不同剂量的He—Ne激光对Raji细胞膜表面SH的影响

本文以离体培养的Ｒａｊｉ细胞为材料,采用ＥＬＬＭＡＮ方法检测了不同剂量的Ｈｅ－Ｎｅ激光对Ｒａｊｉ细胞膜表面ＳＨ含量的影响。发现０．５Ｊ／ｃｍ＾２Ｈｅ－Ｎｅ激光能量可明显增加膜表面ＳＨ含量（Ｐ〈０．０５）。大于或小于此剂量的Ｈｅ－Ｎｅ激光对膜表面ＳＨ含量的影响均不明显（Ｐ〉０．０５）。提示０．５Ｊ／ｃｍ＾２的激光能量对膜有刺激作用。     

氧化修饰高密度脂蛋白对培养人动脉平滑肌细胞细胞周期蛋白D_1基因表达的影响

动脉平滑肌细胞（ｓｍ ｏｏｔｈ ｍ ｕｓｃｌｅ ｃｅｌｌ,ＳＭＣ）是动脉粥样硬化（ａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ,ＡＳ）斑块中的主要细胞,它的增殖在ＡＳ形成过程中极其重要．利用体外培养的人主动脉ＳＭＣ,观察了天然高密度脂蛋白（ｎａｔｉｖｅ ｈｉｇｈ ｄｅｎｓｉｔｙ ｌｉｐｏｐｒｏｔｅｉｎ,Ｎ－ＨＤＬ）及氧化修饰ＨＤＬ（ｏｘｉｄｉｚｅｄ ＨＤＬ,ＯＸ－ＨＤＬ）对培养人主动脉ＳＭＣ ｃｙｃｌｉｎ Ｄ１（细胞周期蛋白Ｄ１）基因转录表达的影响．结果表明：（１）Ｎ－ＨＤＬ对ＳＭＣｃｙｃｌｉｎ Ｄ１基因表达无影响（Ｐ＞ ０．０５）;（２）ＯＸ－ＨＤＬ使ＳＭＣｃｙｃｌｉｎ Ｄ１基因表达显著增强（Ｐ＜０．０１）,其表达量随时间（２、１２、２４ ｈ）延长而增加．上述结果表明,ＯＸ－ＨＤＬ的致ＡＳ作用可能与其刺激ＳＭＣｃｙｃｌｉｎ Ｄ１基因表达增加有关．     

人主动脉硫酸乙酰肝素蛋白聚糖对培养的人血管壁细胞生长的作用

通过培养的人主动脉平滑肌细胞（ｈＡＳＭＣ）及脐静脉内皮细胞（ｈＵＶＥＣ）,应用３Ｈ－ＴｄＲ参入、Ｎｏｒｔｈｅｒｎｂｌｏｔ分析、逆转录多聚酶链反应（ＲＴ－ＰＣＲ）、放射免疫分析（ＲＩＡ）、和紫外比色法等技术观察了人主动脉中硫酸乙酰肝素蛋白聚糖（ＨＳＰＧ）对ｈＡＳＭＣ和ｈＵＶＥＣＤＮＡ合成的作用及对血小板源生长因子（ＰＤＧＦ）、ＰＤＧＦ受体、转化生长因子β（ＴＧＦ－β）、内皮素－１（ＥＴ－１）或碱性成纤维细胞生长因子（ｂＦＧＦ）基因表达和肾素－血管紧张系统（ＲＡＳ）的影响,结果显示,ＨＳＰＧ明显抑制培养的ｈＡＳＭＣ基础的ＤＮＡ合成（ｃｐｍ值为：１０３８５±３２６３ｖｓ,２５５４１±６４２１,Ｐ＜０．０１）及外源性ＰＤＧＦ诱导的ＤＮＡ合成（ｃｐｍ值为：９８７８±１９４７ｖｓ．１３４８１±４４ｌ０,Ｐ＜０．０５）;抑制ＰＤＧＦＡ链、ＴＧＦ－Ｂｐ和ＥＴ－１ｍＲＮＡ表达,提高ＰＤＧＦａ和β受体ｍＲＮＡ的表达;显著降低ｈＡＳＭＣ培养液中血管紧张素Ⅱ（ＡｎｇⅡ）的浓度和血管紧张素转换酶（ＡＣＥ）的活性,推测ＨＳＰＧ抑制ＰＤＧＦＡ链、ＴＧＦ－β及ＥＴ－１ｍＲＮＡ表达,降低ＡＣＥ活性及ＡｎｇⅡ浓度是其抑制ｈＡＳＭＣ增殖的重要机     

肺动脉内皮细胞与肺动脉平滑肌细胞增殖的相互调节

血管内皮细胞和血管平滑肌细胞在结构和功能上关系密切,二者的相互关系在血管舒缩和血管壁结构的调节中起重要作用。本文观察了培养的小牛肺动脉内皮细胞（ＰＡＥＣ）和肺动脉平滑肌细胞（ＰＡＳＭ）在细胞增殖方面的相互调节作用。混合培养的ＰＡＥＣ和ＰＡＳＭ细胞的３Ｈ－ＴｄＲ参入明显降低（Ｐ＜０．００１,与对照组相比）。无论向培养的ＰＡＥＣ和ＰＡＳＭ中分别加入ＰＡＳＭ和ＰＡＥＣ的条件培养基还是二者共培养时,均发现ＰＡＥＣ的３Ｈ－ＴｄＲ参入明显降低,而ＰＡＳＭ的３Ｈ－ＴｄＲ明显升高（Ｐ＜０．０５,与对照组相比）。流式细胞测定也发现共培养时ＰＡＥＣ的Ｇ１期细胞增多,Ｇ２／Ｍ期细胞减少;而ＰＡＳＭ的Ｇ１期细胞减少,Ｇ２／Ｍ期细胞增多。共培养的ＰＡＳＭ细胞内ｃＡＭＰ增加,ｃＧＭＰ含量降低;而ＰＡＥＣ细胞的ｃＡＭＰ和ｃＧＭＰ含量均降低（Ｐ＜０．０１,与对照组相比）。上述结果提示,ＰＡＥＣ和ＰＡＳＭ相互作用可能通过第二信使而调节它们本身的增殖     

吗啡对福尔马林引起大鼠海马内IL-2RβmRNA表达的影响

本实验采用原位杂交法观察足底注射福尔马林（Ｆｏｒ）痛敏对海马内白细胞介素２受体βｍＲＮＡ（ＩＬ－２ＲβｍＲＮＡ）生成的影响及其与吗啡、促肾上腺皮质激素（ＡＣＴＨ）的关系。结果表明：正常大鼠海马有ＩＬ－２ＲβｍＲＮＡ表达,集中分布于ＣＡ１－ＣＡ４区神经元、齿状回颗粒细胞。足底注射Ｆｏｒ后６ｈ双侧海马ＩＬ－２ＲβｍＲＮＡ表达均增加（Ｐ〈０．０５）,１２ｈ达高峰,２４ｈ仍高于正常。在６ｈ时,腹腔注射吗啡     

环腺苷一磷酸对人Ⅰ型17β羟类固醇脱氢酶在绒癌细胞系中表达的调节作用

由Ｈ ＳＤ１７Ｂ１基因编码的人Ⅰ型１７β－羟类固醇脱氢酶（１７β－ｈｙｄｒｏｘｙｓｔｅｒｏｉｄｄｅｈｙｄｒｏｇｅｎａｓｅｔｙｐｅ１简称Ⅰ型１７ＨＳＤ）催化雌酮与雌二醇之间的转化。本文研究环腺苷一磷酸简化（ｃＡＭＰ）对该酶在培养的绒癌胞系（ＪＡＲ和ＪＥＧ－３）中表达的调节作用。用８－ｂｒｏｍｏ－ｃＡＭＰ处理两种绒癌细胞后,观察到在伴随１．３ｋｂⅠ型１７ＨＳＤｍＲＮＡ表达的同时,Ｉ型１７ＨＳＤ蛋白浓度     

NO对大鼠睡眠-觉醒的调节

目的和方法：通过对大鼠侧脑室微量注射ＮＯＳ抑制剂Ｌ－ＮＡＭＥ及ＮＯ的前体Ｌ－精氨酸（Ｌ－Ａｒｇ）观察两种物质对大鼠睡眠－觉醒的影响。结果：注射１ｍｇ Ｌ－ＮＡＭＥ（５μＬ）后４ｈ觉醒（Ｗ）明显增加,尤以注射后第１￣２ｈ显著;４ｈ慢波睡眠（ＳＷＳ）明显减少,该效应同样以注射后第１￣２ｈ显著;异相睡眠（ＰＳ）无明显变化。小剂量Ｌ－ＮＡＭＥ（０．２ｍｇ,５μｌ）对大鼠的Ｗ、ＳＷＳ、ＰＳ无明显影响;同样方     

TNF-α、IL-1β及LPS对血管平滑肌细胞一氧化氮合酶基因表达的影响及作用机制研究

通过ＲＮＡ印迹分析和亚硝酸盐含量测定检查ＴＮＦ－α、ＩＬ－１β和ＬＰＳ对大鼠血管平滑肌细胞（ＶＳＭＣ）诱导型一氧化氮合酶（ｉＮＯＳ）基因表达及ＮＯ生成的影响．结果表明,ＴＮＦ－α、ＩＬ－１β和ＬＰＳ均能显著诱导ＶＳＭＣｉＮＯＳ基因表达和促进ＮＯ生成,其作用强度与浓度和作用时间有关;双因素（ＴＮＦ－α＋ＬＰＳ,ＬＰＳ＋ＩＬ－１β）对诱导ｉＮＯＳ基因表达及ＮＯ生成产生协同作用．ＰｏｌｙｍｙｘｉｎＢ和地塞米松可部分抑制ＴＮＦ－α对ｉＮＯＳ基因表达的诱导作用及ＮＯ生成     

大鼠iNOS基因上游调控区在转录激活中的作用

为了探讨大鼠ｉＮＯＳ基因上游调控区不同部位在对细胞因子诱导应答中所起的作用,将调控区不同部位插入ｐＳＶ０－ＣＡＴ报告基因载体,转染体外培养的血管平滑肌细胞（ＶＳＭＣ）,经ＩＬ－１β诱导后,采用氯霉素乙酰转移酶（ＣＡＴ）活性测定和Ｎｏｒｔｈｅｒｎ印迹杂交,检查了调控区各部位在ＩＬ－１β诱导ｃａｔ表达中所起的作用．结果表明,被转染的细胞在未经ＩＬ－１β刺激时,各种调控区序列启动ｃａｔ表达的活性均很低．在ＩＬ－１β作用下,调控区远端序列（－１０３７～－４３８）、近端序列（－４３７～＋４６）和全长序列（－１０３７～＋４６）均能独立激活ｃａｔ表达,其中以全长序列的作用最强,表明ｉＮＯＳ基因表达调控区远端和近端序列均具有启动子和增强子样功能．同时证实,远端序列和近端序列单独启动ｃａｔ表达的活性分别为全长序列的９１．３％和６７．１％,揭示大鼠ｉＮＯＳ基因调控区远端序列在介导ＩＬ－１β的应答反应中发挥更重要作用．     

IFN—α治疗慢性乙肝抗病毒疗效与细胞因子变化关系分析

观察一乙型病毒性肝炎（ＣＨＢ）患者（２５例）经α－干扰素（ＩＦＮ－α）抗病毒治疗前后血清中细胞因子和受体水平的变化与乙肝病毒消长之间的关系。收集治疗前后血清标本ＥＬＩＳＡ法同步检测,根据治疗后乙肝病毒复制指标（ＨＢＶ－ＤＮＡ）阴转分应答组（１０例）与无应答组（１５例）进行统计学分析。治疗后两组血清中ＩＬ－６水平下降,尤其答应组下降明显;治疗后应答组ＩＬ－２水平明显升高（Ｐ〈０．０１）,ｓＩＬ－２Ｒ     

纳洛酮对发热大鼠下丘脑中cAMP和腹中膈区AVP含量的影响

目的：研究纳洛酮对白细胞介素-1β（IL-1β）致热大鼠发热反应的影响及机制。方法：经大鼠侧脑室微量注射IL-1β建立发热模型,观察纳洛酮对发热大鼠体温的影响,并测定下丘脑中环磷酸腺苷（cAMP）和腹中膈区精氨酸加压素（AVP）含量。结果：纳洛酮减弱了IL-1β致热效应,同时下丘脑中cAMP和腹中膈区AVP含量也相应减少（P〈0．01）。结论：纳洛酮能够抑制大鼠IL-1β性发热,其机制可能是抑制下丘脑中cAMP的合成,并且促进腹中膈区AVP的释放。     

Interleukin-1 mediates endothelin-1-induced fever and prostaglandin production in the preoptic area of rats

The intracerebroventricular injection of endothelin-1 (ET-1) induces fever and increases PG levels in the cerebrospinal fluid of rats. Likewise, the injection of IL-1 into the preoptic area (POA) of the rat hypothalamus causes both fever and increased PG production. In this study, we conducted in vivo and in vitro experiments in the rat to investigate 1) the hypothalamic region involved in ET-1-induced fever and PG biosynthesis and 2) whether hypothalamic IL-1 plays a role as a mediator of the above ET-1 activities. One hundred femtomoles of ET-1 increased body temperature when injected in the POA of conscious Wistar rats; this effect was significantly counteracted by the coinjection of 600 pmol IL-1 receptor antagonist (IL-1ra). In experiments on rat hypothalamic explants, 100 nM ET-1 caused a significant increase in PGE2 production and release from the whole hypothalamus and from the isolated POA, but not from the retrochiasmatic region, in 1-h incubations. Six nanomoles of IL-1ra or 10 nM of a cell-permeable interleukin-1 converting enzyme inhibitor completely counteracted the effect of ET-1 on PGE2 release from the POA. One hundred nanomoles ET-1 also caused a significant increase in IL-1beta immunoreactivity released into the bath solution of hypothalamic explants after 1 h of incubation, although during such time ET-1 failed to modify the gene expression of IL-1beta and other pyrogenic cytokines within the hypothalamus. In conclusion, our results show that ET-1 increases IL-1 production in the POA, and this effect appears to be correlated to ET-1-induced fever in vivo, as well as to PG production in vitro.     

Refractory hypothalamic alpha-mSH satiety and AGRP feeding systems in rats bearing MCA sarcomas

In pre-anorectic tumor-bearing (TB: methylcholanthrene-induced sarcoma) rats, injection of alpha-melanocyte stimulating hormone (alpha-MSH) into the perifornical hypothalamus (PFH) had no significant effect on food intake at a dose (5 microg) that reduced feeding in non-TB control rats. Following the development of anorexia, injection of alpha-MSH MC3/MC4 receptor antagonists, SHU9119 (1 microg) or 4 microg agouti-related protein (AGRP), stimulated feeding in non-TB rats, while having no significant effect in TB rats. Concentrations of alpha-MSH were not altered significantly in ventromedial, dorsomedial or lateral hypothalamic areas of TB rats, and proopiomelanocortin (POMC) messenger RNA was not changed in TB rats in these hypothalamic areas. Determination of cytokines by ELISA in non-operated TB and non-TB rats revealed elevated IL-2 in plasma and hypothalamus as well as increased TNF-alpha in the hypothalamus of anorectic TB rats. IL-1B was not detectable in plasma and was not altered significantly in hypothalamus of TB rats. These results suggest that the POMC alpha-MSH satiety system is refractory in TB rats, even prior to the onset of anorexia. This change in MC3/MC4 receptor response does not appear to be secondary to alterations of endogenous alpha-MSH in TB rats. Cytokine involvement in the altered response to MC3/MC4 receptor stimulation and blockade is a possibility, since TNF-alpha and IL-2 were increased in hypothalamus of anorectic TB rats. Therefore, these results suggest major alterations in POMC neuropeptide systems in TB rats as anorexia progresses. Although these changes do not appear to have occurred due to grossly-altered concentrations of alpha-MSH, elevated cytokine activity in the hypothalamus may be an important factor. Due to the complex multi-factorial nature of feeding control, additional factors are likely to be involved in cancer anorexia.     

Receptor-mediated modulation of murine mast cell function by alpha-melanocyte stimulating hormone.

The proopiomelanocortin (POMC)-derived neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH) is known to modulate some aspects of inflammation through direct effects on T cells, B cells, and monocytes. To determine whether alpha-MSH might similarly influence mast cell responsiveness, mast cells were examined to see if they expressed the receptor for alpha-MSH, melanocortin-1 (MC-1), and whether alpha-MSH altered mast cell function. We thus first identified MC-1 on bone marrow cultured murine mast cells (BMCMC) and a murine mast cell line (MCP-5) employing flow cytometry and through detection of specific binding. Subsequent treatment of mast cells with alpha-MSH increased the cAMP concentration in a characteristic biphasic pattern, demonstrating that alpha-MSH could affect intracellular processes. We next examined the effect of alpha-MSH on mediator release and cytokine expression. IgE/DNP-human serum albumin-stimulated histamine release from mast cells was inhibited by approximately 60% in the presence of alpha-MSH. Although activation of BMCMC induced the expression of mRNAs for the inflammatory cytokines IL-1beta, IL-4, IL-6, TNF-alpha, and the chemokine lymphotactin, mRNAs for IL-1beta, TNF-alpha, and lymphotactin were down-modulated in the presence of alpha-MSH. Finally, IL-3-dependent proliferative activity of BMCMC was slightly but significantly augmented by alpha-MSH. Taken together, these observations suggest that alpha-MSH may exert an inhibitory effect on the mast cell-dependent component of a specific inflammatory response.     

Physiological regulation of hypothalamic IL-1beta gene expression by leptin and glucocorticoids: implications for energy homeostasis

Interleukin-1beta (IL-1beta) is synthesized in a variety of tissues, including the hypothalamus, where it is implicated in the control of food intake. The current studies were undertaken to investigate whether hypothalamic IL-1beta gene expression is subject to physiological regulation by leptin and glucocorticoids (GCs), key hormones involved in energy homeostasis. Adrenalectomy (ADX) increased hypothalamic IL-1beta mRNA levels twofold, measured by real-time PCR (P < 0.05 vs. sham-operated controls), and this effect was blocked by subcutaneous infusion of a physiological dose of corticosterone. Conversely, hypothalamic IL-1beta mRNA levels were reduced by 30% in fa/fa (Zucker) rats, a model of genetic obesity caused by leptin receptor mutation (P = 0.01 vs. lean littermates), and the effect of ADX to increase hypothalamic IL-1beta mRNA levels in fa/fa rats (P = 0.02) is similar to that seen in normal animals. Moreover, fasting for 48 h (which lowers leptin and raises corticosterone levels) reduced hypothalamic IL-1beta mRNA levels by 30% (P = 0.02), and this decrease was fully reversed by refeeding for 12 h. Thus leptin and GCs exert opposing effects on hypothalamic IL-1beta gene expression, and corticosterone plays a physiological role to limit expression of this cytokine in both the presence and absence of intact leptin signaling. Consistent with this hypothesis, systemic leptin administration to normal rats (2 mg/kg ip) increased hypothalamic IL-1beta mRNA levels twofold (P < 0.05 vs. vehicle), an effect similar to that of ADX. These data support a model in which expression of hypothalamic IL-1beta is subject to opposing physiological regulation by corticosterone and leptin.     

Anxiety-like behavior induced by IL-1beta is modulated by alpha-MSH through central melanocortin-4 receptors

The proinflammatory cytokine interleukin-1beta (IL-1beta) influences neuroendocrine activity and produces other effects, including fever and behavioral changes such as anxiety. The melanocortin neuropeptides, such as alpha-melanocyte-stimulating hormone (alpha-MSH), antagonize many actions of IL-1, including fever, anorexia and hypothalamic-pituitary-adrenal (HPA) axis activation through specific melanocortin receptors (MC-R) in the central nervous system. The objective of the present study was to establish the effect of MSH peptides on IL-1beta-induced anxiety-like behavior and the melanocortin receptors involved. We evaluated the effects of intracerebroventricular (i.c.v.) administration of IL-1beta (30 ng) and melanocortin receptor agonists: alpha-MSH, an MC3/MC4-R agonist (0.2 microg) or gamma-MSH, an MC3-R agonist (2 microg) or HS014, an MC4-R antagonist (2 microg), on an elevated plus-maze (EPM) test. Injection of IL-1beta induced an anxiogenic-like response, as indicated by reduced open arms entries and time spent on open arms. The administration of alpha-MSH reversed IL-1beta-induced anxiety with co-administration of HS014 inhibiting the effect of alpha-MSH. However, the associated treatment with gamma-MSH did not affect the anxiety response to IL-1beta. These data suggest that alpha-MSH, through central MC4-R can modulate the anxiety-like behavior induced by IL-1beta.     

A new role for epidermal cell-derived thymocyte activating factor/IL-1 as an antagonist for distinct epidermal cell function

It is known that many immunologic responses to IL-1 are antagonized by the neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH). This led us to investigate the possible reciprocal effects of IL-1 and the functionally related epidermal cytokines, epidermal cell-derived thymocyte activating factor (ETAF) and IL-6, on the melanogenic effect of alpha-MSH on murine Cloudman melanoma cells. When these cells were treated with ETAF in combination with alpha-MSH or its potent analog [Nle4,D-Phe7]-alpha-MSH, the melanotropin induced increase in tyrosinase activity, and thus melanin synthesis, was abrogated. This inhibitory effect of ETAF was not mediated by competitive binding to the melanotropin receptor, because ETAF also blocked the melanogenic response of melanoma cells to isobutyl methylxanthine (IBMX) and to PGE1 and PGE2. ETAF had no effect on cellular proliferation. Inhibition of the stimulated tyrosinase activity by ETAF was not due to diminished cAMP synthesis or increased cAMP degradation. Cells treated concomitantly with ETAF and alpha-MSH, IBMX, or PGE1 had the same cAMP levels as cells treated with alpha-MSH, IBMX, or PGE1 alone. In contrast to ETAF, human rIL-1 alpha or IL-1 beta alone or in combination did not have an inhibitory effect on melanogenesis. IL-6 significantly inhibited the basal level of tyrosinase and partially abrogated the alpha-MSH-induced tyrosinase activity. IL-6 also stimulated cellular proliferation when added alone or in combination with alpha-MSH. Granulocyte-macrophage colony stimulating factor (GM-CSF) did not alter either the tyrosinase activity or cellular replication at the concentrations tested. IL-1 alpha, GM-CSF, and IL-6 or IL-1 alpha and GM-CSF added together did not significantly affect the MSH-induced tyrosinase activity. These results ascribe a new potential function for ETAF and IL-6 as modulators of the melanogenic response of pigment cells.     

Interleukin-1 inhibits serotonin release from the hypothalamus in vitro.

During a 60-min incubation period, the in vitro release of serotonin (5-HT) from the hypothalami of control male rats decreased by 12.3 +/- 3.1%. In contrast, the presence of 25 ng of interleukin-1 beta (IL-1 beta) in the incubation medium more than doubled this decrease to 29.3 +/- 3.3% (P < 0.001), and the presence of 50 ng of IL-1 beta more than quadrupled this decrease to 53.7 +/- 7.4% (P < 0.001). The decrease produced by the higher dose of IL-1 beta was significantly greater than that produced by the lower dose (P < 0.01), indicating a dose response. During the next two 60-min periods when the hypothalami of the control as well as treatment groups were incubated without IL-beta, 5-HT release continued to decrease and then became stabilized in the control group. In contrast, 5-HT release in the treatment groups rebounded before becoming stabilized at levels that were not significantly different from those in the control group. It is concluded that IL-1 beta inhibits the release of serotonin from the hypothalamus in vitro.     

Synergism between interleukin-6 and interleukin-1beta in hypothalamic serotonin release: a reverse in vivo microdialysis study in F344 rats

The effects of interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) perfused locally into the anterior hypothalamus (AHY) on serotonin (5-hydroxytryptamine, 5-HT) release were investigated in the same region using in vivo microdialysis in conscious, freely moving F344 rats. IL-1beta (1 ng/rat) or IL-6 (50 ng/rat) injected directly into the AHY elicited a rapid and transient statistically significant increase in extracellular 5-HT levels (to 161% and 145% of the respective AUC (area under the curve) basal value, 100%). Intra-hypothalamic infusion of IL-1-receptor antagonist IL-1Ra (2 mug/rat) prevented this effect of IL-1beta, but not that of IL-6, suggesting an IL-1beta-independent mechanism for hypothalamic 5-HT release by this latter cytokine. Furthermore, intra-hypothalamic co-perfusion of IL-6 with IL-1beta at sub-optimal doses (10 ng/rat and 0.5 ng/rat, respectively) synergized in releasing hypothalamic 5-HT, thus providing in vivo evidence that both cytokines, IL-6 and IL-1beta are able to modulate the neuronal 5-HT response in the rat AHY.     

应激大鼠肾胞液[^3H]醛固酮结合活性的变化及调节机制的初步研究

为探讨烫伤引起病理性应激时大鼠肾胞液醛固酮结合活性的变化及可能的调节机制,以[～3H]-醛固酮为配体,用放射性配基-受体结合分析法测定了正常对照组、轻度烫伤组和重度烫伤组大鼠肾胞液醛固酮结合活性的结合容量(Rt)和表观解离常数(Kd);采用体内注射TNF-α、IL-1β中和抗体和α-促黑色素细胞刺激激素(α-melanocyte-stimulatinghormone,α-MSH)和合成肽KPV(Ac-D-Lys-L-Pro-D-Val)等措施调节其改变.结果发现,肾胞液存在两种不同结合容量、不同亲和力的醛固酮结合活性受体.与正常对照组的Rt(Rt141.6±7.2fmol/mgpro;Rt2317.6±70.0fmol/mgpro)相比,轻烫组的Rt(Rt141.4±5.0fmol/mgpro;Rt2314.8±45.7fmol/mgpro)无显著差异(P>0.05;P>0.05);重烫组的Rt(Rt122.4±5.4fmol/mgpro;Rt2196.3±32.5fmol/mgpro)则显著下降(P<0.01;P<0.01).体内注射TNF-α与IL-1β中和抗体、α-MSH及KPV均能明显提高重烫组Rt值.结果提示,重度烫伤大鼠肾胞浆醛固酮结合活性降低,TNF-α、IL-1β中和抗体、α-MSH及KPV均可防止重度烫伤引起病理性应激时醛固酮结合活性降低.