癫痫大鼠脑内白细胞介素6的表达特征

有临床资料显示，有癫痫病史或癫痫发作的患者脑脊液和血浆白细胞介素6(IL-6)浓度升高，动物实验也证明，在各种癫痫发作模型中脑内IL-6表达增加。我们试图通过研究红藻氨酸(KA)诱导癫痫发作的动物模型相关脑区中IL-6的表达特征及其与c—Fos表达的比较，进一步探讨IL-6在癫痫发作中的意义及其细胞学来源。     

维生素E对离心运动大鼠骨骼肌超微结构的影响

背景：维生素E作为一种抗氧化剂,具有清除自由基的功效,可减轻运动中抗氧化酶所受的自由基损伤,减缓疲劳出现,从而提高运动能力。 目的：通过维生素E对骨骼肌运动性损伤的干预,探讨其对骨骼肌运动性损伤形态学变化的影响,为骨骼肌运动性损伤的形态学研究和抗损伤机制的探索提供实验依据。 设计、时间及地点：随机分组,动物实验,于2007-05/10在沈阳体育学院国家体育总局重点实验室和中国医科大学电镜中心完成。 材料：雄性SD大鼠16只,随机均分为对照组、运动组、生理盐水组、维生素E组。 方法：维生素E组于实验前1 d腹腔注射维生素E胶丸,注射量为1.0~1.2 mg/kg,总量为4 mL/kg,每8 h注射1次,共4次。生理盐水组以生理盐水为对照,注射方式、注射量及处死时间同维生素E组。运动组只进行运动,不给予药物或生理盐水,对照组仅为常规饲养,无任何干预。采用一次力竭性下坡跑运动建造大鼠损伤模型,运动结束后,取大鼠右侧肱三头肌,制做电镜标本。 主要观察指标：肌原纤维和肌节排列情况;Z线异常变化;细胞膜、细胞核、线粒体、肌浆网、T小管、卫星细胞等形态学改变。 结果：补充维生素E组后,骨骼肌损伤的超微结构改变有明显的改善,虽然肌浆网尚有水肿表现,但肌纤维排列基本整齐,Z线明暗带清晰,细胞核清楚。 结论：补充维生素E可有效地减少离心运动对骨骼肌肌纤维损伤的形态学改变,肌纤维排列更加整齐、肌节更加清晰,其作用可能与维生素E的抗氧化和促进蛋白质的合成功能等因素有关。     

参麦注射液对脑梗死患者血白细胞介素6的影响

正参麦注射液是常用于临床的中成药针剂,主要用于休克的治疗,也可以用于急性脑血管病的治疗,具有较好的疗效。本文应用参麦注射液治疗脑梗死,并观察患者用药前后血白细胞介素6(interleukin 6,IL-6)的水平和神经功能的变化,以探讨参麦注射液治疗脑血管病的机制,现报道如下。1资料与方法1一般资料以2012-04—2015-02在我院神经内科住院治疗的急性脑梗死患者为观察对象。入选标准:年龄55~75     

脑梗死后出血性转化患者血浆白细胞介素1β、6、10含量的变化

目的观察脑梗死后出血性转化患者血浆IL-1β、IL-6、IL-10的变化,探讨脑梗死出血性转化与脑梗死后炎性反应之间的关系。方法 60例脑梗死并发出血性转化患者按出血严重程度分为HI-1型15例,HI-2型15例,PT-1型15例,PT-2型15例。按年龄、性别、神经功能缺损评分(NIHSS)、出血部位、治疗措施相匹配的原则选取无出血性转化的脑梗死患者作为对照组。分别为:HI-1型对照组15例,HI-2型对照组15例,PT-1型对照组15例,PT-2型对照组15例。测定所有患者入院2 d清晨血浆IL-1β、IL-6、IL-10、S-100β蛋白浓度。结果和相对应的对照组相比出血性转化患者发病初期IL-1β、IL-6浓度显著高于对照组,而IL-10、S-100β蛋白的浓度无明显差别。结论在同样程度脑损伤的情况下,急性期的高水平的促炎性细胞因子IL-1β、IL-6可能是通过炎性反应促进了血脑屏障的破坏和脑梗死后出血性转化的发生。     

脑卒中后抑郁患者血清白细胞介素-6水平变化的研究

目的研究脑卒中后抑郁(PSD)患者血清白细胞介素-6(IL-6)水平变化,探讨PSD患者的抑郁与免疫功能变化的关系。方法采用放射免疫法检测59例PSD患者、36例非PSD患者及43例正常人的血清IL-6水平。59例PSD患者随机给予抗抑郁治疗 脑血管病恢复期方案治疗(n=29)或仅给予脑血管病恢复期方案治疗(n=30),观察患者治疗前后血清IL-6水平变化。结果治疗前,PSD组血清IL-6水平显著高于非PSD组(P<0.01)和正常对照组(P<0.01);治疗后,PSD抗抑郁治疗组与PSD未抗抑郁治疗组相比,HAMD评分(P<0.01)和IL-6水平(P<0.01)均显著降低。在PSD组治疗前、PSD抗抑郁治疗组及PSD未抗抑郁治疗组治疗后,HAMD评分与血清IL-6水平相关系数分别为0.375(P<0.01)、0.452(P<0.01)和0.397(P<0.01)呈显著性正相关。结论PSD患者血清IL-6水平明显升高并且与抑郁程度相关。     

多发性硬化患者血清和脑脊液中白细胞介素-6的变化及其意义

本研究应用生物学方法检测27例多发性硬化（MS）患者血清和脑脊液（CSF）白细胞介素-6（IL－6）水平，以探讨IL－6在MS发病中的作用。结果显示MS患者血清IL-6水平显著高于其他非炎症性神经病（NIND）组及正常对照（NC）组，其CSFIL－6水平亦显著高于NIND组；但MS患者血清与CSFIL-6水平不呈线性相关，血清IL-6水平随病情稳定而下降。本研究结果提示IL－6可能参与MS的免疫病理过程。     

急性脑出血患者血清单胺氧化酶和白细胞介素6的表达

目的检测单胺氧化酶(MAO)和白细胞介素6(IL-6)在急性脑出血患者血清中的表达,探讨其与急性脑出血患者病情预后的关系。方法选取52例急性脑出血患者作为实验组,分别于发病后的第1、3、7、14天采集其血清行MAO和IL-6检测;同期选取30例健康志愿者为对照组。结果急性脑出血组MAO和IL-6在第1、3、7、14天的表达明显高于对照组,MAO和IL-6在发病后第1天表达最高,其后逐渐下降。血清中MAO和IL-6的表达在少量脑出血组、中量脑出血组、大量脑出血组依次增高。结论急性脑出血患者血清MAO和IL-6水平明显增高,且与出血量呈正相关,可作为判断脑出血量和病情预后的血液指标。     

维生素E对离心运动后大鼠骨骼肌线粒体内丙二醛、超氧化物歧化酶的影响

背景：许多实验表明自由基的增加与骨骼肌运动性损伤有关，而维生素E作为一种抗氧化剂，具有清除自由基的功效，可减轻运动中抗氧化酶所受的自由基损伤，减缓疲劳出现，进而提高运动能力。 目的：从细胞线粒体自由基代谢的角度，探讨维生素E对离心运动后大鼠骨骼肌细胞线粒体丙二醛、超氧化物歧化酶的影响，以进一步阐明维生素E抗骨骼肌运动性损伤的内在机制。 设计、时间及地点：随机分组，动物实验观察，于2007-05/10在沈阳体育学院国家体育总局重点实验室和中国医科大学重点实验室完成。 材料：雄性SD大鼠48只，体质量(304±12) g。随机分为对照组、运动组、生理盐水组、维生素E组，12只/组。 方法：维生素E组腹腔注射维生素 E胶丸，1.0~1.2 mg/kg，总量为4 mL/kg，初次注射时间为鼠正式实验前1 d，以后每8 h注射1次，共4次。生理盐水组以生理盐水为对照，注射方式、注射量及运动方式、处死时间同维生素E组。运动组只进行运动，不给予药物或生理盐水，对照组仅为常规饲养，无任何干预。采用一次力竭性下坡跑运动建造大鼠损伤模型，运动结束后，取大鼠右侧肱三头肌。 主要观察指标：采用微量测定试剂盒和6010紫外-可见分光光度计测定丙二醛含量及超氧化物歧化酶活力。 结果：肱三头肌细胞线粒体各组丙二醛、超氧化物歧化酶在离心运动后24 h均显著增加(P < 0.01)。与运动组比较，生理盐水组丙二醛、超氧化物歧化酶值均无显著性差异(P > 0.05)，维生素E组丙二醛显著降低(P < 0.01)，而超氧化物歧化酶显著增高(P < 0.01)。 结论：补充维生素E可降低骨骼肌细胞线粒体丙二醛的含量，增加细胞线粒体超氧化物歧化酶的活性，提高骨骼肌细胞的抗氧化能力，进而可减轻自由基对肌肉的损伤作用。维生素E对运动性骨骼肌损伤的预防作用主要是通过维生素E的抗氧化作用完成的。     

补肾益气中药与膝骨性关节炎关节液中白细胞介素1及白细胞介素6的表达*☆

背景：对骨性关节炎的治疗目前尚无逆转和阻断的有效方法,只能缓解症状和延缓病变的进程。 目的：探讨补肾益气法中药预防家兔膝骨性关节炎的作用机制。 方法：4月龄健康日本长耳大白兔随机分为对照组、模型组、中药大、中、小剂量组、盐酸氨基葡萄糖胶囊对照组。造成兔膝骨性关节炎模型同时分别给予不同剂量中药及盐酸氨基葡萄糖胶囊灌胃4周,应用酶联免疫吸附法测定关节液中白细胞介素1及白细胞介素6的变化,同时取关节软骨行大体及光镜检查。 结果与结论：治疗后动物关节软骨有不同程度的色泽变化,骨赘、骨囊肿形成,软骨关节面出现浅表性糜烂,部分标本软骨缺损深达软骨中层,出现软骨剥脱,但程度明显降低。中药大、中、小剂量组及盐酸氨基葡萄糖胶囊对照组关节液中白细胞介素1及白细胞介素6水平均显著降低(P < 0.05),且随用药剂量增大,兔关节液中白细胞介素1及白细胞介素6水平降低幅度增强。提示补肾益气法中药可能通过降低兔关节液中白细胞介素1及白细胞介素6水平,来达到预防骨性关节炎的发生。     

蛛网膜下腔出血患者脑脊液白细胞介素6的变化及其意义

用噻唑兰（ＭＴＴ）法测定２０例原发性蛛网膜下腔出血（ＳＡＨ）及２０例对照组脑脊液白细胞介素６（ＩＬ－６）含量。结果：ＳＡＨ患者ＩＬ－６含量明显高于对照组（Ｐ＜０．０１）；临床出现症状性脑血管痉挛的患者ＩＬ－６含量高于无此并发症者（Ｐ＜０．０５）；ＳＡＨ患者ＩＬ－６水平与ＨｕｎｔａｎｄＨｅｓ临床病情分级有正相关关系（ｒ＝０．４９１７，Ｐ＜０．０５）。提示免疫／炎症反应参与了ＳＡＨ后迟发性脑血管痉挛的发生。     

Ultrastructural changes after concentric and eccentric contractions of human muscle

Four normal subjects performed a 20 min step test using a step of the same relative height. During the test the quadriceps muscle of one leg contracted concentrically throughout by stepping up, while the contralateral muscle contracted eccentrically by controlling the step down. Thus both muscles performed the same amount of work. Three subjects had bilateral needle biopsies just prior to exercise. All four had bilateral biopsies immediately after exercise, and 24-48 hours later when the muscles which had contracted eccentrically were painful. The samples were examined by light and electron microscopy. No abnormalities were seen in pre-exercise samples nor after exercise in muscles which had contracted concentrically. The muscles which had contracted eccentrically showed some damage immediately after exercise. In the samples taken 24-48 hours after exercise the damage was more marked and involved a greater percentage of fibres. In view of the known differences between these types of contractions it is suggested that the initial damage is mechanically induced. The exacerbation of damage with time could be due to mechanical or chemical factors.     

热应激预处理对离心运动大鼠骨骼肌自由基代谢的影响

背景：研究表明热预处理能够提高肌肉抗损伤的能力,但具体的机制尚不清楚。目的：观察热应激预处理对离心运动大鼠骨骼肌超氧化物歧化酶活性及丙二醛含量的影响。方法：雄性Wistar大鼠随机分为对照组、离心运动组、预热应激+离心运动组。热应激温度为43 ℃,时间约35 min。采用-16°下坡跑台跑做大负荷间歇性离心运动,跑速为26.8 m/min,运动5 min,间歇1 min,共进行10组。分别于运动前1 h、运动后1,24,48 h取大鼠腓肠肌,采用硫代巴比妥酸法测定大鼠丙二醛含量,黄嘌呤氧化酶法测定超氧化物歧化酶活性。结果与结论：与对照组比较,离心运动组大鼠腓肠肌丙二醛含量显著增高(P < 0.05),并随运动后时间的延长逐渐升高,超氧化物歧化酶活性随运动后时间的延长显著降低(P < 0.05)。与离心运动组比较,预热应激+离心运动组大鼠腓肠肌超氧化物歧化酶活性显著增高(P < 0.05),丙二醛含量显著降低(P < 0.05)。说明热应激预处理可增强骨骼肌超氧化物歧化酶活性,降低丙二醛含量,对离心运动损伤有保护作用。     

Increased activities of MB and BB isozymes of creatine kinase in denervated neonatal and adult rat muscle

Creatine kinase (CK) activity and isozyme patterns were assessed in newborn and adult rat anterior tibial muscle in response to denervation. Total CK activity was low in the control neonatal muscle, gradually increasing to the adult level within 1 month. Denervation prevented this normal increase, and, therefore, CK activity was reduced to 25% of control at 2 months. In the denervated adult muscle, total CK activity decreased to 50% of control within 3 weeks and remained at that level. Denervation of neonatal muscle resulted in a greater conservation of MB isozyme compared with controls. The alteration in BB isozyme expression was even more dramatic with a 33-fold difference expressed at 2 months in terms of percent total CK in denervated vs. control muscle. In denervated adult muscle, MB and BB isozyme activities increased gradually, attaining levels 3-fold and 13-fold, respectively, above control muscle at the end of the experimental period.     

Exaggerated expression of skeletal muscle-derived interleukin-6, but not TNFalpha, in mice lacking interleukin-10

IL-10 reduces cytokine expression in non-muscle tissues, but its effect on skeletal muscle remains undefined. Therefore, we tested the hypothesis that endogenous IL-10 acts to reduce cytokines in the gastrocnemius muscle by comparing IL-6 and TNFalpha expression in wild-type (IL-10(+/+)) and IL-10 deficient (IL-10(-/-)) mice following an inflammatory insult induced by peripheral LPS. IL-6 mRNA expression increased following LPS for both IL-10(+/+) and IL-10(-/-) mice; the response was greater and prolonged in IL-10(-/-) mice. Muscle TNFalpha mRNA also increased, but without differences between genotypes. IL-6 protein concentrations were elevated by LPS with a greater and prolonged response for IL-10(-/-) mice, but TNFalpha did not change. These results provide the first in vivo evidence that endogenous IL-10 attenuates IL-6 expression by skeletal muscle in response to LPS.     

离心运动对大鼠骨骼肌细胞增殖和波形蛋白表达的时序性影响

背景：骨骼肌损伤后是通过肌卫星细胞的增殖形成新核来生长和修复的,但关于骨骼肌细胞增殖和波形蛋白表达的关系很少报道。 目的：探讨骨骼肌细胞增殖与波形蛋白表达的关系以及运动性骨骼肌微损伤后修复的机制。 设计、时间和地点：随机对照动物实验,于2007-12/2008-09在湖南师大运动人体科学实验中心完成。 材料：健康成年8周龄雄性SD大鼠50只,随机分成对照组和运动后即刻、运动后3 h、运动后24 h和运动后48 h组,每组10只大鼠。 方法：运动组大鼠进行重复3 d的力竭性离心运动,力竭模型采用跑台运动,速度为16 m/min,坡度为-16°,持续运动至力竭,对照组为正常大鼠,未做运动。 主要观察指标：运动组分别于运动后即刻,3,24,48 h取材,对照组一次性取材,免疫组织化学法检测各组大鼠肱三头肌内侧头不同恢复时相增殖细胞核抗原PCNA的表达和波形蛋白的表达。 结果：骨骼肌细胞增殖出现时序性变化,运动后即刻增殖指数显著大于对照组,运动后24 h达到峰值,运动后48 h增殖指数有所下降。骨骼肌细胞中波形蛋白表达出现时序性,而且其免疫反应分值的时序性与增殖指数出现一致性,但与增殖指数不具有相关性。 结论：3 d重复性力竭离心运动后骨骼肌细胞增殖和波形蛋白的表达出现时序性变化。波形蛋白的表达与肌细胞增殖具有一定的关系,但不是惟一的影响的因素。     

Impact of resistance exercise training on interleukin-6 and JAK/STAT in young men

The JAK/STAT signaling pathway is essential for myogenic regeneration and is regulated by a diverse range of ligands, including interleukin-6 (IL-6) and platelet-derived growth factor-BB (PDGF-BB). Our aim was to evaluate the responsiveness of IL-6 and PDGF-BB to intense exercise, along with STAT3 activation, before and after 12 weeks of resistance training. In young men, IL-6 and PDGF-BB protein concentrations were quantified in biopsied muscle and increased at 3 h post-exercise (17.5-fold and 3-fold, respectively). The response was unaltered by 12 weeks of training. Similarly, STAT3 phosphorylation was elevated post-exercise (12.5-fold), irrespective of training status, as was the expression of downstream targets c-MYC (8-fold), c-FOS (4.5-fold), and SOCS3 (2.3-fold). Thus, intense exercise transiently increases IL-6 and PDGF-BB proteins, and STAT3 phosphorylation is increased. These responses are preserved after intense exercise. This suggests they are not modified by training and may be an essential component of the adaptive responses to intense exercise.     

The effects of strength,aerobic, and concurrent exercise on skeletal muscle damage in rats

Introduction: In this study we examined oxidative stress and skeletal muscle damage resulting from acute strength, aerobic, or concurrent exercise in rats. Methods: The animals were divided into control (C), strength (SE), aerobic (AE), and combined (CE) exercise groups. They were euthanized at 3 different time‐points (6, 24, and 48 h) after acute exercise. Results: SE exercise rats had increased dichlorofluorescein oxidation at 6 h post‐exercise and decreased superoxide dismutase activity at all time‐points. Glutathione peroxidase activity and sulfhydryl levels were increased in the AE group at 48 h post‐exercise. Serum lactate dehydrogenase activity was increased in the SE and CE groups at 24 h and in the AE group at 48 h. Echo intensity was elevated at 24 h for all groups. Conclusions: Forty‐eight hours was sufficient for complete recovery from oxidative stress and muscle damage in the SE and CE groups, but not in the AE group. Muscle Nerve 50 : 79–86, 2014     

Sexual dimorphism in rat cerebrum and cerebellum: different patterns of catalytically active creatine kinase isoenzymes during postnatal development and aging

During postnatal development, maturation and aging the Wistar rat cerebrum and cerebellum synthesize, in a different sex-dependent manner, catalytically active dimeric cytosolic (c) muscle-type (MM) and heart-type (MB) creatine kinase (CK), besides the supposedly sole type brain-specific (BB) CK. In both sexes, typical and atypical neuromuscular cCK isoenzymes were present during the study for 26 months. As in rat heart, females showed more cerebral cCK variants (41%) in comparison to males. Female rats exhibited about 93% more cerebellar variants of cCK isoenzymes as compared to males. The male cerebellum showed predominantly BB- and MB-CK during the whole study in comparison to the female one that contained all neuromuscular cCK variants. Only female rats showed decreases and increases of cerebral CK specific activity. In contrast to males, coinciding with the weaning period, cerebral female CK activity decreased 45% from 14 to 21 days and increased about 3-fold in female rats and only 1.3-fold in males from 21 to 45 days of age. Contrary to the remarkable 4-fold increase of chicken brain CK specific activity exhibited at old age, the rat did not show another cerebral CK activity increase during senescence in either sex. However, sex differences of CK specific activity appeared in the cerebellum at all ages. From the sex-specific plateau phase at 45–60 days until 2.2 years of age, about a 41% independent increase of cerebellar CK specific activity was observed in both sexes. After puberty, the differential cerebellum–cerebrum values of CK specific activity were higher for female rats than males during youth, adulthood and senescence. The present work shows that in rat cerebrum and cerebellum, production of ATP through anaerobic transphosphorylation by the CK/PC system is sex-and age-specific, especially in the cerebellum, when glycolysis and the Krebs cycle lose capacity. As in rat heart, under physiological conditions at all ages the several cCK isoenzymes do participate in a gender-specific manner, in favor of females, in diverse functions of the different cell compartments of glial and neuronal cells with regard to their high and fluctuating energy demands not completely covered by anaerobic and aerobic glycolysis.     

Nuclear factor-kappaB p65 and upregulation of interleukin-6 in retinal ischemia/reperfusion injury in rats

We previously demonstrated that endogenous interleukin-6 (IL-6) is upregulated and may be neuroprotective after retinal ischemia. The purpose of this study is to investigate the role of nuclear factor kappa-B (NF-kappaB) in regulating IL-6 expression after ischemia. NF-kappaB p65 mRNA levels were significantly elevated between 2 and 12 h after the insult. A high number of NF-kappaB p65 positive cells were detected in the inner retina at 12 h after ischemia. Activated nuclear NF-kappaB p65 and IL-6 were colocalized in cells, which were also marked by a microglial/phagocytic cell marker (ED1) in the inner retina. Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which inhibits IkappaB degradation and hence prevents the activation and translocation of NF-kappaB into the nucleus) abolished the increase in NF-kappaB p65 mRNA levels after the insult, while there was no effect by helenalin (an inhibitor which inhibits NF-kappaB activity by alkylation of the p65 subunit, thereby blocking its binding to the target DNA). However, MG-132 and/or helenalin significantly diminished the increase in IL-6 mRNA levels after the insult. Small interfering RNAs (siRNAs, inhibit target gene expression through the sequence-specific destruction of the target messenger RNA) against NF-kappaB p65 significantly reduced the increase in NF-kappaB p65 mRNA levels as well as IL-6 mRNA levels after ischemia. The number of retinal ganglion cells (RGCs) was also significantly decreased using the inhibitors of NF-kappaB compared with those of the controls after ischemia. These findings support the hypothesis that upregulation of endogenous retinal IL-6 in retinal I/R injury in microglial/phagocytic cells is controlled predominantly by NF-kappaB p65.     

脑外伤SIRS患者外周血中IL-2、IL-6的临床观察

目的探讨颅脑损伤后全身炎症反应综合征(SIRS)患者外周血IL-2、IL-6表达的临床意义。方法56例符合SIRS诊断的颅脑损伤患者按GCS分为重型、中型和轻型3组,入院24h内进行SIRS评分,同时采取双抗体夹心ELISA法检测外周血IL-2、IL-6含量,并进行组间比较,同时与GCS评分、SIRS评分进行相关性分析。结果轻型、中型和重型组血中IL-2含量分别是(558.9±219.6)μ/ml、(614.2±209.6)μ/ml和(904.5±401.37)μ/ml,重型组明显高于中型和轻型组(P<0.05)。轻型组、中型组和重型组血中IL-5含量分别是(10.39±7.66)pg/ml、(26.75±14.68)pg/ml和(45.8±17.24)pg/ml,各组间有非常显著差异(P<0.01)。GCS评分及SIRS评分均与IL-2、IL-6呈显著负相关(P<0.01)。预后差的患者的IL-2、IL-6含量显著高于全组病人的水平(P<0.01)。结论IL-2、IL-6在颅脑损伤后SIRS患者外周血中有较高的表达,可能是引起SIRS的因素之一。