电针对帕金森病大鼠室管膜下区细胞增殖和胶质原纤维酸性蛋白表达的影响

目的:观察电针对帕金森病(PD)大鼠室管膜下区(SVZ)神经干细胞的影响。方法:SD大鼠随机分为正常对照组(6只)、模型组(6只)和电针组(6只)。右侧前脑内侧束注射六羟基多巴胺制备PD模型。电针组于造模1周开始高频(100Hz)电针"合谷"太冲"穴,每次30min,每日1次,连续电针21d。以酪氨酸羟化酶(TH)、抗增殖细胞核抗原(PCNA)以及胶质原纤维酸性蛋白(GFAP)抗体免疫组化阳性分别显示SVZ多巴胺能神经末梢、分裂细胞和神经干细胞。结果:正常对照组右侧纹状体有较强的TH表达,而模型组和电针组的表达均几乎为零;模型组右侧SVZ的PCNA免疫反应阳性细胞数和表达量均显著低于正常对照组(P<0.01),电针组较模型组均显著增高(P<0.01);模型组右侧SVZ的GFAP表达水平显著低于正常对照组(P<0.01),电针组较模型组显著增高(P<0.05)。结论:电针可不通过增加TH表达而逆转PD大鼠损伤侧SVZ的PCNA和GFAP表达减少,提示其改善PD临床症状的可能机制。     

“夹脊”电针对兔退变腰椎间盘组织中基质金属蛋白酶13和基质金属蛋白酶组织抑制因子1表达的影响

目的:研究"夹脊"电针对兔退变的腰椎间盘中基质金属蛋白酶13(matrix metalloproteinase-13,MMP-13)和基质金属蛋白酶组织抑制因子1(tissue inhibitor of metalloproteinase-1,TIMP-1)表达的影响,探讨夹脊电针治疗腰椎间盘退行性病变的作用机制。方法:36只清洁级成年新西兰大白兔随机分为正常组、假手术组、模型组和电针组,每组9只。采用克氏针横穿椎体后椎体间加压法复制椎间盘退变模型。电针组针刺L 4、L 5"夹脊"穴28d。各组于第1、28、56天应用Western blot方法检测椎间盘组织中MMP-13蛋白的表达,免疫荧光技术检测椎间盘组织中TIMP-1蛋白的表达。结果:建立模型后,MMP-13蛋白表达增强(P0.01);电针进行干预后可降低MMP-13的表达(P0.01)。TIMP-1在荧光激发下,胞质清晰,可见红色荧光,其中各组第1天和正常组、假手术组的第28、56天均呈现强阳性,模型组第56天阳性细胞最少、红色荧光最弱(P0.01),而电针组在第56天阳性细胞升高(P0.01)。结论:电针"夹脊"穴可以通过降低椎间盘组织中MMP-13和增强TIMP-1的表达,纠正基质合成与分解代谢失衡,达到防治椎间盘退变的效果。     

电针对干眼症兔结膜细胞凋亡及相关蛋白Caspase-3、Fas和Bcl-2表达的影响

目的:通过观察电针对干眼症兔结膜细胞凋亡及相关蛋白Caspase-3、Fas和Bcl-2表达的影响,从细胞凋亡角度探讨电针治疗干眼症的作用机制.方法:雄性新西兰兔随机分为正常组、模型组、电针组和假电针组.采用0.1%苯扎氯铵滴眼制作兔干眼症模型.检测各组兔泪液分泌量、泪膜破裂时间;采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定(TUNEL)法检测结膜细胞凋亡情况;应用免疫组化法检测结膜细胞Caspase-3、Fas和Bcl-2蛋白表达.结果:与正常组比较,模型组兔泪液分泌量降低,泪膜破裂时间缩短(均P<0.01);与模型组、假电针组比较,电针组兔泪液分泌量增多,泪膜破裂时间延长(均P<0.05).与正常组比较,模型组兔结膜细胞凋亡增加(P<0.01),Caspase-3和Fas蛋白表达增加(均P<0.05),Bcl-2蛋白表达降低(P<0.01);与模型组、假电针组比较,电针组兔结膜细胞凋亡减少(均P<0.01),Caspase-3和Fas蛋白表达减少(均P<0.05),Bcl-2蛋白表达增加(均P<0.01).结论:电针能抑制干眼症兔结膜细胞凋亡,下调凋亡相关蛋白Caspase-3和Fas表达,上调Bcl-2蛋白表达,该作用可能是电针治疗干眼症的作用机制之一.     

头皮针对脑缺血大鼠模型碱性成纤维细胞生长因子的影响

目的 :研究头皮针对脑缺血大鼠模型碱性成纤维细胞生长因子的影响 ,并与电针组比较。方法 :线栓法制备大鼠脑缺血模型 ,甲醛固定脑组织切片 ,运用免疫组化方法检测各组碱性成纤维细胞生长因子的变化情况。结果 :术后 6hr与术后 1 5天组内神经功能评分比较 ,模型组无明显差异 (P >0 .0 5) ,电针组与针刺组有显著性差异 (P <0 .0 1 )。组间 1 5天时比较 ,电针组与针刺组无明显差异 (P >0 .0 5) ,两组与模型组比较均有显著性差异 (P <0 .0 1 )。在第 1 5天时碱性成纤维细胞生长因子免疫组化染色比较 ,电针组与模型组有明显差异 (P <0 .0 5) ,针刺组与模型组有显著性差异 (P <0 .0 1 ) ,针刺组与电针组有明显差异 (P <0 .0 5)。结论 :头皮针可促进碱性成纤维细胞生长因子产生并延长碱性成纤维细胞生长因子产生时限 ,这可能是头皮针减轻脑缺血损伤并促使肢体功能恢复的机理之一     

电针对高血脂合并脑缺血大鼠巢蛋白和增殖细胞核抗原表达的影响

目的:观察电针对高血脂合并脑缺血大鼠侧脑室外侧壁巢蛋白(Nestin)和增殖细胞核抗原(PCNA)表达的影响。方法:41只成年雄性SD大鼠随机分为正常组和高脂饲料喂养组,高脂饲料喂养组大鼠用高脂饲料喂养42 d造成高脂血症模型后,随机分为假手术组、模型组、电针1组、电针2组。电针1组电针“丰隆”,1次/d,连续7 d。第50天,电针组和模型组用FeCl3化学诱导造成脑缺血,术后电针组电针“丰隆”“百会”,1次/d,连续14 d。用神经功能缺损评分评定行为学变化,生物化学法检测血脂四项,HE染色观察缺血半暗带形态学改变,免疫组化检测缺血侧侧脑室外侧壁Nestin和PCNA的表达。结果:术后14 d模型组TC、LDL升高(P<0.01),HDL降低(P<0.01);电针组TC、LDL降低(P<0.05),HDL升高(P<0.05)。模型组神经功能缺损评分增高,HE染色组织形态呈脑缺血改变,Nestin、PCNA阳性细胞个数增多(P<0.05);电针治疗可降低神经功能缺损评分(P<0.05),缺血半暗带细胞形态接近正常,Nestin、PCNA阳性细胞数升高(P<0.05),术后7 d时达到高峰,且电针1组高于电针2组(P<0.05)。结论:电针“丰隆”“百会”可调节血脂,促进缺血侧侧脑室外侧壁Nestin、PCNA的表达,改善神经功能,且在高血脂阶段进行针刺干预效果更佳。     

ELECTROACUPUNCTURE SHOWS EVIDENCE OF REGENERATIVE POTENTIAL IN DEGENERATED INTERVERTEBRAL DISCS IN VIVO

Study Design: A radiographic, histologic and gene expression study was conducted in a rabbit model to determine the effect of electroacupuncture(EA) at EX-B2 on lumbar disc degeneration.Objective: To determine if the EA is able to protect disc degeneration in vivo.Methods: New Zealand white rabbits(n=40) were used for this study.The rabbits were randomly assigned to one of four groups.Twenty animals were first loaded for 28 days using a custom-made external compression device to stimulate disc degeneration.After 28 days loading time, they were divided into compression group(n=10) and EA group(n=10).Five of each group were sacrificed and the tissues were harvested.Five of the EA treatment group received EA administration, applied to EX-B2, at 2 or 100 Hz for 28 days; five in the compression group using the same device for another 28 days.In a sham compression group, the lumbar body was only punctured without previous loading.Ten served as controls.Before the animals were sacrificed, MRIs were obtained for each group at days 28 and 56 to evaluate the ability of the device to induce the IVD model.Discs were analyzed using immunofluorescence for COL2, biglycan, and bone morphogenetic protein-2.For gene analysis, conventional and quantitative polymerase chain reactions were used for COL2, biglycan, decorin, fibronectin, matrix metalloproteinase-13(MMP-13), and tissue inhibitor of MMP-1(TIMP-1).Results: Immunofluorescence and the gene expression analysis showed a significant reduction of BMP-2-, COL2-, decorin-, biglycanand TIMP-1-positive cells in compressed discs.After 28 days of EA treatment, the disc showed a sign of regeneration; the number of dead cells decreased in comparison with the loaded discs without EA method.Conclusion: EA increased the level of extracellular matrix in degenerated disc.It is able to keep a dynamic balance between extracellular matrix synthesis and degradation.     

Effects of electroacupuncture at shu-points of the five zang-organs on electrophysiologic function of sciatic nerve in the rabbit of Guillain-Barre syndrome

OBJECTIVE: To probe into the mechanism of electroacupuncture at shu-points of the five zang-organs for treatment of Guillain-Barre syndrome (GBS). METHODS: Eighty healthy giant-ear white rabbits were randomly divided into 4 groups, a blank group, a model group, an electroacupuncture (EA) group and an immunoglobulin group, 20 rabbits in each group. The internationally recognized P 2 immune rabbit model was used in the study. The EA group were treated with EA at shu-points of the five zang-organs and the immunoglobulin group with intravenous injection of immunoglobulin 80 mg/kg/day. The sciatic nerve movement conduction velocity (MCV) and F wave incidence rate were investigated respectively at the 7th and 14th days of treatment in the rabbits of GBS. RESULTS: The sciatic nerve MCV significantly reduced in the model group, and it significantly increased (P < 0.01) and F wave abnormal cases was significantly reduced (P < 0.05) after treatment for 14 days in the EA group as compared with those in the model group. CONCLUSION: EA at shu-points of the five zang-organs can increase the sciatic nerve MCV and decrease the abnormal F wave incidence rate of the sciatic nerve in the rabbit of GBS.     

电针对慢性应激抑郁大鼠海马转化生长因子β3和碱性成纤维细胞生长因子表达的影响

目的:观察电针对慢性应激模型大鼠海马转化生长因子β3(TGF-β3)、碱性成纤维细胞生长因子(bFGF)蛋白表达的影响,探讨电针对慢性应激抑郁模型大鼠海马神经的营养再生作用。方法:雄性SD大鼠随机分为空白组、模型组、电针组、氟西汀组,每组10只。除空白组外,其余组均采用慢性应激结合孤养方法造模28d。电针组于造模前1h选取"百会""印堂"穴进行电针,氟西汀组于造模前1h给予盐酸氟西汀混悬液5mL/kg灌胃治疗。通过旷场实验对大鼠进行行为学评价,采用生物素标记抗体芯片技术筛选出海马中差异蛋白TGF-β3、bFGF。结果:造模结束后,与空白组相比,模型组大鼠水平穿越格数、竖立次数均显著减少(P0.01);与模型组相比,电针组和氟西汀组大鼠水平穿越格数、竖立次数均显著增加(P0.01)。与空白组比较,模型组大鼠海马TGF-β3蛋白水平下降(fold change=0.48),bFGF蛋白水平上升(fold change=1.36);与模型组比较,电针组、氟西汀组TGF-β3蛋白水平上升(fold change=1.61,1.61),bFGF蛋白水平下降(fold change=0.61,0.45)。结论:电针可能通过上调TGF-β3蛋白表达水平参与促进神经血管的营养再生,并且良性调节具有神经保护作用的bFGF,使其趋于正常水平,从而改善慢性应激抑郁模型大鼠的行为学症状,这可能是针刺抗抑郁作用的分子机制之一。     

RESEARCH ON THE CHANGES OF THE CONCENTRATION OF IONIZED CALCIUM IN THE POINT NEIGUAN OF RABBITS WITH ACUTE HEART ISCHEMIA AFTER ELECTROACUPUNCTURE

Objective: To explore the mechanism of "Neiguan"(PC6) electroacupuncture in improving acute heart ischemia.Methods: Thirty-two healthy New Zealand rabbits were divided into 4 groups: normal group, sodium chloride group, model group and acupuncture group.Heart ischemia was induced in the rabbits by means of PPI auditive vein injection.We used the technique of microdialysis and inductively coupled plasma optical emission spectroscopy, and collected the extracellular fluid in the point Neiguan(PC6).In the mean time acupuncture of Neiguan was performed.The changes of concentration of ionized calcium in extracellular fluid of Neiguan were observed.Results: The concentrations of ionized calcium of the model group and the acupuncture group were decreased compared with the normal group(P0.05).After acupuncture the concentration of ionized calcium were increased compared with the model group(P0.05), showing that Neiguan electroacupuncture can increase the concentration of ionized calcium.Conclusion: The mechanism of Neiguan(PC6) electro-acupuncture in improving acute heart ischemia is associated with the change of concentration of ionized calcium in extracellular fluid of Neiguan(PC6).     

EFFECTS OF LOW-FREQUENCY ELECTROACUPUNCTURE ON THE IMMUNOLOGIC FUNCTION IN MORPHINE DEPENDENCE RATS

InGoodmanandGilmans’bookPharmaco logicalBasisofTherapeutics[1 ] ,acupuncturetherapyhasbeenregardedasthethirdtypeofremediesforheroinomania .However,uptonow ,majorityoftheresearchesfocusonhowtotreatwithdrawalsymptoms,feweronthereha bilitationofthepatient’simmunefunction .Inthepresentpaper,theeffectoflow frequencyelectroacupuncture (EA)onthecontentofTlymphocytesubgroupsintheperipheralbloodisobservedforrevealingmechanismsofacupunc tureinraisingimmunologicfunction .1　MATERIALSANDMETHOD…     

电针通过抑制下丘脑细胞外调节蛋白激酶5信号通路改善手术创伤大鼠脾脏自然杀伤细胞的功能

目的:观察下丘脑内细胞外调节蛋白激酶(ERK)5信号通路在电针改善手术创伤大鼠脾脏自然杀伤(NK)细胞功能中的作用及机制。方法:SD雄性大鼠随机分为对照组、创伤组、创伤+电针组、创伤+未电针组、创伤+低剂量BIX 02188组、创伤+高剂量BIX 02188组,每组6只。采用手术创伤模型,创伤+电针组选取双侧"足三里"穴,术后立刻电针,创伤+未电针组针刺双侧"足三里"穴,但不接电针仪,均持续30min,创伤+低剂量BIX 02188组、创伤+高剂量BIX 02188组于造模前1周进行侧脑室埋管,手术创伤前30min注射BIX 02188。免疫组化法和Western blot法观察下丘脑ERK 5磷酸化水平和蛋白表达,及促肾上腺皮质激素释放激素(CRF)蛋白表达,乳酸脱氢酶释放法和Real-time PCR法检测脾脏NK细胞杀伤功能及穿孔素(Perforin)和颗粒酶B(Granzyme B)的mRNA表达。结果:创伤组大鼠下丘脑内ERK 5信号通路显著激活,ERK 5磷酸化水平及蛋白表达均升高(P0.01,P0.05),电针及ERK 5抑制剂均可抑制ERK 5的磷酸化(P0.05,P0.01);手术创伤后,脾细胞Perforin及Granzyme B的mRNA明显下调,脾脏NK细胞的杀伤活力下降(P0.01,P0.05),电针治疗可增加Perforin及Granzyme B的基因表达,进而提高脾脏NK细胞的杀伤活力(P0.05);下丘脑内CRF的表达在创伤后明显上升(P0.01),给予ERK 5抑制剂或电针均可下调其表达(P0.01)。结论:电针改善手术创伤引起的脾脏NK细胞杀伤活力降低的机制之一可能是下调下丘脑内ERK 5信号通路的激活,减少CRF的产生,从而抑制下丘脑-垂体-肾上腺轴激活。     

电针对局灶性脑缺血再灌注大鼠受损神经元细胞外信号调节蛋白激酶的影响

目的:探索电针对脑缺血再灌注大鼠大脑受损神经元的保护作用及其细胞外信号转导机制。方法:随机将24只SD大鼠均分为假手术组、模型组、电针组和电针+PD98059组,采用改良Longa线栓法复制局灶性大脑中动脉缺血再灌注模型。电针组取"百会"大椎"穴,选用疏密波,频率80～100Hz,电流强度1～3mA,电压1～3V,持续电刺激60min。电针+PD98059组于腰椎间隙注入丝裂原活化蛋白激酶1的抑制剂PD980592.78mg/kg,并电针。依据Julio氏神经行为学评分法对各组大鼠进行评分,采用免疫组织化学染色法观察电针及PD98059阻滞状态下电针对模型大鼠右侧病灶处颞叶大脑皮层锥体细胞层细胞外信号调节蛋白激酶(ERK)蛋白表达的影响。结果:电针能改善模型大鼠的神经行为学分值(P<0.01),上调脑缺血再灌注大鼠受损神经元ERK的蛋白表达(P<0.01),其作用可被PD98059阻断(P<0.01)。结论:电针可减轻脑缺血再灌注大鼠大脑神经元的损伤,促进损伤修复,这一作用可能与其影响缺血再灌注后ERK信号通路的变化有关。     

针刀干预对颈椎病兔颈肌细胞凋亡的影响

目的:观察针刀干预对颈椎病兔劳损颈肌细胞凋亡的影响,揭示针刀治疗颈椎病可能的疗效机制。方法:6月龄新西兰兔随机分为空白组、模型组、针刀组、电针组,每组各6只,采用长期低头位方法制备颈椎病模型。造模后针刀组于斜方肌起点、胸锁乳突肌乳突附着点、颈椎关节突及局部硬结或条索状物,每次选2~3个点定为针刀进针部位,针刀干预每周1次,共3次;电针组取双侧"天柱""颈百劳""大杼",毫针针刺,同侧"天柱""大杼"穴接韩氏穴位神经刺激仪,每次治疗20min,隔天1次,共3周。干预结束1周后取颈肌行TUNEL检测和Western blot检测Bcl-2、Bax蛋白表达水平。结果:颈肌TUNEL阳性细胞核计数模型组较空白组明显升高(P0.01),针刀组较模型组、电针组明显降低(P0.01)。Western blot结果显示,各组Bcl-2蛋白表达水平差异无统计学意义(P0.05);模型组Bax蛋白表达水平较空白组明显升高(P0.01),针刀组Bax蛋白表达水平较模型组降低(P0.05);模型组Bcl-2/Bax蛋白比值较空白组降低(P0.05),针刀组Bcl-2/Bax蛋白比值较模型组、电针组升高(P0.05)。电针组各项指标与模型组比较差异均无统计学意义(P0.05)。结论:针刀干预颈椎病可降低颈肌细胞凋亡,这可能是针刀治疗颈椎病的疗效机制之一。     

针刀松解法对第3腰椎横突综合征局部软组织张力的影响

目的:探讨针刀治疗第3腰椎横突综合征的作用机制。方法:180例第3腰椎横突综合征患者随机分为针刀组和电针组,每组90例。针刀组在第3腰椎横突尖部(即压痛点处)进行针刀治疗,配合腰部过伸过屈手法,每周1次,共3周;电针组取双侧肾俞、腰阳关、阿是穴(局部压痛点)、患侧委中进行电针治疗,每周3次,共3周。采用JZL-Ⅱ软组织张力计测量两组治疗前、治疗后及治疗后6个月随访时第3腰椎横突局部软组织500g压力位移和能量吸收比的变化,采用日本骨科协会(JOA)下腰痛评分表评价两组的临床疗效。结果:针刀组500g压力位移在治疗后和随访时较治疗前升高(均P<0.01),而电针组较治疗前降低(P<0.05,P<0.01);针刀组组织能量吸收比在治疗后和随访时均较治疗前升高(均P<0.01),而电针组治疗后与治疗前比较差异无统计学意义(P>0.05),仅随访时较治疗前升高(P<0.01)。治疗后和随访时两组总体疗效等级分布,针刀组优于电针组(P<0.05,P<0.01)。结论:针刀治疗能显著提高第3腰椎横突局部软组织的500g压力位移和能量吸收比,降低局部软组织的张力,从而改善或减轻疼痛,且临床疗效优于电针。     

EFFECT OF ELECTROACUPUNCTURE OF THE HEART MERIDIAN ACUPOINTS ON ISCHEMIC CARDIAC FUNCTION IN THE RABBIT

Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart Meridian and the heart. Methods: Acute myocardial ischemia (AMI) was produced by intravenous infusion of pituitrin (40 u + 5% glucose injection 500 ml, 60 drips/min) in the rabbit. Left intraventricular pressure (LVP), maximal rising velocity of LVP (dp/dt max), isovolumetric pressure (IP) and end-diastolic pressure (EDP) of the left cardiac ventricle were used as the indexes. Three points of Heart Meridian [HM, from "Shenmen" (HT 7) to "Lingdao" (HT 4)] and the three points of Lung Meridian [LM, from "Taiyuan" (LU 9) to "Lieque" (LU 7)] were punctured with filiform needles and stimulated with hand-manipulation and electrically with ZY2-1 EA Therapeutic Apparatus. 30 rabbits anesthetized with urethane (1 g/kg) were randomly and evenly divided into control group, HM group and LM group. Resul     

电针“委中”穴对大鼠腰多裂肌损伤后TGF-β1、CTGF、Vimentin表达的影响

目的观察电针"委中"穴对大鼠腰多裂肌损伤修复过程中转化生长因子-β1(TGF-β1)、结缔组织生长因子(CTGF)和波形纤维蛋白(Vimentin)表达的影响,从肌肉再生修复角度探讨针刺治疗的最佳疗程。方法选取54只雄性SD大鼠,随机分成空白组、模型组、电针委中组,每组18只,各组再随机分成1、3、7 d时间点。模型组和电针委中组用0.5%布比卡因进行造模,造模后,电针委中组每天进行1次电针治疗,模型组同步固定,空白组不进行任何处理,3组分别在对应的时间点进行取材。通过Masson染色观察各组多裂肌胶原纤维和肌纤维的变化,通过免疫组化法检测各组多裂肌中TGF-β1、CTGF和Vimentin的表达变化。结果造模后模型组各时间点TGF-β1、CTGF、Vimentin表达水平升高(P <0.01),电针委中组各时间点TGF-β1表达均低于模型组(P <0.01),1、3 d电针委中组CTGF表达含量低于模型组(P <0.05),7 d组的表达含量显著低于模型组(P <0.01),1、3 d电针委中组的Vimentin表达含量均高于模型组(P <0.01),7 d电针委中组与模型组相比表达水平升高(P <0.05)。结论电针委中穴可以通过降低TGF-β1和CTGF的表达,同时增加Vimentin的表达来促进肌纤维再生,以利于骨骼肌损伤修复。     

臭氧穴位注射治疗下腰痛临床观察

目的:探讨穴位注射臭氧治疗下腰痛的临床价值。方法:120例下腰痛患者随机分为电针组、当归穴位注射组、臭氧穴位注射组,分别于气海俞、大肠俞、关元俞、局部阿是穴予以电针、当归穴位注射、浓度为30μg/mL臭氧注射。结果:臭氧注射组有效率为97·5%,高于电针组、当归注射液穴位注射组的85·0%和87·5%,差异具有非常显著或显著性意义(P<0·01或P<0·05),而电针组与当归穴位注射组比较,差异无显著性意义(P>0·05)。结论:臭氧穴位注射治疗下腰痛方法易行、疗效高,是值得推荐的理想方法。     

电针经p38 MAPK信号通路对坐骨神经损伤大鼠脊髓中AQP1和AQP4表达的影响＊

目的 探讨电针（electroacupuncture，EA）治疗对坐骨神经损伤大鼠脊髓中水通道蛋白AQP1和AQP4表达的影响，并揭示其可能作用机制。方法 将60只SD大鼠随机分成假手术组（Sham组）、模型组（Model组）、电针组（EA组）、抑制剂组（SB203580组）和电针 + 抑制剂组（EA + SB203580组），每组12只。采用钳夹法复制坐骨神经损伤大鼠模型，并给予电针和p38抑制剂SB203580干预14天。分别于干预前及干预后第7天和14天检测坐骨神经功能指数（SFI）；HE染色观察损伤处远端坐骨神经组织病理学变化；BL-410电生理系统检测大鼠神经传导速度（NCV）；qRT-PCR检测脊髓AQP1和AQP4 mRNA表达水平；Western blot检测脊髓AQP1、AQP4、p-p38MAPK和p38MAPK蛋白表达水平。结果 与Sham组比较，Model组大鼠坐骨神经组织结构不完整，出现明显炎症浸润和病理损伤，EA组和SB203580组大鼠坐骨神经组织相较于Model组坐骨神经组织炎症浸润和病理损伤得到明显缓解，EA + SB203580组与SB203580组的差异不大。与Sham比较，Model组大鼠脊髓中AQP1和AQP4 mRNA和蛋白表达水平以及p-p38MAPK/p38MAPK蛋白比值均显著增加，而SFI值和NCV显著降低（P < 0.01）；与Model组比较，EA组和SB203580组大鼠脊髓中AQP1 和AQP4 mRNA和蛋白表达水平、p-p38MAPK/p38MAPK蛋白比值均显著降低，而SFI值和NCV显著升高（P < 0.01）；与SB203580组比较，EA + SB203580组检测指标无显著性变化（P > 0.05）。结论 电针刺激可抑制脊髓中AQP1和AQP4表达，改善大鼠坐骨神经损伤，其可能与抑制p38MAPK信号通路活化有关。