慢性脑缺血致认知功能障碍大鼠神经细胞Caspase-3表达及GDNF给药的影响

目的观察慢性脑缺血后致认知功能障碍大鼠神经细胞半胱氨酸蛋白酶(Caspase-3)表达,并探讨胶质细胞源性神经营养因子(GDNF)对大鼠认知功能障碍和Caspase-3表达的影响。方法采用双侧颈总动脉永久结扎方法制备慢性前脑缺血大鼠模型,随机分为对照组、GDNF组和生理盐水组,分别在术后1月、2月,根据逃避潜伏期对各组大鼠进行记忆功能测定,应用免疫组织化学方法检测Caspase-3表达。结果双侧颈总动脉结扎1、2月组与对照组相比,逃避潜伏期明显延长;GDNF组与生理盐水组比较,逃避潜伏期明显缩短;与对照组相比,缺血组大鼠额叶皮层、海马的Caspase-3阳性细胞数明显增多,与生理盐水组比较,1、2月GDNF组大鼠额叶皮层、海马的Caspase-3阳性细胞数明显减少。结论GDNF可改善认知功能,其机制可能是通过影响Caspase-3凋亡关键蛋白酶表达,抑制神经细胞凋亡。     

川芎嗪对肝星状细胞增殖及结缔组织生长因子表达的影响

目的探讨川芎嗪(TMP)对肝星状细胞HSC-T6增殖及结缔组织生长因子(CTGF)表达的影响。方法不同剂量的TMP作用于HSC-T6细胞不同时间后,MTT法检测细胞的增殖;ELISA法检测Ⅰ型、Ⅲ型胶原和透明质酸(HA)的合成;West-ern blot法测定CTGF的表达。结果100～1000mg/L的TMP作用于HSC-T6细胞后,细胞的增殖明显受到抑制,且呈剂量依赖性;Ⅰ型、Ⅲ型胶原和HA的合成减少,CTGF的表达也减少,二者下降程度呈正相关(r分别为0.727、0.643和0.769)。结论TMP能够有效抑制肝纤维化形成,其可能的机制为抑制HSC增殖并降低CTGF的表达,从而阻断细胞内基质的形成。     

迷走神经刺激对癫痫大鼠海马缝隙连接蛋白43表达的影响

目的观察迷走神经刺激(vagus nerve stimulation,VNS)对海人酸(kainic acid,KA)致癫痫大鼠海马星形胶质细胞缝隙连接蛋白43(Connexin 43,Cx43)表达的影响,探讨Cx43与癫痫之间的关系及其在VNS治疗癫痫中的作用。方法将SD大鼠随机分为对照组、KA组和VNS+KA组,每组10只;KA组和VNS+KA组大鼠左侧脑室注射3μl 0.05%KA溶液,制备癫痫模型,对照组注射等量生理盐水;VNS+KA组行VNS。观察各组大鼠行为变化,记录皮层脑电图(electrocorticogram,ECoG);采用免疫组织化学法和Western blot法检测各组大鼠海马星形胶质细胞Cx43的表达。结果大鼠左侧脑室注射KA 3⁵ min后,KA组大鼠为RacineⅣ5 min后,KA组大鼠为RacineⅣ^Ⅴ级重型癫痫发作,脑电图可见棘波、棘慢波及簇状高尖波等异常脑电发放;VNS+KA组大鼠为RacineⅠⅤ级重型癫痫发作,脑电图可见棘波、棘慢波及簇状高尖波等异常脑电发放;VNS+KA组大鼠为RacineⅠ^Ⅲ级轻型发作,脑电发放较KA组减轻,对照组无癫痫发作及异常脑电发放。KA组大鼠海马Cx43阳性细胞数和相对表达量均明显高于对照组和VNS+KA组(P均<0.01)。结论癫痫大鼠海马Cx43的表达与癫痫发病机制密切相关,VNS可降低癫痫大鼠海马Cx43的表达,抑制癫痫发作。     

短暂前脑缺血再灌注对大鼠海马脑区脑源性神经营养因子蛋白及mRNA表达的影响

目的探讨短暂前脑缺血再灌注(transient forebrain ischemia-reperfusion,I/R)对脑源性神经营养因子(brainderived neurotrophic factor,BDNF)蛋白及mRNA表达的影响,为进一步探索大鼠海马CA1区神经元损伤机制提供新的思路。方法将雄性SD大鼠随机分为control组、sham组和I/R组,利用Western blot和荧光定量PCR分析I/R后大鼠BDNF蛋白及mRNA表达的变化;染色质免疫共沉淀(chromatin immunoprecipitation,ChIP)试验检测I/R后大鼠BDNF基因启动子上H3K27的乙酰化水平。结果与control组相比,sham组大鼠CA1和CA3区BDNF蛋白和m RNA表达差异无统计学意义(P> 0. 05)。与sham组相比,I/R组大鼠CA1区BDNF蛋白表达显著下降(P <0. 001),而CA3区BDNF蛋白表达增高(P <0. 05);I/R组大鼠CA1区BDNF mRNAⅠ、Ⅱ和Ⅵ的表达均显著增高(P <0. 01),而mRNAⅣ的表达...     

丹参酮ⅡA对大鼠脊髓损伤后星形胶质细胞增殖的MAPK通路的影响

目的探讨丹参酮ⅡA(tanshinoneⅡA,TⅡA)对大鼠脊髓损伤(spinal cord injury,SCI)后星形胶质细胞增殖的MAPK通路的影响。方法建立大鼠SCI模型,获得星形胶质细胞,培养14 d后,采用免疫荧光法检测星形胶质细胞中胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)的表达;MTT法选择TⅡA抑制星形胶质细胞生长的最适浓度和时间;Western blot法检测MAPK通路各蛋白的磷酸化情况。结果星形胶质细胞中有GFAP特异性表达;TⅡA抑制星形胶质细胞生长的最适浓度为15μg/mL,最适作用时间为36 h;15μg/m L TⅡA作用0和4 h,星形胶质细胞中p-JNK高于8和12 h,ERK1/2和p38无变化。结论 TⅡA主要通过JNK依赖性途径对星形胶质细胞的生长进行调控。     

小胶质细胞对阿尔兹海默病发生发展的影响作用

阿尔兹海默病(老年性痴呆,AD)是由β淀粉样蛋白(Aβ)和微管相关蛋白(Tau)聚集形成的具有毒性作用的寡聚物而引起的老年人主要以记忆力下降和脑部形成老年斑、神经纤维缠绕为特征的神经退行性疾病. 小胶质细胞作为中枢神经系统中的固有免疫细胞,是脑内免疫监视的关键成分,发挥内源性免疫防御作用. 正常生理状态的小胶质细胞能有效吞噬和清除毒性Aβ寡聚体,阻止AD发生. 在AD病理过程中,过度激活的小胶质细胞通过补体依赖途径过度吞噬突触,导致突触丧失,同时大量释放炎症因子,促进Tau相关病理变化,对神经元造成直接损伤,导致认知功能下降. 由此可见,小胶质细胞在AD发生发展过程中起着双刃剑的作用,探明小胶质细胞的极化状态及其在AD疾病机理中的作用将为攻克AD的药物研发提供突破性思路.     

短暂前脑缺血再灌注对大鼠海马中脑源性神经营养因子启动子与组蛋白去乙酰化酶3结合的影响及其作用机制

目的 评价短暂前脑缺血再灌注(ischemia-reperfusion,I/R)对大鼠海马中脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)启动子与组蛋白去乙酰化酶3(histone deacetylase 3,HDAC3)结合的影响,并探讨其作用机制。方法 采用Pulsinelli四血管夹闭法建立SD大鼠的I/R模型(I/R组),同时设假手术组(Sham组)。尼氏染色法观察大鼠海马中神经元存活情况;染色质免疫共沉淀(chromatin immunoprecipitation,ChIP)法检测大鼠海马中BDNF启动子(Bdnf-p1、Bdnf-p2、Bdnf-p4和Bdnf-p6)与HDAC3的结合情况;qPCR法检测大鼠海马中反义脑源性神经营养因子(brain derived neurotrophic factor antisense,BDNF-AS)的表达情况。结果 与Sham组比较,I/R组大鼠海马CA1区神经元数目大幅减少,CA3和DG区神经元数目变化较小。I/R组大鼠海马CA1区中Bdnf-p1和Bdnf-p2与HDAC3结合...     

在小鼠胚胎干细胞系嵌入碳酸盐碳灰石DNA载体的上皮细胞钙粘蛋白及纤维蛋白元细胞粘附蛋白对转基因的运输和表达的影响

干细胞有通过基因操作分化为某一特定类型的细胞的潜力，因此，在再生药品中代表了有一个新的和多能的细胞替换来源。然而，常规方法将基因转移到这些祖细胞，有一些弊端，特别是涉及安全性和有效性问题。最近报道了生物功能的碳酸盐碳灰石的DNA载体嵌入纤维连接蛋白和上皮细胞钙粘蛋白载体嵌合体的发展，导致其与胚胎干细胞表面高亲和力的相互影响，并为随后的表达加快转基因运输。在这里，我们展示利用DNA，细胞粘附蛋白和无机晶体合成高功能复合粒子的分子基础，最后为对细胞基础治疗具有应用潜力的小鼠干细胞系建立一个高度转染机制。     

丁酸钠对CHO细胞生长及rhEPO表达量的影响

目的:通过对比实验的方式,在培养基中添加不同浓度的丁酸钠(NaBu),以此获取CHO细胞生长与产物rhEPO表达量的影响.方法:在24孔板上采用不同浓度的丁酸钠(0mM、0.25mM、0.5mM、0.75mM)培养CHO细胞生长,设定对照组与研究组,并借助血球计数板测定细胞密度,以此保持各组相同的细胞接种数据,测定实验...     

肿节风注射液对荷瘤小鼠T淋巴细胞增殖活力及NK细胞活性的影响

目的研究肿节风注射液(ZJF)对荷瘤小鼠T淋巴细胞增殖活力及NK细胞活性的影响,探讨其抗肿瘤作用的机制。方法无菌取C57BL/6纯系小鼠脾脏,制成5×106个/ml的单个脾细胞悬液,MTT法检测不同浓度(50、25、12.5、6.25和3.13 mg/ml,以生药量计)的ZJF对正常小鼠T淋巴细胞增殖的影响。将近交系615小鼠经左腋皮下注射小鼠前胃癌Fc细胞(1×106个/ml,0.2 ml/只),复制荷瘤小鼠模型,并随机分成5组:ZJF低、中、高剂量组(给药剂量分别为2、10、20 mg/kg,以生药量计)、CTX组[0.3 g/(kg·3 d)]及阴性对照组(生理盐水0.1 ml/10 g),MTT法检测ZJF对荷瘤小鼠T淋巴细胞增殖及NK细胞活性的影响。结果 ZJF可显著促进正常小鼠T淋巴细胞的增殖(P<0.05),且呈剂量依赖性;ZJF低、中、高剂量组荷瘤小鼠T淋巴细胞的增殖活力明显高于阴性对照组(P<0.05),且呈剂量依赖性,ZJF中、高剂量组荷瘤小鼠NK细胞的活性明显高于阴性对照组(P<0.05)。结论 ZJF可促进正常小鼠与荷瘤小鼠T淋巴细胞的增殖活力,增强NK细胞活性,为其抗肿瘤作用机制的研究提供了实验依据。     

Effect of polyphenols on oxidative stress and mitochondrial dysfunction in neuronal death and brain edema in cerebral ischemia

Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti-inflammatory, anti-carcinogenic, anti-viral, anti-ulcer, and anti-apoptotic properties. One important consequence of ischemia is neuronal death and oxidative stress plays a key role in neuronal viability. In addition, neuronal death may be initiated by the activation of mitochondria-associated cell death pathways. Another consequence of ischemia that is possibly mediated by oxidative stress and mitochondrial dysfunction is glial swelling, a component of cytotoxic brain edema. The purpose of this article is to review the current literature on the contribution of oxidative stress and mitochondrial dysfunction to neuronal death, cell swelling, and brain edema in ischemia. A review of currently known mechanisms underlying neuronal death and edema/cell swelling will be undertaken and the potential of dietary polyphenols to reduce such neural damage will be critically reviewed.     

丝裂原活化蛋白激酶信号转导通路在脑缺血再灌注损伤中的作用及机制

目的探讨丝裂原活化蛋白激酶(mitogen activated protein kinase,MAPK)信号转导通路在脑缺血再灌注损伤(cerebral ischemia/reperfusion,I/R)中的作用及机制。方法将大鼠随机分为6组:未使用p38MAPK抑制剂SB203580的假手术组(Sham组)、使用抑制剂的假手术组(Sham/SB组)、未使用抑制剂再灌注24 h组(I/R 24 h组)、未使用抑制剂再灌注48 h组(I/R 48 h组)、使用抑制剂再灌注24 h组(SB 24 h组)和使用抑制剂再灌注48 h组(SB 48 h组)。采用大脑中动脉线栓法(middle cerebral artery occlusion,MCAO)复制大鼠局灶性脑缺血再灌注模型,使用抑制剂的各组于造模前30 min经腹腔注射SB203580(5 mg/kg,溶于5 mg/ml DMSO)。采用免疫荧光双标法检测大鼠大脑中动脉(middle cerebral artery,MCA)和脑微血管(microvascular,Mic.V)周围IgG的渗出;Western blot和RT-PCR法检测大鼠脑组织中p38、一氧化氮合酶(inducible nitric oxide synthase,iNOS)、基质金属蛋白酶-9(matrix metalloproteinase,MMP-9)、胶原Ⅳ型(collagenⅣ)蛋白和基因表达的变化。结果随着再灌注时间的延长,大鼠脑血管内IgG渗出量增加(P<0.01);经p38MAPK抑制剂预处理后,IgG的渗出程度有所减轻。脑缺血再灌注后,大鼠脑组织中p38、iNOS、MMP-9蛋白的表达水平和基因mRNA的转录水平均明显升高(P<0.05),经p38MAPK抑制剂预处理后,能显著抑制p38、iNos、MMP-9蛋白的表达水平和基因mRNA的转录水平(P<0.05);collagenⅣ蛋白的表达水平和基因mRNA的转录水平随着缺血时间的延长而逐渐下降(P<0.05),经p38MAPK抑制剂预处理后,其下降程度有所减轻(P<0.05)。结论 MAPK通路中的关键蛋白p38、iNOS、MMP-9在脑缺血时表达显著增加,其过度表达直接导致血脑屏障的破坏,抑制其表达,从而遏制对血脑屏障的破坏,有望为I/R的治疗提供新的途径。     

Effect of oxidative damage due to excessive protein ingestion on pancreas function in mice

The present study was undertaken to evaluate the effect of oxidative damage due to excessive protein diet on pancreas function in mice. For this purpose, thirty male (C57BL/6J) mice were randomly divided into three groups and fed on different diets as follows: group 1 was fed on a normal diet, group 2 was fed on an excessive protein diet and group 3 was fed on an excessive protein diet supplemented with 0.06 g/kg cysteamine. Each group was fed for 2 weeks, and then pancreas samples were collected to examine oxidative and antioxidant parameters and pancreas function. The results showed that ingestion of an excessive protein diet markedly increased contents of malondialdehyde (MDA) and decreased T-AOC and activities of antioxidants SOD and GSH-Px, compared with a normal diet (P < 0.05). Pancreas weight and concentration of protein, DNA and RNA were significantly higher (P < 0.05), digestive enzyme activities were significantly lower and levels of somatostatin and insulin were higher in mice fed with an excessive protein diet than those fed with a normal protein diet. In the group fed with excessive protein diet supplemented with cysteamine, oxidative stress was mitigated and pancreas function was improved. These data demonstrate that excessive protein ingestion could increase oxidative damage of free radicals on pancreas function through destroying the balance of oxidants and antioxidants.     

睡眠剥夺对小鼠肾组织中IL-6、TNF-α表达水平的影响

目的探讨睡眠剥夺(sleep deprivation,SD)对小鼠肾组织中炎症因子IL-6和TNF-α表达的影响。方法将C57雄性小鼠随机分为空白对照组及SD 24、48和72 h组,利用COBAS INTEGRA 800全自动生化分析仪检测小鼠血清中尿素氮(urea nitrogen,BUN),肌酐(creatinine,CREA)和尿酸(uric acid,URCA)的含量;黄嘌呤氧化酶法检测肾脏组织中超氧化物歧化酶(superoxide dismutase,SOD)活性,硫代巴比妥酸法检测丙二醛(malonaldehyde,MDA)含量;对动物进行组织学检查,ELISA法检测肾脏组织中IL-6和TNF-α含量。结果与空白对照组比较,随SD时间延长,小鼠血清中BUN、CREA和URCA含量在SD 24 h后显著增高(P 0. 01),48和72 h持续增高(P 0. 01);小鼠肾脏组织中SOD活性随SD时间延长持续下降(P 0. 01),MDA含量持续增加(P 0. 01);HE染色可见肾小管上皮细胞空泡样变性、轻度水肿,肾小球和间质内可见炎症细胞浸润和红细胞,肾小囊腔闭塞;IL-6、TNF-α含量随SD时间延长持续增加(P 0. 01)。结论 SD诱发肾组织氧化损伤,引起脂质过氧化,使得肾脏结构和功能受损,促进炎症因子IL-6和TNF-α的大量释放,激活炎症反应,加重对肾脏的损伤。     

重组金黄葡萄球菌肠毒素B及热休克蛋白65融合蛋白的原核表达及其在小鼠体内的体液免疫效果

目的原核表达重组金黄葡萄球菌肠毒素B(recombinant Staphylococcus aureus enterotoxin B,r SEB)及热休克蛋白65(heat shock protein 65,HSP65)融合蛋白r SEB-HSP65,并探讨其在小鼠体内的体液免疫效果。方法采用分子生物学方法将修改过TCR Vβ结合区的r SEB基因与HSP65基因融合,构建重组表达质粒p ET-28a-r SEB-HSP65,转化E.coli BL21(DE3),IPTG诱导表达,经铜柱亲和层析纯化。将纯化蛋白经小鼠背部皮下注射,分别于第0、14、28天各免疫1次,分别于第14、28、42 d经小鼠尾静脉采血,分离血清,间接ELISA法检测小鼠血清中抗-SEB的Ig G水平。结果重组表达质粒p ET-28a-r SEB-HSP65经双酶切及PCR鉴定,证明构建正确。表达的重组蛋白r SEB-HSP65的相对分子质量约85 000,主要以包涵体形式表达,表达量约占全菌总蛋白的40.81%,纯化蛋白纯度约为90%。各组免疫小鼠均可产生较高滴度抗体,且在第14、28及42天大部分含铝佐剂疫苗组的效价显著高于相同剂量的无铝佐剂疫苗组(P<0.05),第42天时无铝佐剂低剂量疫苗组与含铝佐剂低剂疫苗量组间差异无统计学意义(P>0.05)。结论成功在E.coli BL21(DE3)中表达了重组蛋白r SEB-HSP65,且可诱导小鼠产生较高的抗体水平。     

Effect of Peucedanum japonicum Thunb on the expression of obesity-related genes in mice on a high-fat diet

The present study describes the effect of Peucedanum japonicum Thunb (PJT) intake on the expression of obesity-related genes in mice fed a high-fat diet. To explore the mechanism underlying the effect of PJT, This study focused on the expression of genes, especially those related to obesity and metabolism syndrome, in the liver and adipose tissues. In agreement with our previous observations, intake of 10 % PJT for 4 weeks significantly reduced serum triglyceride (TG), leptin, abdominal fat, and adipocyte size. PJT also significantly increased fecal excretion of TG, decreased that of bile acid, and tended to increase the fecal excretion of total cholesterol. Microarray analysis was used to monitor changes in 324 metabolic syndrome-related genes in the liver. Statistically significant upregulation of PPP1R10, RORC, and PBEF1 genes and downregulation of DUSP1, INSIG2, and SERPINA12 genes were noted and confirmed by real-time RT-PCR. These changes were indicative of increased fatty acid oxidation in the maintenance of lipid homeostasis and insulin sensitivity in the livers of PJT-fed mice. PJT increased the expression of PPARγ, FXRα, DGAT1, and ATGL genes, suggesting an enhancement of adipocyte differentiation and normalization of functionality of adipose tissue.     

人脐血干细胞在局灶性脑缺血大鼠体内的迁移与分化

目的观察人脐血干细胞(human umbilical cord blood stem cells,HUCBSCs)在局灶性脑缺血大鼠体内的迁移与分化,探讨HUCBSCs移植对缺血性脑损伤大鼠神经功能恢复可能的作用机制。方法采用线栓法制备大鼠大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)再灌注模型,将造模成功的20只大鼠随机分为2组:移植组15只,造模成功后24 h,经尾静脉移植1 ml(2×106个)DAPI/CM-Dil荧光染料标记的HUCBSCs;模型组5只,造模成功后24 h,经尾静脉移植等量生理盐水。分别于移植前及移植后3、7、15 d进行神经功能缺损评分(neurological severity score,NSS),并取脑组织,制备冰冻切片,HE染色观察脑组织形态,荧光显微镜观察HUCBSCs在脑组织中的迁移和分布,免疫荧光法检测脑组织中巢蛋白(Nestin)和神经元特异性烯醇化酶(neuron specific enolase,NSE)的表达。结果移植组大鼠HUCBSCs移植后7 d起,其改良的NSS(m NSS)显著低于对照组(P<0.05)。移植后15 d,大鼠脑组织病理改变明显减轻。移植后3 d起,可见病灶及其周围部位有阳性细胞存在,随着时间的推移,脑缺血病灶部位的阳性细胞增多;移植后7 d,迁移至病灶部位的细胞数增加;移植后15 d,迁移至病灶部位的细胞数量达观察期内的高峰,各时间点阳性细胞数差异有统计学意义(P<0.05)。移植后15 d,大鼠脑组织中CM-Di I/NSE-FITC和CM-Di I/Nestin-FITC双阳性细胞率分别为85.2%和81.6%。结论 HUCBSCs经静脉移植后,能在大鼠体内存活,并向损伤部位迁移,具有向神经元细胞方向分化的潜能,对脑缺血大鼠的神经功能恢复具有促进作用。     

细胞膜表面异位表达热休克蛋白70的CD4~+T细胞诱导EAE小鼠保护性免疫作用

目的探讨细胞膜表面异位表达热休克蛋白70(heat shock protein 70,HSP70)在T细胞疫苗(T cell vaccine,TCV)诱导保护性免疫中的作用。方法建立髓鞘少突胶质细胞糖蛋白多肽35-55(myelin oligodendrocyte glycoprotein,MOG35-55)诱发的C57BL/6小鼠实验性自身免疫性脑脊髓炎(experimental auto-immune encephalomyelitis,EAE)模型,以MOG35-55肽特异性CD4~+T细胞为疫苗,经尾静脉免疫小鼠。对EAE小鼠的临床神经功能进行评分,流式细胞术检测小鼠脾脏中CD4~+CD25~+Foxp3~+调节T细胞(Treg)百分比、ELISA法检测脾细胞培养上清中细胞因子IFNγ、IL-4、IL-10和IL-17含量。结果射线照射可诱导活化CD4~+T细胞表面异位表达HSP70;HSP70~+T组小鼠症状显著轻于HSP70-T封闭组(P 0. 01);HSP70~+T组小鼠脾脏中CD4~+CD25~+Foxp3~+Treg细胞百分比、脾细胞上清中IL-4、IL-10含量均显著高于HSP70-T组(P 0. 01),而IFNγ、IL-17含量均显著低于HSP70-T组(P 0. 01)。结论细胞膜表面异位表达HSP70在活化T细胞诱导的保护性免疫中发挥重要作用。     

Effect of supplement with lactic-acid producing bacteria on fatigue and physical activity in patients with chronic fatigue syndrome

Disturbances in intestinal microbial ecology and in the immune system of the host have been implicated as a part of the pathogenesis in chronic fatigue syndrome. Probiotic lactic acid producing bacteria have been shown to prevent and alleviate gastrointestinal disturbances and to normalize the cytokine profile which might be of an advantage for patients suffering from chronic fatigue syndrome. The aim of the study was to evaluate the effect of Lactobacillus paracasei ssp. paracasei F19, Lactobacillus acidophilus NCFB 1748 and Bifidobacterium lactis Bb12 on fatigue and physical activity in CFS patients. Fifteen patients fulfilling the criteria set by international researchers in the field at the US Centre for Disease Control and Prevention in 1994 for chronic fatigue syndrome, were included in the study. The patients had high fatigue severity scores and high disability scores. During the first two weeks baseline observations without treatment were assessed, succeeded by four weeks of intake of a probiotic product and a four-week follow-up period. The fatigue, health and physical activity was assessed by the use of the Visual Analogue Scales and the SF-12 Health Survey. Faecal samples were collected and the normal microflora was analysed. Neurocognitive functions improved during the study period while there were no significant changes in fatigue and physical activity scores. No major changes occurred in the gastrointestinal microflora. At the end of the study 6 of 15 patients reported that they had improved according to the assessment described. The findings in this study that improvement of health is possible to achieve should encourage further studies with interventions with probiotics in patients with CFS.