针刺对抑郁模型大鼠皮层及海马脑源性神经营养因子基因和蛋白表达的影响

目的:观察针刺对慢性应激抑郁模型大鼠额叶皮层和海马脑源性神经营养因子(BDNF)基因和蛋白表达的影响,初步探讨针刺治疗抑郁症的机制。方法:将24只SD大鼠随机分为4组:空白组、空白+针刺组、模型组、模型+针刺组,每组6只。采用孤养结合慢性应激的方法造模。针刺干预选用"百会"透刺"印堂"穴,直刺单侧"内关"穴,留针20min,隔日1次。采用实时荧光定量PCR方法检测大鼠额叶皮层和海马BDNF mRNA表达,免疫印迹技术检测大鼠额叶皮层和海马BDNF蛋白表达水平。结果:与空白组相比,模型组大鼠额叶皮层、海马BDNF mRNA与蛋白表达水平明显下降(P<0.01,P<0.05);空白+针刺组大鼠额叶皮层、海马BDNF mRNA与蛋白表达水平无显著性变化(均P>0.05)。与模型组相比,模型+针刺组大鼠额叶皮层和海马BDNF mRNA与蛋白表达水平均明显升高(P<0.05,P<0.01)。结论:慢性应激抑郁模型大鼠额叶皮层和海马内BDNF含量减少,针刺治疗可以上调额叶皮层和海马区BDNF的表达水平,这可能是针刺发挥抗抑郁治疗作用的途径之一。     

眼针疗法对脑缺血再灌注大鼠海马组织BDNF表达的影响（英文）

目的:探讨眼针改善脑缺血再灌注损伤的机制。方法:健康SD大鼠32只按随机数字表分正常组、假手术组、模型组和眼针组4组,每组8只。模型组及眼针组应用线栓法复制脑缺血再灌注损伤大鼠模型。眼针组于脑缺血再灌注即刻、12 h及23.5 h,取肝区、上焦区、下焦区、肾区进行眼针治疗20 min。正常组未进行处理;假手术组插入栓塞线深度0.5 ～ 1.0 cm,其余同模型组。于再灌注即刻及24 h进行神经功能缺损评分,采用Western blot、实时荧光定量聚合酶链反应(RT-PCR)方法测定右侧海马组织脑源性神经营养因子(BDNF)蛋白及mRNA表达。结果:再灌注即刻眼针组与模型组大鼠神经功能缺损评分无差别,再灌注24 h眼针组评分为1.50±0.53,与模型组3.13±0.64比较,明显下降(P<0.01);Westernblot检测海马组织BDNF蛋白表达为正常组0.71±0.02、假手术组0.70±0.04、眼针组0.69±0.04,与模型组0.37±0.03比较均有统计学差异(P<0.01);各组大鼠BDNF mRNA表达趋势同蛋白表达。结论:眼针疗法能通过增加内源性BDNF的表达以促进大鼠脑缺血再灌注损伤过程中神经干细胞的修复,实现对脑缺血组织保护的目的。     

针刺对海洛因复吸大鼠海马△FosB和CREB表达的影响

ObjectiveTo investigate the effect of acupuncture on the addiction memory of rats.MethodsA model for heroin re-addicted rats was made by coupling heroin injection in increasing doses on the platform of a Morris water maze with high-frequency sounds cues. The animals were randomly divided into control group, relapse group, acupuncture group, and drug group, with 10 individuals in each group. For the acupuncture group, Băihuì (

GV 20) and “Dàzhuī”

GV 14) were selected. Morris water maze was used to assess the time elapsed and the distance traveled before a rat reached the platform. The expression levels of Δ FosB and cAMP response element binding protein (CREB) in hippocampal CA 1 area were assessed with immunohistochemical staining.ResultsUpon completion of three treatments, the acupuncture group had significantly longer lengths of latency and swimming distance compared to the relapse group (P<0.05). Furthermore, the acupuncture group had significantly lowered expression levels of Δ FosB and CREB compared to the relapse group (P<0.05).ConclusionAcupuncture can downregulate Δ FosB and CREB expression in rats' hippocampal area and inhibit the addiction memory.     

针刺对强迫游泳应激大鼠海马c-jun氨基末端激酶信号通路的影响

目的:观察针刺对强迫游泳应激大鼠海马c-jun氨基末端激酶(JNK)信号转导通路影响,探讨针刺抗抑郁的作用机制。方法:SD大鼠随机分为空白组、空白+JNK通路阻断剂(SP 600125,以下简称SP)组、模型组、模型+SP组、针刺组、针刺+SP组、氟西汀组、氟西汀+SP组,每组6只。采用强迫游泳应激结合孤养法造模。针刺干预选取"百会""印堂"穴,每次20min,每天1次,共治疗2d;阳性对照药物给予氟西汀1.8mg/kg灌胃,每天1次,共治疗2d。通过游泳不动时间对大鼠进行行为学评价;采用Western blot法检测海马中JNK上游激酶MKK 4和MKK 7、JNK、磷酸化JNK(p-JNK)蛋白表达。结果:与空白组比较,空白+SP组游泳不动时间差异无统计学意义(P0.05),模型组游泳不动时间显著增加(P0.01);与模型组比较,模型+SP组、针刺组、针刺+SP组、氟西汀组、氟西汀+SP组游泳不动时间明显缩短(P0.05,P0.01)。不同组别之间JNK蛋白表达水平差异无统计学意义(均P0.05)。与空白组比较,模型组海马中MKK 4、MKK 7、p-JNK蛋白表达显著升高(均P0.01);与模型组比较,氟西汀+SP组MKK 4、MKK 7蛋白表达显著降低(均P0.05),其余组有降低趋势,但差异无统计学意义(均P0.05),模型+SP组、针刺组、针刺+SP组、氟西汀组、氟西汀+SP组p-JNK蛋白表达显著降低(P0.05,P0.01)。结论:针刺治疗能降低急性应激模型大鼠海马JNK的磷酸化水平及蛋白表达,有效抑制JNK信号转导通路活性,进而改善强迫游泳应激抑郁模型大鼠的行为学症状,这可能是针刺发挥抗抑郁效应的分子机制之一。     

针刺对戊四唑诱发惊厥大鼠海马葡萄糖调节蛋白78和C/EBP同源蛋白表达的影响

目的:观察针刺对惊厥大鼠海马神经元内葡萄糖调节蛋白78(Grp 78)和C/EBP同源蛋白(CHOP)蛋白表达的影响,探讨针刺抗惊厥的可能机制。方法:SD大鼠随机分为正常对照组(n=6)、模型组(n=18)、针刺组(n=18)。腹腔注射戊四唑(50mg/kg)复制惊厥大鼠模型。针刺组立即针刺"百会""大椎"30min。各组分别于造模后2、12、48h采用免疫组化法观察各组大鼠海马CA 1区Grp 78和CHOP蛋白表达情况。结果:模型组大鼠在惊厥发作2、12h海马CA 1区Grp 78蛋白表达与正常组比较明显增强(P0.01);针刺组大鼠在惊厥发作12h和48h与模型组比较Grp 78蛋白表达显著增加(P0.01,P0.05)。在惊厥发作各个时段与正常组比较,模型组大鼠海马CA 1区CHOP蛋白表达明显上调(P0.01);针刺组海马CA 1区CHOP蛋白阳性表达在惊厥发作各个时段与模型组比较明显减少(P0.05,P0.01)。结论:针刺能明显调节惊厥大鼠海马神经元Grp 78蛋白和CHOP蛋白的表达,从而起到保护惊厥性脑损伤作用。     

Imperatorin ameliorates learning and memory deficits through BDNF/TrkB and ERK/CaMKIIα/CREB signaling in prenatally‐stressed female offspring

Prenatal stress (PS) can lead to impaired spatial learning and memory in offspring. Imperatorin (IMP) is a naturally occurring furanocoumarin with many pharmacological properties. However, the effects of IMP on cognitive impairment induced by PS and the underlying molecular mechanisms remain unclear. We investigated the protective effect of IMP treatment after PS on learning and memory deficits in female offspring at postnatal 60 days. After treating prenatally‐stressed offspring with IMP (15 and 30 mg/kg) for 28 days, we found that IMP increased body weight and ameliorated spatial learning and memory and working memory deficits in female offspring rats. Meanwhile, hippocampal Glu and serum corticosterone levels in prenatally‐stressed offspring were significantly decreased after IMP administration. Additionally, IMP treatment significantly increased BDNF, TrkB, CaMKII, and CREB mRNA expression in the hippocampus of offspring rats. Furthermore, PS‐mediated induction of RKIP protein and mRNA expression and glucocorticoid receptor protein expression in the hippocampus of offspring rats were significantly decreased by IMP treatment, and the protein expression of BDNF and TrkB and relative levels of p‐EKR/ERK, p‐CaMKIIα/CaMKIIα, and p‐CREB/CREB were remarkably increased after IMP treatment. Taken together, IMP can ameliorate PS‐induced learning and memory deficits through BDNF/TrkB and ERK/CaMKIIα/CREB signaling pathway and hypothalamic–pituitary–adrenal axis.     

Effects of acupuncture at pai-hui on the deficit of memory storage in rats

In this study, we investigated the effects of Pai-Hui by acupuncture on cycloheximide (CXM)-induced impairment of the passive avoidance response in rats. Acupuncture at Pai-Hui (Go-20) treated 15 min before or immediately after training trial for 15 min significantly attenuated CXM-induced impairment of passive avoidance response in rats, but did not have the same effect 30 and 60 min before or 30 min after the training trial or before the retention trial. Acupuncture at Pai-Hui 15 min before the training trial for 15, 30 and 60 min significantly attenuated CXM-induced impairment of passive avoidance response in rats, and its efficacy paralleled the acupuncture duration. Furthermore, acupuncture at Pai-Hui did not attenuate scopolamine (SCOP)-induced impairment of passive avoidance response, but was slightly inhibited by SCOP at 0.3 mg/kg. Second, acupuncture at Pai-Hui attenuated p-chloroamphetamine (PCA)-induced impairment of passive avoidance response and was significantly antagonized by PCA at 1 mg/kg. These results suggest that acupuncture at Pai-Hui mainly affects the memory storage process and has preventive and immediate therapeutic effects on CXM-induced impairment of passive avoidance response. Its efficacy paralleled the acupuncture duration. The preventive effect of acupuncture at Pai-Hui on CXM-induced impairment is significantly reduced by serotonergic 5-HT releaser, and slightly by cholinergic manipulations.     

EFFECTS OF ELECTROACUPUNCTURE AT “CHANGQIANG” ACUPOINT(GV1) ON BDNF PROTEIN EXPRESSION IN HIPPOCAMPUS CA3 OF RATS WITH AUTISM

Objective: To study the effects of "Changqiang" acupoint(GV1) electroacupuncture on BDNF protein expression in the hippocampus CA3 of an autistic rat model.Methods: The autism model was established by intraperitoneal injection of sodium valproate(VPA) in pregnant Wistar rats.Eighteen young rats with autism were selected and randomly divided into a model group, a non-acupoint group, and an electroacupuncture at "Changqiang"(GV1)(EA for short) group.Another 6 normal young rats were selected as a blank group.In the EA group, acupuncture was applied at Houhai(as Changqiang), and then EA apparatus was connected with continuous wave, 2 Hz, 20 min, once a day for consecutive 20 d.The same EA manipulation as the non-acupoint group, where was in the right rib, was selected.Blank group and model group were reared under the same conditions without any intervention.The BDNF protein expression in hippocampal CA3 was measured by immunohistochemical techniques.Results: BDNF protein expression in the non-acupoint group was significantly different with the control group and the model group(P0.05), and BDNF protein expression in the EA group was not significantly different with the control group and the model group(P0.05); compared with the model group, BDNF protein expression in the EA group showed significant difference(P0.05), and BDNF protein expression in the non-acupoint group showed no significant difference(P0.05); when electroacupuncture group was compared with non-acupoint group, there was a significant difference(P0.05).Conclusion: Electroacupuncture at Changqiang(GV1) can increase the expression of BDNF protein in the hippocampal CA3 of an autistic rat model.     

针刺对慢性应激抑郁大鼠海马核转录因子kappa B信号通路的影响

目的:观察针刺对慢性应激抑郁模型大鼠海马炎性反应信号通路中核转录因子kappa B(NF-κB)、环氧化酶-2(COX-2)、前列腺素E2(PGE2)表达的影响,探讨针刺抗抑郁的作用机制。方法:将SD大鼠随机分为正常组、模型组、针刺组、氟西汀组,每组9只。采用慢性不可预知应激结合孤养的方法建立抑郁模型。针刺组穴位选取"百会"和"内关",隔日针刺1次,共14次;氟西汀组给予氟西汀10mg/kg灌胃治疗,每日1次,共28次。采用蛋白印记法检测大鼠海马NF-κB的表达,酶联免疫吸附法检测海马COX-2、PGE2的含量。结果:与正常组比较,模型组大鼠海马NF-κB表达及COX-2、PGE2含量显著上升(P0.01)。针刺和氟西汀治疗显著下调NF-κB、COX-2和PGE2(P0.01,P0.05),两个治疗组的差异无统计学意义(P0.05)。结论:针刺治疗可能通过抑制NF-κB信号通路,下调炎性反应因子表达,从而发挥抗炎作用,保护海马神经元,这可能是针刺治疗抑郁症的机制之一。     

针刺“百会”、“大椎”对拟血管性痴呆大鼠脑内谷胱甘肽过氧化物酶及细胞凋亡的影响

目的 :建立拟血管性痴呆 (VD)的动物模型 ,探讨针刺“百会”及“大椎”对VD大鼠脑内谷胱甘肽过氧化物酶 (GSH PX)的影响并观察海马区内细胞凋亡情况。方法 :选用纯系Wistar老年大鼠 3 6只 ,随机分为假手术组、模型组、针刺组和西药组 ,采用 2 血管阻断法 ( 2 VO)制作VD大鼠模型 ,之后进行“百会”、“大椎”针刺治疗。检测大鼠穿梭箱实验成绩及脑内GSH PX的活力 ,采用TdT介导的原位末端标记法观察海马区内细胞凋亡情况。结果 :经统计学处理数据表明 ,针刺VD大鼠的“百会”、“大椎” ,可明显减少VD大鼠在穿梭箱实验中的电击次数和电击时间 ,增强脑内GSH PX的活力 ,明显减轻VD大鼠海马区内神经元的损伤。结论 :针刺“百会”、“大椎”能提高VD大鼠的学习记忆能力 ,改善自由基代谢 ,促进受损神经元的恢复。     

电针对慢性应激所致大鼠空间学习记忆障碍及海马胆碱能功能的影响

目的 :探讨电针对慢性应激致空间学习记忆障碍大鼠海马胆碱能功能的影响。方法 :采用电击足底结合噪声应激建立大鼠学习记忆障碍模型 ,Morris水迷宫观察动物的空间学习记忆能力 ,放免法检测乙酰胆碱 (Ach)含量、胆碱乙酰转移酶 (ChAT)和乙酰胆碱酯酶 (AchE)活性。结果 :慢性应激可引起大鼠空间学习记忆功能障碍 ,海马Ach含量减少 ,ChAT和AchE活性降低。电针对上述改变有显著的保护作用。结论 :电针改善慢性应激引起的大鼠空间学习记忆功能障碍可能与其增强海马胆碱能系统的功能有关。     

针刺对脑缺血大鼠海马区凋亡细胞及Caspase-9蛋白表达的影响

目的观察针刺对脑缺血损伤大鼠大脑海马区凋亡细胞及Caspase-9蛋白表达的影响,探讨针刺对脑缺血损伤的神经保护机制。方法雄性SD大鼠,随机分为正常对照组、脑缺血模型组、脑缺血治疗组,每组10只,采用化学刺激诱导血栓性闭塞大脑中动脉造成大鼠局灶性脑缺血模型。针刺“百会”、“水沟”,每日1次,治疗7d。应用苏木素-伊红染色（HE）及免疫组化方法观察针刺前后大鼠缺血区凋亡细胞及海马区Caspase-9蛋白表达的变化。结果大鼠局灶性脑缺血后Caspase-9表达增加,针刺对脑缺血损伤大鼠Caspase-9的过度表达有明显抑制作用。HE染色显示,缺血灶内大量神经元变性坏死,出现脑水肿表现,针剌治疗后变性坏死细胞明显减少。结论针刺可减轻Caspase-9的过度表达,改善脑缺血状态,从而减轻脑损害程度,这可能是针刺减轻脑缺血损伤的机制之一。     

针刺对脑缺血小鼠脑组织胶质纤维酸性蛋白表达的影响

目的 :观察针刺对脑缺血小鼠脑组织胶质纤维蛋白的影响。方法 :选用NIH雄性小鼠3 8只 ,随机分为正常组 (n =10 )、假手术组 (n =10 )、模型组 (n =8)、针刺组 (n =10 )。针刺“百会”、“神庭”、“率谷”、“脑户”穴 ,1天 1次 ,共 10次。用免疫组化法观测胶质纤维酸性蛋白 (GFAP)的表达。结果 :模型组海马结构中GFAP免疫组化染色阳性反应普遍增强 ,正常组和假手术组的阳性反应一致 ,而针刺组的阳性反应介于模型和正常鼠之间。结论 :针刺对小鼠学习记忆能力的改变与使GFAP阳性反应数减少有关     

基于轮廓分析的电针长强穴对FMR1基因敲除小鼠CREB表达的多脑区联动效应研究＊

目的 观察电针长强穴对脆性X智障基因（Fragile X mental retardation 1，FMR1）敲除小鼠不同脑区环磷腺苷效应元件结合蛋白（cAMP-response element binding protein，CREB）及磷酸化CREB（p-CREB）蛋白表达量影响，以探讨针刺的多脑区联动效应。方法 选取适龄FMR1基因敲除小鼠，通过PCR鉴定其基因表型。将24只纯合子基因敲除小鼠通过随机数字表法分为3组，每组8只，即空白组（仅给予抓取动作）、非经非穴组（电针肋弓最低点上1 cm处）和长强组（电针长强穴）。2组针刺组采用电针仪进行干预，电针刺激频率2 Hz，强度2 mA，连续波，每日20 min，连续干预14 天。干预结束后通过免疫组化法检测海马、皮质及小脑CREB及p-CREB蛋白的表达情况。结果 空白组海马的CREB表达量较皮质（P<0.05）、小脑（P<0.001）显著升高；非经非穴组及长强组皮质的CREB表达量较海马（P<0.05，P<0.01）、小脑（P<0.05）显著升高。空白组小脑的p-CREB表达量及p-CREB率较皮质（P<0.01，P<0.001）、海马（P<0.05，P<0.001）显著升高；非经非穴组的小脑p-CREB表达量较海马（P<0.01）显著升高；非经非穴组小脑p-CREB率较皮质（P<0.01）、海马（P<0.05）显著升高；二者在长强组的三个脑区均无显著性差异（P＞0.05）。轮廓分析结果示：CREB平行轮廓分析示差异有统计学意义（P＜0.05），提示三个脑区的总体轮廓不平行，即脑区的联动变化不一致。p-CREB及p-CREB率水平轮廓分析差异有统计学意义（P＜0.01），提示三个脑区联动变化一致，且各组间变化程度一致，但各组中蛋白表达不相等，其中小脑最高。结论 通过轮廓分析能初步观察针刺的多脑区联动效应，且针刺刺激可能通过影响CREB磷酸化使得FMR1基因敲除小鼠多脑区效应方式发生改变。     

Bushenhuoxue improves cognitive function and activates brain-derived neurotrophic factor-mediated signaling in a rat model of vascular dementia

OBJECTIVE: To explore the protective mechanisms of the Traditional Chinese Medicine Bushenhuoxue(BSHX) in a rat model of vascular dementia(VD).METHODS: A rat model of VD was developed using bilateral common carotid artery occlusion(BCCAO).Rats were administered BSHX(10.14 or 5.07 g/kg),nimodipine(11.06 mg/kg; positive control), or saline(control) by gavage daily for 30 d post-surgery.Learning and memory abilities were assessed using the Morris water maze. Morphological changes in the hippocampus were observed using light microscopy(hematoxylin and eosin staining) and transmission electron microscopy(TEM). The m RNA and protein expression levels of brain-derived neurotrophic factor(BDNF), tyrosine receptor kinase B(Trk B), phosphatidyl inositol 3-kinase(PI3 K), serine/threonine kinase(AKT), and c AMP response element binding protein(CREB) were measured by real-time polymerase chain reaction(RT-PCR) and Western blot, respectively.RESULTS: Compared with the sham group, rats with BCCAO exhibited impaired learning and memory abilities(Morris water maze) and showed abnormalities in neuronal morphology(light microscopy)and ultrastructure(TEM) in the hippocampus. They also had decreased m RNA and protein expressions of BDNF, Trk B, PI3 K, AKT, and CREB in hippocampal tissue(all P 0.05). In rats with BCCAO, administration of BSHX attenuated deficits in learning and memory, improved the morphology and ultrastructure of hippocampal neurons, and enhanced m RNA and protein expression levels of BDNF, Trk B, PI3 K,AKT, and CREB(all P 0.05).CONCLUSION: BSHX may protect hippocampal neurons and improve learning and memory abilities, at least in part via the activation of BDNF/Trk B/PI3 K/AKT/CREB signaling.     

电针对PSD大鼠前额叶和海马BDNF、CREB表达调控的影响

目的观察电针对卒中后抑郁(PSD)模型大鼠行为学以及前额叶和海马脑源性神经营养因子(BDNF)、环磷腺苷反应元件结合蛋白(CREB)表达调控的影响。方法将旷场实验得分相近的40只大鼠随机分为正常组、模型组、西药组和电针组,每组10只。正常组孤养不作任何处理。其他组采用线栓法大脑中动脉阻塞联合慢性不可预知温和应激法制备PSD模型。模型组给予2 mL 0.9%生理盐水灌胃,西药组给予2 mL盐酸氟西汀溶液灌胃,电针组大鼠选取百会、丰隆、太冲、三阴交穴针刺治疗,丰隆、太冲接电针治疗仪,共治疗21 d。观察大鼠行为学的改变及前额叶和海马BDNF、CREB、BDNF mRNA、CREB mRNA表达的变化。结果应激21 d后,模型组、西药组、电针组大鼠较正常组神经功能缺损评分明显升高,体质量下降,旷场实验水平和垂直得分降低,糖水消耗量降低(P<0.05)。治疗21 d后,西药组、电针组较模型组大鼠神经功能缺损评分降低,体质量增加,自发活动增多,对新环境探索能力增强,糖水消耗量增加(P<0.05)。模型组大鼠前额叶和海马BDNF、CREB、BDNF mRNA、CREB mRNA表达较正常组明显减少(P<0.05);电针组和西药组BDNF、CREB、BDNF mRNA、CREB mRNA的表达较模型组明显升高(P<0.05)。结论电针能明显促进PSD模型大鼠前额叶和海马BDNF、CREB的表达,改善抑郁行为。     

针灸对拟痴呆大鼠记忆功能及皮层胆碱能系统的影响

目的:观察针灸对拟痴呆大鼠记忆功能及皮层胆碱能系统的影响。方法:建立拟痴呆大鼠动物模型,运用 Morris 迷宫作为检测工具,分别观察对照组、模型组、针刺组、艾灸组游泳时的差异及针刺、艾灸对拟痴呆大鼠大脑皮层组织中胆碱能 M-受体结合容量、胆碱酯酶活性(ACHE)的影响。结果:针刺组、艾灸组与模型组大鼠比较,游泳时差异有显著性。模型组大鼠皮层 M-受体结合容量值较针刺组、艾灸组明显降低。模型组与针刺组、艾灸组皮层的 ACHE 活性比较差异亦有显著性。结论:通过对拟痴呆大鼠的记忆力、皮层 M-受体结合容量及胆碱酯酶活性的观察,证明针灸有防治脑功能减退、改善记忆的功能。     

电针对局灶性脑缺血大鼠脑源性神经营养因子影响的研究

目的 :研究电针督脉经穴“大椎”、“百会”对局灶性脑缺血大鼠脑源性神经营养因子的影响。方法 :凝闭大鼠一侧大脑中动脉 1 0hr后致局灶性脑缺血 ,采用免疫组化染色S P法进行观察。结果 :电针治疗能增强局灶性脑缺血大鼠脑组织脑源性神经营养因子的表达 ,从而阻止神经细胞内Ca2 +超载 ,稳定细胞内环境。结论 :电针对缺血性脑损伤具有一定的保护作用 ,为临床针灸治疗缺血性脑血管疾病奠定了理论基础。     

针刺对糖尿病合并脑缺血再灌注大鼠学习记忆行为的影响

目的:建立糖尿病合并脑缺血再灌注导致学习记忆障碍大鼠模型,观察针刺对其学习记忆行为的改善作用。方法:Wistar大鼠87只,分为正常对照组、糖尿病+假手术组、脑缺血组、糖尿病+脑缺血组(模型组)、糖尿病+脑缺血+针刺组。腹腔注射链脲佐菌素建立糖尿病模型,3d后双侧颈总动脉夹闭再灌注2次。术后1个月,用跳台和Morris水迷宫判断其学习记忆能力;取海马组织,HE染色观察CA1区的细胞分布。针刺治疗从术后1周开始,取穴为“百会”、双侧“三阴交”“脾俞”或“百会”、双侧“肾俞”“足三里”,两组穴位交替进行,手针治疗,刺入后提插捻转,以手下有涩紧感为度,留针30min,隔日1次,共治疗15次。结果:电击后15min模型组的被动回避反应下台潜伏期明显缩短(P<0.01),24h后仍小于其它各组(P<0.05);针刺组下台潜伏期明显延长(P<0.05)。模型组学会主动回避反应的训练次数显著多于其它4组(P<0.001);针刺组明显少于模型组(P<0.05)。模型组在目标象限停留的时间最短(P<0.01),游泳的距离也最短(P<0.05)。模型组大鼠海马CA1区呈现明显的神经元缺失,脑缺血组的神经元也有所减少,针刺治疗后神经元缺失有所减轻。结论:糖尿病合并脑缺血再灌注可在短期内造成学习记忆障碍,糖尿病可加重脑缺血造成的脑损伤,针刺可改善糖尿病合并脑缺血再灌注造成的学习记忆障碍。     

针刺对脑缺血再灌注损伤大鼠双侧脑组织白细胞介素-1β、肿瘤坏死因子-α表达的影响

目的:探讨脑缺血再灌注损伤大鼠双侧脑组织白细胞介素-1β(IL-1β)及肿瘤坏死因子-α(TNF-α)的表达变化及针刺的干预作用。方法:以右侧大脑中动脉线栓法制备脑缺血再灌注损伤大鼠模型,将大鼠随机分为模型组、假手术组和针刺组,每组再按照再灌注后时间分12、24、48、72、96、144h6个时间点,每个时间点6只大鼠,另设正常组6只。针刺组电针刺激"百会"和"足三里"穴,每日1次,每次20min。应用免疫组化法检测大鼠双侧脑组织IL-1β及TNF-α的表达量。结果:IL-1β在脑缺血大鼠患侧脑区呈双峰表达,模型组峰值时间为48h和96h,针刺组为72h,针刺组IL-1β表达量显著低于模型组,但高于假手术组和正常组(均P<0.05);IL-1β在脑缺血大鼠健侧脑区表达高于假手术组和正常组,除72h组外,针刺组各个时间点的表达低于模型组(均P<0.05)。TNF-α在患侧脑区呈单峰表达,模型组和针刺组峰值时间均为72h,针刺组表达量显著低于模型组,但高于假手术组和正常组(均P<0.05);TNF-α在脑缺血大鼠健侧脑区表达高于假手术组和正常组(均P<0.05)。结论:针刺可通过调节脑缺血大鼠双侧脑组织IL-1β及TNF-α的表达,干预脑缺血再灌注损伤大鼠的炎性反应。