OBJECTIVE:To observe the effect of moxibustion preconditioning on learning-memory ability, Toll like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB) signal pathway related proteins and microglia in rats with Alzheimer's disease (AD), so as to explore its possible mechanisms underlying improvement of AD. METHODS:Male SD rats were randomly divided into normal, sham operation, AD model and pre-moxibustion groups, with 9 rats in each group. Moxibustion was applied to "Baihui"(GV20), "Shenshu"(BL23) and "Zusanli"(ST36) for 15 min, once daily, 6 days as a course of treatment for 3 courses. At the end of moxibustion, the AD model was established by injection of Aβ25-35 aggregation solution into the bilateral hippocampus. The sham operation group was only injected with the same amount of 0.9% Nacl solution. The spatial learning-memory ability of rats was detected by Morris water maze test, the ultrastructure of hippocampal neurons was observed by transmission electron microscope (TEM). The histopathological changes of hippocampus tissue were observed by HE staining, and the protein expression levels of TLR4 and NF-κB p65 in the hippocampus detected by Western blot, and the positive expressions of Iba-1, CD80 and CD206 in the hippocampal CA1 region were detected by immunofluorescence labeling. The contents of inflammatory factors IL-1β, TNF-α and IL-10 in the hippocampus were measured by ELISA. RESULTS:Compared with the sham operation group, the escape latency was significantly increased (P<0.01), and the number of platform quadrant crossing times was decreased (P<0.01) in the model group. In comparison with the model group, the increased escape latency and the decreased platform quadrant crossing times were reversed in the pre-moxibustion group (P<0.01). TEM and light microscope observation showed loose arrangement of cells, enlarged cell space, degeneration, swelling and deformation of hippocampal neurons, rupture of membranes of a large number of cells, reduction of mitochondria, dilation of endoplasmic reticulum, and matrix vacuoles, uneven distribution of organelles and cytoplasm, and being difficult in distinguishing the nuclear cytoplasm in the model group, which was relatively milder in the pre-moxibustion group. The expression levels of hippocampal NF-κB p65 and TLR4, the mean immunofluorescence density of Iba-1 and CD80, as well as the contents of IL-1β and TNF-α in hippocampal CA1 region were significantly increased in the model group than those in the sham operation group (P<0.01), and obviously decreased in the pre-moxibustion group than those in the model group (P<0.05, P<0.01). Whereas the expression of CD206 and the content of IL-10 were evidently decreased in the model group than those in the sham operation group (P<0.01), and strikingly increased in the pre-moxibustion group than those in the model group (P<0.01). No significant differences were found between the sham operation group and the normal group in all the indexes mention above (P>0.05). CONCLUSION:Pre-moxibustion at GV20, BL23 and ST36 can improve learning-memory ability in AD rats, which may be associated with its functions in promoting the polarization of microglia from M1 to M2 and reducing the neuroinflammatory response by way of TLR4/NF-κB signaling pathway.

目的 观察逆灸对阿尔茨海默病(Alzheimer's disease,AD)伴抑郁大鼠血浆心房利钠肽(atrial natriuretic peptide,ANP)及皮质酮(corticosterone,CORT)水平的影响,探讨逆灸防治AD认知障碍伴抑郁的可能作用机制.方法 将雄性SD大鼠随机分为空白组、假手术组、模型组和逆灸组,每组 9 只.采用双侧海马注射β淀粉样蛋白25-35(amyloid β25-35,Aβ25-35)的方法复制AD大鼠模型.逆灸组大鼠取"百会""肝俞""肾俞"穴施以逆灸.糖水偏好实验评估大鼠情绪状态,Morris水迷宫检测大鼠空间学习记忆能力,电镜观察海马超微结构,ELISA法检测大鼠血浆ANP、CORT浓度.结果 与假手术组比较,模型组大鼠糖水偏好指数明显下降(P<0.01),逃避潜伏期显著延长(P<0.01),平台停留时间与平台穿越次数显著减少(P<0.01);海马神经元细胞损伤明显,胞浆基质溶解,空化;血浆ANP浓度明显降低(P<0.01),CORT浓度显著提高(P<0.01).与模型组比较,逆灸组大鼠糖水偏好指数明显升高(P<0.01),逃避潜伏期明显缩短(P<0.01),平台停留时间与穿越平台次数明显增加(P<0.05,P<0.01);海马神经元细胞基本正常,突触结构清晰;血浆ANP浓度升高(P<0.01),CORT浓度降低(P<0.01).结论 逆灸可以有效减缓AD大鼠抑郁样行为的发生发展,上调大鼠血浆ANP表达、降低CORT水平.调节下丘脑-垂体-肾上腺轴功能可能是其防治阿尔茨海默病引发的抑郁样行为的重要机制之一.

目的 观察逆灸对β-淀粉样蛋白(amyloidβ-peptide,Aβ)25-35诱导的阿尔茨海默病(Alzheimer's disease,AD)大鼠海马CA1区酪氨酸蛋白激酶-2(Janus kinase-2,JAK2)、信号转导和转录激活因子-3(signal transducer and ac-tivator of transcription-3,STAT3)的影响,探究逆灸防治AD的作用机制.方法 将健康雄性SD大鼠随机分为正常组、假手术组、模型组和逆灸组,每组9只.逆灸组于"百会""肾俞""足三里"穴上方进行悬灸治疗,逆灸结束后通过双侧海马内注射聚集态Aβ25-35寡聚体制备AD大鼠模型,假手术组仅注射等量生理盐水.Morris水迷宫实验检测大鼠学习记忆和空间探索能力,苏木精—伊红染色法观察海马组织形态,ELISA法检测海马组织中白细胞介素-6(interleukin 6,IL-6)水平,RT-qPCR法检测海马CA1区JAK2、STAT3 mRNA表达水平,Western blot法检测海马CA1区JAK2、STAT3蛋白磷酸化表达水平.结果 与正常组和假手术组比较,模型组大鼠逃避潜伏期显著延长(P<0.05),穿越平台次数显著减少(P<0.05);海马组织中神经细胞数量明显减少,细胞核形态改变,核膜界限模糊,细胞间隙增大,海马周围神经细胞出现坏死、空泡变性,血管肿胀变形;海马组织内IL-6水平显著升高(P<0.05);CA1区JAK2 mRNA、STAT3 mRNA相对表达水平显著升高(P<0.05),JAK2、STAT3蛋白磷酸化表达水平显著增加(P<0.05).与模型组比较,逆灸组大鼠逃避潜伏期显著缩短(P<0.05),穿越平台次数显著增加(P<0.05);海马神经细胞数量明显增多,结构基本完整,少许细胞核轻度不规则;海马组织中IL-6水平显著降低(P<0.05);CA1区JAK2 mRNA、STAT3 mRNA相对表达水平显著降低(P<0.05),JAK2、STAT3蛋白磷酸化表达水平显著降低(P<0.05).结论 逆灸"百会""肾俞""足三里"穴能改善AD大鼠学习记忆功能,减少神经炎症因子的释放,延缓神经炎症反应的发生发展,其作用机制可能与抑制脑内JAK2/STAT3信号通路有关.

脑性瘫痪是一组持续存在的中枢性运动和姿势发育障碍症候群,解决患者运动障碍对促进功能恢复具有重要意义.应将现代康复理念与中医辨证论治思想结合,指导不同运动障碍类型脑性瘫痪的针刺治疗.痉挛型可采用头针联合体针疗法,补虚泻实、和阴阳以解痉;不随意运动型以头针为主,结合体针疗法,可舒筋通络、调和脏腑;共济失调型以头皮针为主,辅以体针治疗,以补脾益肾.

加速康复外科(enhanced recovery after surgery,ERAS)作为21世纪外科术后康复的主题,提倡多学科协作模式以促进患者更好更快康复为目标.将中医药与ERAS理念相结合,探讨围手术期中医快速康复外科(Chinese medicine in enhanced recovery after surgery,CMERAS)的潜在价值和可行性,可为ERAS的建设提供新思路.术前阶段,中医药能降低焦虑水平,缩短禁食时间;术中阶段,优化麻醉管理,辅助体温控制;术后阶段,减轻疼痛,减少恶心、呕吐,促进快速康复.

OBJECTIVE To observe the effect of electroacupuncture (EA) on miRNA-126-3p and mammalian target of rapamycin (mTOR)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway in rats with cerebral ischemia (CI), so as to explore the underlying mechanism of EA on angiogenesis. METHODS Male SD rats were randomly divided into control group, model group, EA group and EA+inhibitor group (inhibitor group), which were further divided into 3, 7 and 14 d subgroups, with 12 rats in each sub-group. The CI model was established by occlusion of the middle cerebral artery. EA (2 Hz/20 Hz, 0.5 mA) was applied to "Dazhui" (GV14), "Baihui" (GV20) for 20 min, once daily for 14 days at most. Rats of the inhibitor group were given an intraperitoneally injection of mTOR inhibitor (0.1 mg/mL, 0.3 mg/kg) before daily EA. The neurological function was evaluated by modified neurological severity score (mNSS). The ultrastructure of cortical neurons and microvascular endothelial cells in ischemic penumbra was observed by transmission electron microscope, and the microvessel density (MVD) of cortical endothelium in ischemic penumbra was detected by immunohistochemistry. Western blot and quantitative real-time PCR were used to detect the protein and mRNA expression of mTOR, HIF-1α and the expression of miR-126-3p in the cortex of ischemic penumbra, respectively. RESULTS After modeling, compared with the control group at the same time point, the mNSS of the model group was increased (P<0.01), and decreased over time (P<0.01). The cortical neurons and brain microvascular endothelial cells in the ischemic penumbra were edema, and the cell structure was damaged obviously in the model group.The MVD value and the expressions of mTOR、HIF-1α proteins and mRNAs were increased (P<0.01), while the expression of miR-126-3p decreased (P<0.01) in the model group relative to the control group. Compared with the model group at the same time point, the mNSS of both intervention groups was significantly reduced (P<0.01, P<0.05), the neuron and cerebral microvascular structure improved to varying degrees, and the MVD value, the expressions of mTOR and HIF-1α protein and mRNA, and the expression of miR-126-3p of the two treatment groups were increased (P<0.01, P<0.05) at all time points (excep MVD at day 7 in the inhibitor group). Compared with the EA group at the same time point, MVD, the expressions of mTOR, HIF-1α proteins and mRNAs and miR-126-3p in the inhibitor group were all decreased (P<0.05,P<0.01). Compared with the group itself at 4 hours after modeling and day 3 and day 7, the mNSS was decreased at day 14 （P<0.01） in the model, EA and inhibitor groups. Compared with the group itself at day 3, the MVD value and the expression of mTOR protein were increased at day 7 and day 14 in the model, EA and inhibitor groups (P<0.01, P<0.05). Compared with the group itself at day 3 and day 7, the expression of mTOR mRNA and miR-126-3p were up-regulated at day 14 in the model and EA groups (P<0.01, P<0.05).Compared with the group itself at day 3, the mRNA expressions of mTOR and HIF-1α were increased at day 7 and day 14 (P<0.01, P<0.05) in the inhibitor group. CONCLUSION EA at GV14 and GV20 can alleviate neurological deficit and improve angiogenesis in rats with CI, which may be related with its effect in up-regulating the expression of mTOR and HIF-1α, improving activation of miR-126-3p in the cortex of ischemic penumbra.

OBJECTIVE To observe the effect of pre-moxibustion at "Baihui"(GV20), "Shenshu"(BL23) and "Zusanli"(ST36) on expression of Tau protein and related protein kinases as glycogen synthase kinase-3β (GSK-3β), etc. in the hippocampal CA3 region of Alzheimer's disease (AD) rats, so as to explore its mechanism underlying prevention and treatment of AD cognitive impairment. METHODS Male SD rats were randomly divided into 4 groups: normal control, sham operation， model and pre-moxibustion，with 9 rats in each group. Rats of the pre-moxibustion group received moxibustion of GV20, BL23 and ST36 for 15 min, once a day, 6 days a week for 3 weeks. After completion of moxibustion, the AD model was reproduced by injection of amyloid beta-peptide 25-35(Aβ 25-35) aggregation solution 1 μL (5 μg/μL) into the bilateral hippocampus, rats of the sham operation group received injection of the same dose of normal saline into the hippocampus. The spatial learning-memory ability was detected using Morris water maze test, and changes of the ultrastructure of hippocampal neurons were observed using electron microscope, and those of histopathological changes of hippocampus tissue observed using hematoxylin eosin (H.E.) staining. The expression levels of hippocampal GSK-3β, p-Tau, CDK5 and Synapsin I proteins were detected by Western blot and immunohistochemistry, respectively. RESULTS No significances were found between the normal control and sham groups in all the indexes (P>0.05). Compared with the control group, the escape latency of place navigation test of Morris water maze test, expression of GSK-3β and CDK5 and the immunoactivity of GSK-3β, CDK5 and p-Tau were significantly increased (P<0.01), and the residence time in the platform quadrant and the number of platform crossing of spatial prob test and the expression of Synapsin Ⅰ significantly reduced in the model group (P<0.01). Following the intervention, the increase of escape latency, expression of GSK-3β and CDK5 and the immunoactivity of GSK-3β, CDK5 and p-Tau, and the decrease of residence time in the platform quadrant, number of platform crossing and the expression of Synapsin Ⅰ were reversed in the pre-moxibustion group (P<0.05, P<0.01). Outcomes of ultrastructure and histopathological observations respectively showed edema of hippocampal nerve cells at varying degrees, moderate edema of the cytoplasma, chromatin condensation at the edge of the nucleus, partial mitochondrial vacuole-like degeneration, fracture of tubular crest, edema and expansion of Golgi body, disappearance of polarity, fracture of the rough endoplasmic reticulum, degeneration of ribosome and partial myelin axon and reduced synaptic vesicles in the presynaptic capsule; and reduced number of neurons with shrank body, disappearance of nucleolus and blurred nuclear boundary and vacuole-like degeneration in some of them in the model group, which were relatively milder in the pre-moxibustion group. CONCLUSION Pre-moxibustion at GV20, BL23 and ST36 plays a role in slowing down the occurrence and development of cognitive impairment in AD rats, which may be related to its functions in inhibiting tau protein hyperphosphorylation and reducing the expression of some related protein kinases in the hippocampus.

肩手综合征(shoulder-hand syndrome,SHS)是脑卒中后常见的以肩手肿胀、疼痛为主要特征的并发症,早期诊断和治疗对患者功能恢复具有积极意义.将现代康复理念与中医基础理论相结合,基于Brunnstrom理论探讨SHS不同时期的多学科综合治疗策略具有重要意义.BrunnstromⅠ期促进患者运动能力的建立,BrunnstromⅡ～Ⅲ期平衡肌群间肌张力,BrunnstromⅣ～Ⅵ期纠正异常运动模式、强化运动协调性.