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion (MCAO) using the suture method in the remaining rats. Forty successful rat models were randomly and equally divided into the following two groups: (1) TCST group: subsequent to TCST, MCAO was performed for 2 hours, followed by 24 hours reperfusion; (2) model group: rats underwent experimental procedures similar to the TCST group, with the exception of TCST. Rats in the sham-operated group were subjected to experimental procedures similar to the model group; however, the thread was only introduced to a depth of 10 mm. MAIN OUTCOME MEASURES: Following 24 hours of reperfusion, functional neurological deficits were scored. Brain tissue sections from ten rats of each group were used to measure cerebral infarct volume by TTC staining. Hippocampal tissue sections of an additional ten rats from each group were used to detect iNOS levels using the s  相似文献   

2.
BACKGROUND: Cerebral ischemia/reperfusion injury has been shown to induce inflammatory reactions, including white blood cell activation and adhesion molecule expression. These reactions often lead to aggravated neuronal injury. OBJECTIVE: To observe corticocerebral pathology, as well as ultrastructural changes, in a rat model of focal cerebral ischemia/reperfusion injury through optical and electron microscopy, and to investigate interventional effects of "Xingnao Kaiqiao" acupuncture (a brain-activating and orifice-opening acupuncture method). DESIGN, TIME AND SETTING: A randomized, controlled, neuropathology, animal experiment was performed at the Laboratory of Molecular Biology, First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine between April and June 2004. MATERIALS: A total of 50 healthy, male, Wistar rats were randomized into 5 groups, with 10 rats per group: control, sham-operated, model, non-acupoint, and "Xingnao Kaiqiao ". Transmission electron microscope (TEM 400ST) was provided by Philips, Netherlands. Electro-acupuncture treatment apparatus (KWD-8082) was provided by Changzhou Wujin Great Wall Medical Instrument, China. METHODS: Focal cerebral ischemia/reperfusion injury was induced by occlusion of the middle cerebral artery in the model, non-acupoint, and "Xingnao Kaiqiao" groups. Rats from the control group did not undergo any treatment. The sham-operated group received identical experimental procedures as the model group, except that the nylon suture was not inserted into the right internal carotid artery. At 1, 3, 6, and 12 hours following focal cerebral ischemia/reperfusion injury induction, rats from the Xingnao Kaiqiao group underwent 1-minute acupuncture at the bilateral "Neiguan" (PC 6) acupoint, using a reducing method of lifting-thrusting and twirling-rotating. Subsequently, the rats were subjected to acupuncture at the "Renzhong" (DU26) acupoint 10 times by a heavy bird-pecking method. The non-acupoint group  相似文献   

3.
BACKGROUND: Ligustrazine can reduce the production of free radicals and the content of malonaldehyde, and improve the enzymatic activity of adenosine-triphosphate in cerebral anoxia. It also can increase the expression of heat shock protein-70 and Bcl-2, thus alleviating brain tissue injury caused by cerebral ischemia/reperfusion. This study aimed to address the question of whether ligustrazine can protect the membrane structure of neurons. OBJECTIVE: To establish rat models of cerebral ischemia/reperfusion, observe the membrane structure and main organelles of neurons with electron microscope after ligustrazine intervention, and to analyze the dose-dependent effects of ligustrazine on neuronal changes. DESIGN: A randomized controlled study. SETTING: Department of Anatomy Research and Electron Microscopy, Hebei North University. MATERIALS: Forty Wistar rats of SPS grade, weighing 180-250 g and equal proportion of female and male, were provided by Hebei Medical University Animal Center (No. 060126). The ligustrazine injection (40 g/L, No. 05012) was produced by Beijing Yongkang Yaoye. LKB4 Ultramicrotome was purchased from LKB Company in Sweden. JEM100CXII electron microscope was purchased from JEOL in Japan. METHODS: The experiment was performed in the Laboratory of the Department of Anatomy and Electron Microscopy, Hebei North University from June to August 2006. (1) Wistar rats were allowed to adapt for 3 days, and were then randomly divided into four groups, according to the numeration table method: normal group, model group, low-dose ligustrazine group, and high-dose ligustrazine group. There were 10 rats in each group. (2)Rats in the model group, low-dose ligustrazine group, and high-dose ligustrazine group underwent cerebral ischemia/reperfusion model, according to Bannister's method. The carotid artery was opened for reperfusion after 90 minutes of cerebral ischemia. Samples were collected from the cerebral cortex after 24 hours. Animals from the ligustrazine low-dose group  相似文献   

4.
5.
BACKGROUND: Recent studies have suggested that mitochondrial ATP-sensitive K+ channel openers could reduce myocardium infarct size, and protect the function of the mitochondria. OBJECTIVE: To investigate the changes of cerebral infarction volume and the activity of marker enzymes in brain mitochondria of rats given the ATP-sensitive K+ channel opener, nicorandil, before focal cerebral ischemia/reperfusion (I/R). DESIGN, TIME AND SETTING: Randomized, controlled animal experiment, completed at the Brain Scientific Research Center of the Affiliated Hospital of Qingdao University from July to November 2007. MATERIALS: Sixty healthy male Wistar rats weighing 280-300 g. Nicorandil, 5-hydroxydecanoate (5-HD) and cytochrome C were purchased from Sigma in the USA. Standard malondialdehyde (MDA) and protein were purchased from Nanjing Jiancheng Biotechnology Institute. METHODS: Sixty rats were randomly divided into a sham operation group, a middle cerebral artery occlusion (MCAO) group, a nicorandil group and a nicorandil+5-HD group. MCAO for 2 hours was performed in the MCAO group, nicorandil group and nicorandil+5-HD group. A total of 5 mL saline were given to the MCAO group before MCAO. The nicorandil group was injected with the ATP-sensitive K+ channel opener nicorandil 10 mg/kg intraperitoneally 30 minutes before MCAO. The nicorandil+5-HD group was injected with 5-HD 10 mg/kg intravenously 15 minutes before the same treatment as the nicorandil group. MAIN OUTCOME MEASURES: Infarct volume by total brain slice calculation, activities of succinate dehydrogenase (SDH) and cytochrome oxidase (CO), and content of MDA were observed at 22 hours of reperfusion after 2 hours MCAO. RESULTS: Sixty rats were included in the final analysis, without any loss. (1) Infarct volume: compared with the MCAO group and nicorandil+5-HD group, the percentage of infarct volume was significantly decreased in the nicorandil group (P 〈 0.01). (2) The content of MDA, expression of  相似文献   

6.
BACKGROUND: Recently, grape seed procyanidin (GSP) has been shown to be exhibit antioxidant effects, effectively reducing ischemia/reperfusion injury and inhibiting brain cell apoptosis. OBJECTIVE: To study the effects of GSP on nerve growth factor (NGF) expression and neurological function following cerebral ischemia/reperfusion injury in rats. DESIGN: Randomized controlled study based on SD rats. SETTING: Weifang Municipal People's Hospital. MATERIALS: Forty-eight healthy adult SD rats weighing 280-330 g and irrespective of gender were provided by the Experimental Animal Center of Shandong University. GSP derived from grape seed was a new high-effective antioxidant provided by Tianjin Jianfeng Natural Product Researching Company (batch number: 20060107). Rabbit-anti-rat NGF monoclonal antibody was provided by Beijing Zhongshan Biotechnology Co., Ltd., and SABC immunohistochemical staining kit by Wuhan Boster Bioengineering Co., Ltd. METHODS: The present study was performed in the Functional Laboratory of Weifang Medical College from April 2006 to January 2007. Forty-eight SD rats were randomly divided into the sham operation group, ischemia/reperfusion group, high-dose GSP (40 mg/kg) group, or low-dose GSP (10 mg/kg) group (n = 12 per group). Ischemia/reperfusion injury was established using the threading embolism method of the middle cerebral artery. Rats in the ischemia/reperfusion model group were given saline injection (2 mL/kg i.p.) once daily for seven days pre-ischemia/reperfusion, and once more at 15 minutes before reperfusion. Rats in the high-dose and low-dose GSP groups were injected with GSP (20 or 5 mg/mL i.p., respectively, 2 mL/kg) with the same regime as the ischemia/reperfusion model group. The surgical procedures in the sham operation group were as the same as those in the ischemia/reperfusion model group, but the thread was approximately 10 mm long, thus, the middle cerebral artery was not blocked. MAIN OUTCOME MEASURES: NGF expression in the  相似文献   

7.
BACKGROUND: Ischemic cerebrovascular disease causes injury to the blood-brain barrier. The occurrence of brain edema is associated with aquaporin expression following cerebral ischemia/reperfusion. OBJECTIVE: To analyze the correlation of aquaporin-4 expression to brain edema and blood-brain barrier permeability in brain tissues of rat models of ischemia/reperfusion. DESIGN, TIME AND SETTING: The randomized control experiment was performed at the Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, China from December 2006 to October 2007. MATERIALS: A total of 112 adult, male, Sprague-Dawley rats, weighing 220-250 g, were used to establish rat models of middle cerebral artery occlusion and reperfusion by the suture method. Rabbit anti-aquaporin-4 (Santa Cruz, USA) and Evans blue (Sigma, USA) were used to analyze the tissue. METHODS: The rats were randomized into sham-operated (n = 16) and ischemia/reperfusion (n = 96) groups. There were 6 time points in the ischemia/reperfusion group, comprising 4, 6, 12, 24, 48, and 72 hours after reperfusion, with 16 rats for each time point. Rat models in the sham-operated group at 4 hours after surgery and rat models in the ischemia/reperfusion group at different time points were equally and randomly assigned into 4 different subgroups. MAIN OUTCOME MEASURES: Brain water content on the ischemic side and the control side was measured using the dry-wet weight method. Blood-brain barrier function was determined by Evans Blue. Aquaporin-4 expression surrounding the ischemic focus, as well as the correlation of aquaporin-4 expression with brain water content and Evans blue staining, were measured using immunohistochemistry and Western blot analysis. RESULTS: Brain water content on the ischemic side significantly increased at 12 hours after reperfusion, reached a peak at 48 hours, and was still high at 72 hours. Brain water content was greater on the ischemic hemispheres, compared with the control hemispheres at 6, 12, 24, 48, an  相似文献   

8.
9.
BACKGROUND: The integrity of the blood brain barrier (BBB) plays an important role in the patho-physiological process of cerebral ischemia/reperfusion injury. It has been recently observed that metalloproteinase-9 (MMP-9) is closely related to cerebral ischemia/reperfusion injury OBJECTIVE: This study was designed to observe MMP-9 expression in the rat brain after cerebral ischemia/reperfusion injury and to investigate its correlation to BBB permeability. DESIGN, TIME AND SETTING: This study, a randomized controlled animal experiment, was performed at the Institute of Neurobiology, Central South University between September 2005 and March 2006. MATERIALS: Ninety healthy male SD rats, aged 3-4 months, weighing 200-280 g, were used in the present study. Rabbit anti-rat MMP-9 polyclonal antibody (Boster, Wuhan, China) and Evans blue (Sigma, USA) were also used. METHODS: All rats were randomly divided into 9 groups with 10 rats in each group: normal control group, sham-operated group, and ischemia for 2 hours followed by reperfusion for 3, 6, 12 hours, 1, 2, 4 and 7 days groups. In the ischemia/reperfusion groups, rats were subjected to ischemia/reperfusion injury by suture occlusion of the right middle cerebral artery. In the sham-operated group, rats were merely subjected to vessel dissociation. In the normal control group, rats were not modeled. MAIN OUTCOME MEASURES: BBB permeability was assessed by determining the level of effusion of Evans blue. MMP-9 expression was detected by an immunohistochemical method. RESULTS: All 90 rats were included in the final analysis. BBB permeability alteration was closely correlated to ischemia/reperfusion time. BBB permeability began to increase at ischemia/reperfusion for 3 hours, then it gradually reached a peak level at ischemia/reperfusion for 1 day, and thereafter it gradually decreased. MMP-9 expression began to increase at ischemia/reperfusion for 3 hours, then gradually reached its peak level 2 days after perfusion, and thereafter it grad  相似文献   

10.
11.
BACKGROUND: Although the curative effects of acupuncture have been confirmed by various treatments of cerebral infarction, few studies have investigated when acupuncture can attain the best clinical effect. OBJECTIVE: Four different time points were selected for acupuncture treatment of cerebral infarction to evaluate the appropriate time course for Xingnao Kaiqiao therapy in terms of improved neurological function. DESIGN: Controlled observation. SETTING: Department of Traditional Chinese Medicine Rehabilitation and Physiotherapy of the Affiliated Hospital of Medical College of Chinese Armed Police Forces. PARTICIPANTS: A total of 120 inpatients with cerebral infarction of different stages, including 75 males and 45 females, aged 41-75 years, were selected from November 2005 to December 2006 at the Department of Traditional Chinese Medicine Rehabilitation and Physiotherapy in Affiliated Hospital of Medical College of Chinese Armed Police Forces. Diagnostic criteria: in accordance with "main points of diagnosis on different cerebrovascular disease" secondly revised in the Second Cerebrovascular Disease Academic Meeting of Chinese Medicine Association in 1986. All accepted subjects provided confirmed consent, and the experiment received ethical permission from the hospital's ethics committee. METHODS: ① Experiment grouping: All inpatients were divided into four groups with non-stochastic concurrent control method according to the disease course: Group Ⅰ (onset within 7 hours), group Ⅱ (onset from 7 hours to 3 days), group Ⅲ (onset within 4-7 days), and group IV (onset within 21-180 days). On the basis of symptomatic treatment with western medicine, each group received Xingnao Kaiqiao therapy after onset within 7 hours, 7 hours to 3 days, 4 to 7days, and 21 to 180 days. ① The principal acupoints were Neiguan, Renzhong, and Sanyinfiao. ② The auxiliary acupoints were Jiquan, Chize, and Weizhong. ③Acupuncture manipulations: initially, Neiguan (PC6, bilateral)  相似文献   

12.
BACKGROUND: The pharmacological effects of aspirin on apoptosis are complex. The underlying mechanisms have not been properly defined. OBJECTIVE: To observe the effect of different doses of aspirin on brain cell apoptosis following focal cerebral iscbemia-reperfusion injury (CIRI) in rats. DESING, TIME AND SETTING: A randomized, controlled, animal experiment, performed at the School of Medicine and Pharmaceutics, Jiangnan University between June and October 2006. MATERIALS: Twenty-six male, adult, Sprague Dawley rats (grade Ⅱ), weighing 240-290 g, were obtained from Shanghai Experimental Animal Center, Chinese Academy of Sciences. Aspirin was provided by Sigma (USA). METHODS: The rats were randomly divided into four groups: sham-operation (SO), CIRI + vehicle, CIRI + aspirin (6 mg/kg), and CIRI + aspirin (60 mg/kg). Rats in the lesion groups were intragastrically administrated saline, aspirin (6 mg/kg), or aspirin (60 mg/kg), respectively. MAIN OUTCOME MEASURES: The number of pyramidal neurons with normal appearance in the cerebral cortex at 24 mm from the midline; apoptotic cell death as measured by TUNEL; Bcl-2 and Bax protein localization was determined by immunohistochemistry; malondialdehyde (MDA) and super oxidation (SOD) content were determined by biochemistry method; adenosine triphosphate (ATP) content measured by capillary electrophoresis. RESULTS: Following CIRI, the following parameters were altered compared with sham-operated animals: the number of neurons with normal appearance was significantly reduced in the cerebral cortex; the number of apoptotic cells increased; Bax protein expression was enhanced; and the ratio between Bcl-2 and Bax decreased. In addition, MDA content increased significantly, whereas ATP content decreased (P 〈 0.01). Aspirin ameliorated the loss of healthy pyramidal neurons. Both 6 and 60 mg/kg aspirin increased the ratio between Bcl-2 and Bax, with no significant difference between the treatment group  相似文献   

13.
BACKGROUND: Certain components of tetramethylpyrazine, a traditional Chinese medicine, exhibit protective effects against brain injury. OBJECTIVE: To investigate the effects of different Naoxintong doses on expression of nuclear factor-kappa B ( kB), interleukin-6, tumor necrosis factor-α, and complement 3 in rats following focal cerebral ischemia. DESIGN, TIME AND SETTING: The randomized experiment was performed at the Laboratory of Neurology, Second Hospital of Hebei Medical University from June 2004 to June 2006. MATERIALS: A total of 150 adult, healthy, male, Sprague Dawley rats, weighing 280-320g, were selected. Naoxintong powder (mainly comprising szechwan lovage rhizome, milkvetch root, danshen root, and radix angelicae sinensis) was obtained from Buchang Pharmacy Co., Ltd. in Xianyang City of Shanxi Province of China, lot number 040608. METHODS: The rats were randomly assigned into sham operation, saline, high-dose Naoxintong, moderate-dose Naoxintong, and low-dose Naoxintong groups, with 30 rats in each group. Rat models of middle cerebral artery occlusion were established using the suture method, with the exception of the sham operation group. Rats in the high-dose, moderate-dose and low-dose Naoxintong groups received 4, 2, and 1 g/kg Naoxintong respectively, by gavage. Rats in the saline group were treated with 1 mL saline by gavage All rats were administered by gavage at 5 and 23 hours following surgery, and subsequently, once per day. MAIN OUTCOME MEASURES: At 6, 24, 48, 72 hours, and 7 days following model establishment, brain water content was measured. Histopathological changes in brain tissues were detected using hematoxylin-eosin staining. Expression of nuclear factor- kB, interleukin-6, tumor necrosis factor- α, and complement 3 was examined by immunohistochemistry. RESULTS: A total of 150 rats were included in the final analysis with no loss. Brain water content was significantly increased in the ischemic hemisphere of rats from the saline, as well as the high-dose, mo  相似文献   

14.
微小核糖核酸(microRNA,miRNA)是一类非编码的小分子RNA,它们基于与靶mRNA的序列互补来降解mRNA和抑制蛋白质翻译,从而影响靶蛋白的表达。miRNA与脑缺血的发生、发展密切相关,可成为诊断脑缺血的生物标记物。现对miRNA与脑缺血的相关性做一综述,为脑缺血的临床预防、诊断、治疗提供依据和思路。  相似文献   

15.
BACKGROUND: The change in expression of synaptophysin (Syp) and postsynaptic density-95 (PSD-95) alters after cerebral infarction, and the plasticity of synapses contributes greatly to nerve function recovery. Chinese medicinal substances may play an important role in the expression of Syp and PSD-95. OBJECTIVE: To observe the effect of Panaxtriol Saponins (PTS), an active component in Sanqi tongshu capsules, on the expression of Syp and PSD-95 after cerebral infarction at different time points in rats, so as to examine the cerebral function remodeling mechanism. DESIGN, TIME AND SETTING: A randomized and controlled observation which was performed in Dongzhimen Hospital, Beijing University of Traditional Chinese Medicine from January to March, 2007. MATERIALS: Twenty-six healthy male Sprague Dawley rats were used to establish middle cerebral artery occlusion based on the Longa method. Sanqi tongshu capsules (containing 100 mg PTS per tablet) were provided by the Chengdu Huashen Group and nimodipine tablets (30 mg) by Tianjin Zhongyang Pharmaceutical Co., Ltd. METHODS: Twenty-six rats were randomly divided into an operation group (n = 21 ) and a control group (n = 5). The operation group underwent the EZ Longa procedure to make the middle cerebral artery occlusion model. After surgery rats were randomly divided into a model group, a PTS group and a nimodipine group, with seven rats in each group. Rats were intragastrically administrated with saline (2 mL/d) in the model group, with Sanqi tongshu capsule (5.4 mg/100 g/d) in the PTS group, and with nimodipine (1.73 mg/100 g/d) in the nimodipine group. Rats in the control group did not undergo model establishment and drug administration. MAIN OUTCOME MEASURES: The expressions of Syp and PSD-95 were measured by immunohistochemical and image analysis at days 3, 7 and 28 after the operation. RESULTS: The expression of Syp and PSD-95 in the operation group was significantly lower than in the control group at days 3, 7  相似文献   

16.
基质金属蛋白酶-9(MMP-9)是一种锌依赖的蛋白水解酶并可特异性的降解细胞外基质。脑梗死急性期MMP-9的表达显著增加并参与了血脑屏障的破坏、血管源性水肿、缺血再灌注及出血性转化等病理过程,且其血浆水平与脑梗死面积、神经功能缺损程度及溶栓后出血转化等显著相关。现就MMP-9与脑梗死的相关关系进行综述,以更好地了解外周血MMP-9水平变化与脑梗死的关系。  相似文献   

17.
18.
19.
Objective To investigate effects of K_ATP opener on the expressions of caspase-12 mRNA and protein, and to explore the role of endoplasmic reticulum (ER) stress pathway in the mechanism of K_ATP opener protecting against neuronal apoptosis after cerebral ischemia-reperfusion. Methods Two hundred rats were randomly divided into four groups: sham operation group, ischemia-reperfusion group, K_ATP opener group, and K_ATP blocker group. The middle cerebral artery occlusion (MCAO) model was established by intraluminal suture occlusion method; neuronal apoptosis was detected by TUNEL staining. The mRNA and protein expressions of caspase-12 were detected by semi-quantitative RT-PCR and immunohisto-chemical staining, respectively. Results In ischemia-reperfusion group, K_ATP opener group and K_ATP blocker group, the number of apoptotic cells and the mRNA and protein expressions of caspase-12 gradually increased following cerebral reperfusion, and reached the peak at 24 h. In K_ATP opener group, The number of apoptotic cells was significantly less than that in ischemia-reperfusion group and K_ATP blocker group at 12 h, 24 h, 48 h and 72 h (P 〈 0.05 or P 〈 0.01); while the mRNA and protein levels of caspase-12 were significantly less than those in ischemia-reperfusion group and K_ATP blocker group at all times (P 〈 0.05 or P〈0.01). There were no differences between the ischemia-reperfusion group and K_ATP blocker group at each time (P〉 0.05). Conclusion K_ATP opener may protect neurons from apoptosis following the cerebral ischemia-reperfusion by inhibiting ER stress pathway.  相似文献   

20.
目的 探讨脑梗死患者低密度影出现时间与梗死体积之间的关系.方法 60例脑梗死患者,以CT显示低密度影时间,结合DWI、CTA和DSA等影像学资料,借鉴脑出血出血体积的计算方法:V=4π/3(A/2)x(B/2)x(C/2)=(AxBxC)/2,计算梗死体积.探讨低密度影出现时间与梗死体积间的关系.结果 60例患者CT均于不同时间段内出现低密度影,6-24 h内较集中,DWI检查可见相应区域高信号,CTA及DSA检查发现责任血管不同程度狭窄或闭塞.CT低密度影出现时间与梗死体积有直线回归关系.结论 CT低密度影出现时间越早,梗死体积越大,责任血管病变越严重.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号