铅对星形胶质细胞活力影响的检测评价

近 2 0年来 ,人们对脑组织中星形胶质细胞的结构和功能有了更深入的了解。它在神经系统的正常生理活动、脑的发育和神经病理过程中都具有重要作用[1,2 ] 。对星形胶质细胞的体外研究表明 ,星形胶质细胞可合成铅特异结合蛋白 ,对铅有主动摄取和储存作用 ,被称为铅在脑组织中的储藏池[3 ] 。同时 ,研究也表明它对铅毒性作用远较内皮细胞敏感[4] 。所以 ,探索低水平铅暴露对星形胶质细胞的影响及防护方法是十分必要的。到目前为止 ,有关铅毒性的判定 ,基本上采用细胞形态观察 ,该方法不仅烦琐 ,而且主观。更主要的是 ,它不能反映铅对细胞活力的…     

星形胶质细胞的研究

近年来星形胶质细胞应用研究是神经科学研究的热点,该文综述了星形胶质细胞的形态、调节机制、功能、与疾病的联系等,星形胶质细胞在神经系统的生长及修复中起重要作用。     

氯丙烯对神经细胞胞浆膜和线粒体膜 Ca~(2 )-ATP 酶,Na~ ,K~ -ATP 酶活性的影响

氯丙烯对神经细胞胞浆膜和线粒体膜Ｃａ２＋┐ＡＴＰ酶，Ｎａ＋，Ｋ＋┐ＡＴＰ酶活性的影响张磊谢克勤高树君孙克任（山东医科大学毒理学研究室，济南２５００１２）用鸡胚脑神经细胞研究１－烯丙基氯－３对细胞胞浆膜和线粒体膜Ｃａ２＋－ＡＴＰ酶，Ｎａ＋，Ｋ＋－ＡＴＰ...     

苯丙胺对星形胶质细胞的影响及星形胶质细胞分泌液在苯丙胺致PC12细胞毒性中的保护作用

目的:探索苯丙胺(amphetamine,AMPH)对星形胶质细胞(astrocyte,AS)的影响以及星形胶质细胞分泌液astrocytic secretory fluid,ASF)在AMPH致PC 12细胞损伤中的作用。方法:观察不同浓度的AMPH对AS数量和形态变化的影响。在PC12细胞中加入AMPH,建立细胞毒性模型,随后加入ASF、神经生长因子(nerve growth factor,NGF)及其抗体,观察PC12细胞形态的变化以及存活率的差异。结果:(1)AMPH浓度达到9mM时,AS数量减少,而胞体肥大。(2)ASF和NGF均可起保护受损的PC12细胞,其中ASF效果显著优于NGF(P<0.0001)。加入抗体中和ASF中的NGF后,ASF仍然有较好的保护作用。结论:高剂量的AMPH对AS有损伤作用。ASF对AMPH损伤的PC12细胞的保护作用显著优于NGF。     

星形胶质细胞转分化为神经元的研究进展

近年来, 转分化技术在干细胞和再生学领域迅速发展, 具有较大的研究价值。研究发现, 随着转分化诱导条件的成熟, 可以改变其他细胞的谱系来获得神经元。并且, 星形胶质细胞 （As） 广泛分布于中枢神经系统的灰质和白质中, 其过度增生会形成胶质纤维瘢痕, 是阻碍神经功能恢复的关键。因此, As 转分化为神经元成为目前研究的热点。As 的转分化既可以阻止胶质瘢痕的形成, 又能获得新的神经元。本文就 As 的功能及其转分化为神经元的相关研究进行综述。     

星形胶质细胞对神经干细胞分化的影响实验研究

目的研究星形胶质细胞对神经干细胞分化的影响。方法随机在我院动物实验中心选取3只大鼠为研究对象,将本次实验均分为普通星形胶质细胞的培养的对照组以及星形胶质细胞与神经干细胞互不接触状态下共同培养的实验组。对比两组星形胶质细胞对神经干细胞分化的影响效果。结果实验组的纯化星形胶质细胞胶质纤维酸性蛋白抗体标记为阳性,其细胞纯度高到96%,且在神经元特异性烯醇化酶阳性细胞与酪氨酸羟化酶阳性细胞均比对照组多。结论星形胶质细胞不仅可以加快神经干细胞向神经元细胞的分化以及向多巴胺神经元细胞的分化,而且可以延长神经元存活时间,降低神经元凋亡率。     

丹红注射液对体外培养星形胶质细胞的影响

目的 观察丹红注射液对星形胶质细胞（astrocyte, As）增殖作用. 方法 不同浓度丹红注射液作用于体外培养的大鼠As, 噻唑蓝染色（MTT）比色法对丹红注射液进行细胞毒性分析, 流式细胞技术分析细胞增殖情况. 结果 MTT比色分析得出丹红注射液对细胞生长的半数抑制率（IC50）约为17.8%（丹红注射液与培养基的体积比）, 安全作用浓度<8%;流式细胞分析结果：药物组细胞DNA合成期细胞所占百分比（S%）和增殖指数（PI值）（S+G2/M）×100%较正常对照组显著增高（P<0.01）. 结论 适当浓度丹红注射液可促进星形胶质细胞增殖.     

线粒体KATP开放剂二氮嗪促进星形胶质细胞摄取谷氨酸

目的研究线粒体ATP敏感性钾通道(mitochondrial ATP-sensitive potassium channel, mitoKATP)开放剂二氮嗪(diazoxide)对星形胶质细胞摄取谷氨酸(glutamate)的影响.方法取新生大鼠脑星形胶质细胞作原代培养,用液体闪烁计数仪测定[3H]-D,L-谷氨酸的摄入量判断细胞的谷氨酸摄取功能.结果二氮嗪呈浓度依赖性地促进星形胶质细胞摄取谷氨酸,且能抑制1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium,MPP+)对星形胶质细胞摄取谷氨酸的损伤作用;浓度在100μmol·L-1以上时,二氮嗪可完全逆转MPP+对星形胶质细胞摄取谷氨酸的抑制作用;二氮嗪的上述作用可被选择性mito KATP 阻断剂5-羟基癸酸 (5-hydroxydecanoate,5-HD)拮抗.结论二氮嗪通过开放mitoKATP增强星形胶质细胞谷氨酸转运体(glutamate transporters, GluTs)的功能.     

星形胶质细胞在癫痫发病中的作用研究

癫痫的发病机制十分复杂,近年来星形胶质细胞在癫痫发生发展中的关键作用逐渐显现。通过对星形胶质细胞的干预,可能为癫痫的治疗提供新的靶点。本文综述星形胶质细胞在癫痫发病中的作用研究。     

星形胶质细胞肿胀与肝性脑病

<正>肝性脑病(encephalopathy,HE)是由严重肝病引起的,以代谢紊乱为基础的中枢神经系统功能失调综合征。EH神经症状复杂多样,但脑部病理变化并     

Cytotoxic effects induced by hexachlorobenzene in Squilla mantis (L.) (Crustacea, Stomatopoda).

Contamination of marine environments by hexachlorobenzene (HCB) represents a serious concern for potential consequences on ecosystem and human health. Despite this, information on cytotoxic effects on marine organisms is still largely lacking. In this study, we investigated cytotoxic effects induced by HCB on gonads and muscular tissue of Squilla mantis by analysing Na(+)/K(+)-ATPase activity and plasma membrane fluidity. This crustacean species was selected as a model for its habitat, trophic level, feeding behavior, and commercial exploitation for human consumption. Time course experiments revealed that low concentrations of HCB (i.e. 50 nM) determine an exponentially decrease of Na(+)/K(+)-ATPase activity and a significant modification of cellular membrane fluidity. Significant negative relationships between Na(+)/K(+)-ATPase activity and membrane fluidity were observed, suggesting that changes in the structure and packing of cellular membranes induced by HCB may be the primary factor affecting the activity of essential bilayer-associated enzymes. Overall these findings suggest that even small concentrations of HCB may determine important changes on cell metabolism with potential cascade effects on recruitment of this commercial species.     

Placental oxidative stress in malnourished rats and changes in kidney proximal tubule sodium ATPases in offspring

• 1 Intrauterine malnutrition has been linked to the development of adult cardiovascular and renal diseases, which are related to altered Na⁺ balance. Here we investigated whether maternal malnutrition increases placental oxidative stress with subsequent impact on renal ATP‐dependent Na⁺ transporters in the offspring.
• 2 Maternal malnutrition was induced in rats during pregnancy by using a basic regional diet available in north‐eastern Brazil. Placental oxidative stress was evaluated by measuring thiobarbituric acid‐reactive substances, which were 35–40% higher in malnourished dams (MalN). Na⁺ pumps were evaluated in control and prenatally malnourished rats (at 25 and 90 days of age).
• 3 Identical Na⁺/K⁺‐ATPase activity was found in both groups at 25 days (approximately 150 nmol P_i/mg per min). However, although Na⁺/K⁺‐ATPase increased by 40% with growth in control rats, it remained constant in pups from MalN.
• 4 In juvenile rats, the activity of the ouabain‐insensitive Na⁺‐ATPase was higher in MalN than in controls (70 vs 25 nmol P_i/mg per min). Nevertheless, activity did not increase with kidney and body growth: at 90 days, it was 50% lower in MalN than in controls. The maximal stimulation of the Na⁺‐ATPase by angiotensin (Ang) II was 35% lower in MalN than in control rats and was attained only with a much higher concentration of the peptide (10^?10 mol/L) than in controls (10^?14 mol/L).
• 5 Protein kinase C activity, which mediates the effects of AngII on Na⁺‐ATPase was only one‐third of normal values in the MalN group.
• 6 These results indicate that placental oxidative stress may contribute to fetal undernutrition, which leads to later disturbances in Na⁺ pumps from proximal tubule cells.

     

知母皂苷对脂多糖引起星形胶质细胞炎症因子释放的影响及机制

目的研究知母皂苷(SAaB)对脂多糖(LPS)诱导的星形胶质细胞(AC)炎症因子释放的抑制作用及JNK信号传导通路对其的影响。方法实验设对照组、LPS组、SAaB组和阻断剂组。ELISA法和Griess法分别测定各组AC培养液中TNF-α和NO的含量;Western blot检测AC磷酸化JNK和磷酸化c-Jun蛋白表达水平的改变;免疫荧光染色法观察AC的磷酸化ATF-2蛋白表达水平。结果 AC在LPS(10mg.L-1)刺激下TNF-α和NO的分泌、磷酸化JNK1、磷酸化c-Jun和磷酸化ATF-2蛋白表达水平与正常对照组比较均明显增高。特异性JNK特异性阻断剂SP600125(10μmol.L-1)可明显抑制LPS引起的TNF-α和NO产生增加以及磷酸化ATF-2蛋白表达水平;SAaB(1、10、100μmol.L-1)则可明显降低TNF-α和NO产生,下调磷酸化JNK、磷酸化c-Jun和磷酸化ATF-2的蛋白表达水平。结论 SAaB能明显抑制LPS诱导的大鼠皮层AC炎症因子的释放,这种作用可能与其下调JNK信号转导通路有关。     

Comparing the effects of two neurotoxins in cortical astrocytes obtained from rats of different ages: involvement of oxidative damage

Oxidative stress has been recognized as a potential mediator of cell death. Astrocytes play an active role in brain physiology responding to harmful stimuli by activating astrogliosis, which in turn has been associated either with survival or degenerative events. The characterization of the mechanistic actions exerted by different toxins in astrocytes is essential to understand the brain function and pathology. As age plays a critical role in degenerative processes, the aim of this study was to determine whether the administration of equimolar concentrations of two neurotoxins evoking different toxic patterns can induce differential effects on primary astrocytes obtained either from newborn or adult rats, with particular emphasis on those events linked to oxidative stress as a potential source of damage. Primary cortical astrocyte cultures derived from rat brains were exposed to 1‐methyl‐4‐phenylpyridinium (MPP+) or beta‐amyloid peptide (β‐amyloid). Mitochondrial functionality and cell viability were determined as physiological parameters, whereas lipid and protein oxidation were used as markers of oxidative damage. The results of these experiments pointed towards a higher vulnerability to MPP + over β‐amyloid, on most of the tested markers. Hence, in order to allow a comprehensive evaluation of astrocytic responses against MPP + intoxication, a third astrocyte group was included for dose‐response experiments: astrocytes derived from aged rats. The present data indicate that the differences associated with age were mainly found in astrocytes exposed to MPP + (25 and 50 μM) at 1‐h treatment. Results are discussed in terms of the differential mechanisms involved in each model. Copyright © 2012 John Wiley & Sons, Ltd.     

粉防己碱对肾型高血压左室肥厚大鼠心肌ATP酶活性的影响

目的　观察粉防己碱对肾型高血压左室肥厚大鼠心肌 Ａ Ｔ Ｐ 酶活性的影响。方法　采用二肾一夹肾型高血压形成大鼠左室肥厚,用光电比色、无机磷显色法测定心肌细胞膜 Ｎａ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶及线粒体 Ｎａ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶、 Ｃａ２ ＋ Ａ Ｔ Ｐ酶活性。结果　左室肥厚组大鼠心肌细胞 Ａ Ｔ Ｐ 酶活性明显降低,粉防己碱５０ ｍｇ·ｋｇ － １·ｄ － １ｉｇ 连续给药８ ｗｋ 可逆转左室肥厚,显著增加心肌细胞膜 Ｎａ ＋ , Ｋ＋ Ａ Ｔ Ｐ 酶及线粒体 Ｃａ２ ＋ Ａ Ｔ Ｐ酶活性。结论　粉防己碱因其钙拮抗作用,在降低血压、逆转左室肥厚的同时,可使细胞膜钠泵活性、线粒体钙泵活性恢复     

Carbon disulfide cytotoxicity on cultured cardiac myocytes of rats

Although epidemiological studies have suggested that carbon disulfide produces cardiovascular effects in occupationally exposed workers, little is known about its cellular mechanism. The purpose of the present study was to evaluate the functional and histological effects on cardiac myocytes cultured under a condition of carbon disulfide exposure. Cardiac myocytes were isolated from neonatal rat ventricles by trypsin, dispersed and cultured for 3 days in a full Dulbecco's Modified Eagle Medium containing 2% calf serum. Then the myocytes (10(6) myocytes/mL) were incubated with carbon disulfide at concentrations of 0, 20, 40, and 80 micromol/mL for 24 h. The beating arrest rate of myocytes for each group was examined, succinodehydrogenase (SDH) activity in the myocardial cells was assessed using a cytochemical method, and a morphological examination was performed. We found that the beating arrest rate of cardiac myocytes increased with increasing exposure levels. Vacuolization and pseudopodia could be seen in the cytoplasm of the exposed group. SDH activity decreased with increasing exposure levels. The results suggest that CS2 has a direct and dose-dependent cytotoxic effect. The biochemical mechanism may be a reduction of the availability of energy (adenosine triphosphate) to cardiac myocytes, resulting in a decrease of contractility by lack of energy.     

谷氨酸和γ-氨基丁酸对原代培养星形胶质细胞神经甾体合成释放的影响

目的研究氨基酸类神经递质对原代培养大鼠大脑皮质星形胶质细胞神经甾体合成释放的影响。方法采用原代培养的大鼠大脑皮质星形胶质细胞,分别加入不同浓度的谷氨酸和γ-氨基丁酸处理48h;采用固相萃取结合高效液相色谱质-谱联用分析方法提取分离和测定细胞培养液中游离型(脱氢表雄酮,DHEA;孕烯醇酮,PREG;别孕烯醇酮,AP)及结合型神经甾体(脱氢表雄酮硫酸酯,DHEAS;孕烯醇酮硫酸酯,PREGS)。结果与生理盐水对照组比较,谷氨酸处理使PREG和PREGS水平明显下降,DHEAS水平明显升高;γ-氨基丁酸处理使PREG水平明显降低,AP水平增加。结论谷氨酸和γ-氨基丁酸两种神经递质对原代培养的星形胶质细胞PREG合成释放均呈抑制作用;谷氨酸对DHE-AS、γ-氨基丁酸对AP的合成释放分别呈现明显促进作用;高剂量的谷氨酸还可以抑制PRGES的合成和释放。     

抗虫活性菌株SIPI—9764的产物研究

放线菌ＳＩＰＩ－９７６４的发酵液经溶媒萃取、硅胶柱层析和结晶等，分离出２个异黄酮类化合物，命名为ＳＩＰＩ－９７６４－１和－Ⅱ。通过对其理化性质和ＵＶ、ＩＲ、ＭＳ、ＮＭＲ图谱的分析，确定化全物ＳＩＰＩ－９７６４－１和－Ⅱ分别为４‘，５，７－Ｔｒｉｈｙｄｏｘｙｉｓｏｆｌａｖｏｎｅ和４’，７－Ｄｉｈｙｄｒｏｘｙｉｓｏｆｌａｖｏｎｅ，与已知的金雀异黄素和黄豆苷元相一致。两个化合物显示出一定的Ｎａ／ＫＡＴＰ     

Resveratrol improves cardiovascular function and reduces oxidative organ damage in the renal, cardiovascular and cerebral tissues of two-kidney, one-clip hypertensive rats

Objectives The putative protective effects of resveratrol against oxidative injury in the heart, kidney and brain tissues of rats induced with the two‐kidney, one‐clip (2K1C) hypertension model were investigated. Methods Wistar albino rats were divided into sham‐operated (n = 8) or 2K1C groups, in which rats received either resveratrol (10 mg/kg per day, i.p., n = 8), or saline (n = 8) starting at Week 3 after the surgery and continuing for the following 6 weeks. Indirect blood pressure recordings and echocardiographic images were made to evaluate cardiac function. At the end of Week 9 the animals were decapitated and plasma, heart, kidney and brain were taken for biochemical assays, while aortic rings were prepared for vascular reactivity studies. Key findings 2K1C hypertension resulted in increased blood pressure, aortic hypercontractility and reduced left ventricular function, leading to increased lipid peroxidation and myeloperoxidase activity, concomitant with significant reductions in tissue glutathione, superoxide dismutase, Na⁺/K⁺‐ATPase and catalase activities in the cardiac, renal and brain tissues, indicating the presence of oxidative tissue damage in peripheral target organs. Elevated plasma levels of lactate dehydrogenase, creatine kinase, as well as reduced plasma levels of antioxidant capacity and nitric oxide further verified the severity of oxidative injury. A 6‐week treatment with resveratrol reversed all the measured parameters, ameliorated hypertension‐induced oxidative injury in the target organs and improved cardiovascular function. Conclusions Resveratrol improved cardiovascular function through the augmentation of endogenous antioxidants and the inhibition of lipid peroxidation by maintaining a balance in oxidant/antioxidant status, which also ameliorated hypertension‐induced oxidative injury in the cardiac, renal and cerebral tissues.     

锌对铅致大鼠心肌氧化性损伤的保护作用

目的　探讨硫酸锌 (ZnSO4)对低水平醋酸铅 (PbAc2 )暴露的雄性SD大鼠心肌微粒体膜 (MMS)氧化性损伤保护作用的可能机制。方法　暴露组 :PbAc2 3 0mg (kg·d) ;干预组 (3个 ) :剂量为PbAc2 3 0mg (kg·d)分别 +ZnSO42 5、5、1 0mg(kg·d) ;对照组 :给等容积蒸馏水。连续灌胃 9周后断头取血分析铅、血锌含量 ;取尿液分析尿铅含量 ;取心肌制备其MMS分析Na+,K+ ATP酶 (Na泵 )、Ca2 + ATP酶 (Ca泵 )、超氧化物歧化酶 (SOD)活力、丙二醛 (MDA)含量。离体实验将大鼠MMS悬液与最终浓度PbAc2 0 4mmol L组成混合液 ,把此混合液分为 4组 ,其中 3组分别加ZnSO40 3、0 6、1 2mmol L ,37℃共同温育 30min后 ,观察ZnSO4对PbAc2 致MMS氧化性损伤的保护作用。结果　在体实验 3个染PbAc2 +ZnSO4干预组血铅平均值分别为 0 1 7、0 1 6、0 1 5μmol L;MMSMDA含量平均值分别为 2 2 8、2 1 7、2 0 7μmol g;Ca泵活性平均值分别为 1 3 1 7、1 2 98、1 2 52mmol (h.g) ,均明显低于染PbAc2 3 0mg (kg·d)组 (P <0 0 5或P <0 0 1 ) ;而 3个染PbAc2 +ZnSO4干预组血锌、尿铅含量、MMSNa泵和SOD活力平均值分别为 72、78、88μmol L ,0 33、0 36、0 39μmol L ,1 0 0 5、1 1 39、1 1 95mmol (h .g) ;1 3、1 4、1