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蝎毒对癫痫大鼠海马内强啡肽原mRNA表达的影响 总被引:7,自引:0,他引:7
姜春玲 《中国应用生理学杂志》2000,16(1):72-74
目的和方法:本工作用红藻氨酸癫痫模型,通过对癫痫大鼠蝎毒处理后民内哟啡肽原mRNA(KPUYNmRNA)表达的原位杂交观察,对国产蝎粗毒抗癫痫反复发作的细胞分子机制进行初步探讨。结果:原位杂交的实验显示,三周KA后,实验对照组与空白对照组相比,腹侧海马尤其是海马门区PDYNmRNA阳性数目明显减少(P〈0.01)。实验给药组大鼠8例,其中有6例腹侧海马门区PDYNmRNA阳性神经元数目未见减少且有 相似文献
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脑啡肽对大鼠海马神经细胞IL-6基因表达的影响 总被引:3,自引:0,他引:3
本文研究了大鼠海马内微量注射甲硫-脑啡肽(M-ENK)对海马细胞的白细胞介素-6(Interleukin-6,IL-6)基因表达的影响。大鼠双侧海马内微量注射细菌内毒素脂多糖各1μl(LPS,浓度:50ng/ml),于90min后用原位杂交技术检测到海马结构IL-6的基因表达,以齿状回颗粒细胞层显著。当海马内预先注射M-ENK(每侧1μl,浓度:10μg/μl),30min后再给予脂多糖则未见IL-6基因表达。结果表明M-ENK及LPS可影响脑内IL-6的基因表达,在中枢调节机体免疫功能中,IL-6可能具有重要作用。 相似文献
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白细胞介素受体的一种共享分子──IL-2Rγ黄仕和,秦椿华(卫生部武汉生物制品研究所,武昌430060)(同济医科大学工业毒理研究室,汉口430030)关键词IL-2Rγ迄今为止,已有10种白细胞介素受体(IL-IR~IL-10R)被克隆出来。这些受... 相似文献
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丹参酮对阿尔茨海默病样大鼠海马内白介素1β和白介素6 mRNA表达的影响 总被引:5,自引:0,他引:5
目的探讨丹参酮(tanshinone, Tan)抗β-淀粉样肽神经元毒性的分子机制.方法应用凝聚态β-淀粉样肽1-40片段(amyloid β-peptide1-40, Aβ1-40)在大鼠双侧海马齿状回背侧细胞带进行微量注射以建立拟人类阿尔茨海默病(Alzheimer's disease, AD)样动物模型;采用明暗箱被动回避法、穿梭法测试学习记忆功能;用半定量逆转录-聚合酶链反应(RT-PCR)方法测定海马内白介素1β(IL-1β)和白介素6(IL-6)mRNA含量;以丹参酮(tanshinone, Tan)(50mg/ kg)对Aβ1-40处理的大鼠连续灌胃14d,观察其干预效果.结果海马内注射Aβ1-40 14 d后,经行为学检测大鼠学习记忆功能明显减退,海马内IL-1β和IL-6 mRNA表达均显著高于对照组(P< 0.01);Tan(50mg/ kg)连续灌胃14 d能显著抑制大鼠学习记忆功能的减退和上述病理变化.结论 Tan对Aβ1-40诱导的大鼠学习记忆功能障碍具有显著改善作用,并能有效地抑制其海马内IL-1β和IL-6 mRNA的升高,这可能为Tan治疗AD样大鼠的分子机制. 相似文献
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秋水仙素对大鼠前脑生长抑素mRNA表达的影响 总被引:2,自引:0,他引:2
本实验用地高辛标记生长抑素(SOM)反意。RNA探针原位杂交组织化学研究了秋水仙素对大鼠前脑SOMmRNA表达的影响。结果表明秋水仙素对前脑各核区SOMmRNA的表达有明显的影响。结果表明秋水仙素对前脑各核区SDMmRNA的表达有明显的核区特异性:大脑新皮质各区,隔核和脚内核中SOMmRNA阳性神经元数目及含量增加;海马复合体和下丘脑室周核和弓状核中SOMmRNA阳性神经元数目及含量下降;嗅脑,尾壳核和丘脑等核区的则无明显变化、秋水仙素对SOMmRNA表达的核区特异性对正确分析秋水仙素条件下获得的神经肽或神经递质的定位资料具有重要的指导意义。 相似文献
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低氧预处理对大鼠海巴神经元缺氧耐受性和IL—1β表达 … 总被引:3,自引:0,他引:3
目的:观察低氧预处理对大鼠海巴神经元缺氧耐受性和白细胞介素-1β(IL-1β)表达的影响。方法:取培养12d的两组(对照组和低氧预处理组)培养神经元,同时置于缺氧环境(0.9L/LN2,0.1L/LCO2)中培养2、4、8和12h。分别观察它们的形态变化和神经元存活数,并用抗rhIL-1β单克隆抗体进行免疫组织化学染色,观察缺氧对大鼠海马培养神经元IL-1β表达的影响。结果:经低氧预处理的海马神经 相似文献
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利用原位杂交和原位DNA-3’末端标记的方法研究了胰岛素样生长因子-I(IGF-I),IGF-I受体,IGF结合蛋白-2,和促性腺激素受体的信使核糖核酸(mRNA)在不同生长与闭锁阶段的大鼠卵巢卵泡中表达的变化,结果表明:IGF-I主要在正常生长的初级卵泡,窦前卵泡和小窦状卵泡中表达。在各生长与成熟阶段的卵泡中都检测到IGF-I受体mRNA,闭锁卵泡的IGF-I受体表达降低,窦前与窦状的生长和闭锁 相似文献
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Hwang HJ Lee HJ Kim CJ Shim I Hahm DH 《Journal of microbiology and biotechnology》2008,18(10):1641-1647
Amygdalin is a cyanogenic glycoside plant compound found in the seeds of rosaceous stone fruits. We evaluated the antiinflammatory and analgesic activities of amygdalin, using an in vitro lipopolysaccharide (LPS)-induced cell line and a rat model with carrageenan-induced ankle arthritis. One mM amygdalin significantly inhibited the expression of TNF-alpha and IL-1beta mRNAs in LPS-treated RAW 264.7 cells. Amygdalin (0.005, 0.05, and 0.1 mg/kg) was intramuscularly injected immediately after the induction of carrageenan-induced arthritic pain in rats, and the anti-arthritic effect of amygdalin was assessed by measuring the weight distribution ratio of the bearing forces of both feet and the ankle circumference, and by analyzing the expression levels of three molecular markers of pain and inflammation (c-Fos, TNF-alpha, and IL-1beta) in the spinal cord. The hyperalgesia of the arthritic ankle was alleviated most significantly by the injection of 0.005 mg/kg amygdalin. At this dosage, the expressions of c-Fos, TNF-alpha, and IL-1beta in the spinal cord were significantly inhibited. However, at dosage greater than 0.005 mg/kg, the painrelieving effect of amygdalin was not observed. Thus, amygdalin treatment effectively alleviated responses to LPStreatment in RAW 264.7 cells and carrageenan-induced arthritis in rats, and may serve as an analgesic for relieving inflammatory pain. 相似文献
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慢性束缚应激大鼠海马脑啡肽mRNA和前强啡肽mRNA 表达及中药复方的影响 总被引:7,自引:0,他引:7
目的:研究慢性束缚应激时大鼠海马脑啡肽和前强啡肽mRNA基因表达的变化以及逍遥散、四君子汤、金匮肾气丸三种中药复方对其的影响.方法:用特制束缚架连续束缚7 d与21 d,每天3 h的方法制作大鼠束缚应激模型;以RT-PCR反应,扩增脑啡肽和前强啡肽基因,同时以β-actin作为内对照,用凝胶图像分析系统进行扫描并分析,把目的基因的光密度与内参照条带的光密度进行比较后进行半定量分析.结果:7 d模型组大鼠海马前强啡肽mRNA的表达明显增强(P<0.01),21 d模型组海马脑啡呔mRNA和前强啡肽mRNA的表达明显增强(P<0.01);三个复方均能降低海马内前强啡肽mRNA的表达(P<0.01),逍遥散和四君子汤能降低脑啡呔mRNA的表达(P<0.01).结论:逍遥散对脑啡呔mRNA前强啡肽mRNA的基因表达的改善作用明显优于金匮肾气丸组. 相似文献
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S B Milam V L Magnuson B Steffensen D Chen R J Klebe 《Journal of cellular physiology》1991,149(2):173-183
The purpose of this study was to examine the effects of IL-1 beta on integrin expression in MG-63 human osteosarcoma cells. Human recombinant IL-1 beta (rIL-1 beta) produced significant increases in both alpha 2- and alpha 5-subunit mRNA levels, as well as a smaller increase in alpha v-subunit mRNA. In contrast, IL-1 beta decreased alpha 4-subunit mRNA levels by approximately 30% relative to untreated controls. These findings suggest that human IL-1 beta differentially regulates expression of integrins. When cultures were treated with both IL-1 beta and the cyclooxygenase inhibitor, indomethacin, the expression of alpha 2-, alpha 5-, and alpha v-subunit mRNA levels were dramatically increased relative to untreated controls; co-treatment with 0.5 mM prostaglandin E2 (PGE2) partially reversed this effect. Indomethacin alone did not affect integrin mRNA levels. Treatment with IL-1 beta or IL-1 beta + indomethacin also induced significant changes in MG-63 morphology (i.e., increased cell elongation) and increased the ability of cells to contract collagen gels. PGE2 reversed the above effects on cell morphology and gel contraction. These findings indicate that (a) IL-1 beta differentially regulates the expression of integrins and (b) that PGE2, which is induced by IL-1 beta, may provide a negative feedback loop which counteracts the stimulatory effect of IL-1 beta on integrin gene expression. It is suggested that products of inflammation may affect cell behavior by differentially regulating the expression of various integrins. 相似文献
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Mononuclear cells from atopic blood donors showed increased IL-3 steady state mRNA levels. This finding complemented our earlier observations that cells from atopics also showed increased IL-4 but decreased IFN-gamma, IL-1 beta and IL-6 mRNA levels. Therefore, we investigated the effect of human recombinant IL-4 on cytokines mRNA levels in mononuclear cells from normals and atopics. In the presence of IL-4 steady state levels of IL-1 beta and IL-6 mRNA were decreased even if cells were co-stimulated with polyclonal activators such as PMA, PWM or PHA. No influence of IL-4 on granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3 or IFN-gamma mRNA levels was observed with the exception of a decreased IFN-gamma mRNA level in PWM stimulated cells. 相似文献
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IL-2 induction of IL-1 beta mRNA expression in monocytes. Regulation by agents that block second messenger pathways 总被引:2,自引:0,他引:2
E J Kovacs B Brock L Varesio H A Young 《Journal of immunology (Baltimore, Md. : 1950)》1989,143(11):3532-3537
We have previously shown that in mixed cultures of PBL incubation with human rIL-2 induces the rapid expression of IL-1 alpha and IL-1 beta mRNA. Because studies have demonstrated that IL-2R can be expressed on the surface of human peripheral blood monocytes, we chose to investigate whether IL-1 beta mRNA could be directly induced in purified human monocytes by treatment with Il-2 and, if so, to analyze the second messenger pathways by which it may be controlled. Human monocytes do not spontaneously express IL-1 beta mRNA, but can express the gene as soon as 1 h after treatment with IL-2. The level of IL-1 beta mRNA induced by IL-2 at 5 h in human monocytes was about one-fourth that induced by LPS. LPS induction of IL-1 beta mRNA in human monocytes can be blocked by either an inhibitor of protein kinase C (PKc) 1-(5-isoquinolinesulfonyl)-2-methylpiperazine or an inhibitor of calcium/calmodulin (CaM) kinase N-(6-aminohexyl) 5-chloro-1-naphthalenesulfonamide, suggesting that both PKc and CaM kinase are involved in transducing signals initiated by LPS. In contrast, IL-2 induction of IL-1 beta mRNA expression is blocked only by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine, suggesting that PKc, and not CaM kinase, is activated by IL-2. These data suggest that overlapping but distinct second messenger pathways are involved in the transduction of signals initiated by IL-2 and LPS. 相似文献
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The majority of T lymphocytes that infiltrate psoriatic lesions express cutaneous lymphocyte antigen (CLA), a skin homing receptor involved in the influx of memory T cells to cutaneous sites. We investigated CLA expression on normal human peripheral blood mononuclear cells (PBMCs) and evaluated its association with IL-12 receptors, chemokine receptor, CXCR3, and IL-2Ralpha. PBMCs were stimulated in vitro with or without polyclonal activators (mitogen, or superantigens, or anti-CD3+anti-CD28) in the presence or absence of exogenous rhIL-12. The percentage of CLA+ T lymphocytes increased significantly after superantigen stimulation compared to anti-CD3+anti-CD28 or mitogen activation. The majority of activation induced CLA+ T lymphocytes co-expressed IL-12Rbeta1, IL-12Rbeta2, CXCR3, and CD25 in the presence of rhIL-12. Our results indicate that CLA expression on activated T lymphocytes is IL-12 and activation dependent and correlates with the expression of IL-12 receptors, IL-2Ralpha, and CXCR3. Monitoring the levels of Th1 differentiation markers such as CXCR3 and IL-12Rbeta2 along with activation marker, CD25 on skin homing CLA+ T lymphocytes may provide insight into the mechanism of action of immunotherapies directed against Th1 type skin inflammatory diseases. 相似文献
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TNF-alpha and H2O2 induce IL-18 and IL-18R beta expression in cardiomyocytes via NF-kappa B activation 总被引:5,自引:0,他引:5
Chandrasekar B Colston JT de la Rosa SD Rao PP Freeman GL 《Biochemical and biophysical research communications》2003,303(4):1152-1158
Myocardial ischemia/reperfusion is characterized by oxidative stress and induction of proinflammatory cytokines. Interleukin (IL)-18, a member of the IL-1 family, acts as a proinflammatory cytokine, and is induced during various immune and inflammatory disorders. Therefore, in the present study we investigated whether IL-18 expression is regulated by cytokines and oxidative stress in cardiomyocytes. TNF-alpha induced rapid and sustained activation of NF-kappaB whereas H(2)O(2) induced delayed and transient activation. Both TNF-alpha and H(2)O(2) induced IL-18 mRNA and precursor protein in cardiomyocytes, and IL-18 release into culture supernatants. However, only TNF-alpha led to sustained expression. Expression of IL-18Rbeta, but not alpha, was induced by both agonists. TNF-alpha and H(2)O(2) induced delayed expression of IL-18 BP. Pretreatment with PDTC attenuated TNF-alpha and H(2)O(2) induced IL-18 and IL-18Rbeta, but not basal expression of IL-18Ralpha. These results indicate that adult cardiomyocytes express IL-18 and its receptors, and proinflammatory cytokines and oxidative stress regulate their expression via activation of NF-kappaB. Presence of both ligand and receptors suggests IL-18 impacts myocardial biology through an autocrine pathway. 相似文献