前列腺素E2与肿瘤的关系

流行病学,动物实验和临床研究表明,肿瘤的发生发展与患者癌组织分泌的前列腺素E2有着密切关系。研究表明前列腺素E2在肿瘤组织中高表达,并且前列腺素E2的含量与肿瘤的大小、肿瘤的分期、肿瘤有无转移、肿瘤的预后以及肿瘤的复发等方面都有相关性。因此使用前列腺素E2的抑制剂及其含量的检测,将在肿瘤的预防,治疗等方面起着重要的作用。     

吲哚美辛的临床新用途

吲哚美辛为吲哚类有机酸非甾体抗炎药,广泛应用于解热镇痛,抗风湿及急性痛风性关节炎等症。近几年发现不少新用途,现介绍如下。1 吲哚美辛的抗肿瘤作用近几年来研究表明,前列腺素E_2与肿瘤的发生、发展及转移极为密切,虽然其机理不清,但在许多人体和动物肿瘤组织及宿主血浆中都检测到超常量的前列腺素E_2,而且随着肿瘤的生长增殖,前列腺素E_2水平逐渐升高。吲哚美辛是前列腺素生物合成     

胃黏膜EGF及PEG2与肝源性溃疡患者的相关研究

目的探讨胃黏膜EGF(表皮生长因子)及PEG2(前列腺素E2)与肝源性溃疡患者的相关研究。方法本实验选取了160例在2010年8月份～2011年12月份在某医院进行治疗的患者为对象进行研究,其中38例肝硬化肝源性溃疡患者(A组),42例肝硬化非肝源性溃疡患者(B组),35例慢性胃炎患者(C组),45例非溃疡性消化不良(D组),统计及比较A组和B组的胃黏膜表皮生长因子含量和前列腺素E2含量情况以及A组、C组和D组的胃黏膜表皮生长因子含量和前列腺素E2含量情况。结果 A组患胃黏膜表皮生长因子含量为(0.521±0.292)pg/mg,前列腺素E2含量为(519±294)pg/mg;B组患者胃黏膜表皮生长因子含量为(0.911±0.507)pg/mg,前列腺素E2含量为(908±532)pg/mg。两组数据均进行比较,得出P﹤0.05,差异有统计学意义。A组患者胃黏膜表皮生长因子含量(0.521±0.292)pg/mg,前列腺素E2含量为(519±294)pg/mg;C组患者胃黏膜表皮生长因子含量(1.853±0.751)pg/mg,前列腺素E2含量为(1749±638)pg/mg;D组患者胃黏膜表皮生长因子含量(1.871±0.746)pg/mg,前列腺素E2含量为(1707±616)pg/mg。A组与C组相比较,P﹤0.01;A组与D组相比较,P﹥0.05。结论肝源性溃疡患者的胃黏膜表皮生长因子和前列腺素E2不明显与肝硬化患者的肝功能分级相互关系,也就是说不会影响到肝功能变化对肝源性溃疡患者胃黏膜的保护作用。     

阿司匹林对结肠癌术后结肠组织中前列腺素E2含量的影响

该文探讨阿司匹林对结肠癌手术前后组织中前列腺素E2(PGE2)含量的影响。结果表明,结肠癌组织中PGE2含量明显高于正常黏膜组织中PGE2含量。阿司匹林通过抑制PGE2的合成,减少结肠癌术后结肠组织中PGE2含量,与降低结肠癌的术后复发率可能有一定的关系。     

前列腺素E2及其受体在卵泡发育中的作用

颗粒细胞受黄体生成激素（LH）刺激后分泌的前列腺素E2(PGE2),通过旁分泌和自分泌,结合卵丘细胞上的前列腺素受体2,进而激活腺苷酸环化酶,增加胞内cAMP含量并促进透明质酸合酶2和肿瘤坏死因子α介导蛋白6的合成,引起卵丘细胞扩展。PGE2还通过调控颗粒细胞类固醇代谢通路影响孕酮分泌,从而调节黄体的功能。本文就PGE2在卵泡发育的作用进行综述。     

前列腺素与呼吸系统疾病

肺脏是人体含前列腺素浓度最高的组织之一。肺组织能合成PGE_2和PGF_(2α)。PGF含量多于PGE;PGF_(2α)含量为8～500毫微克/每克肺组织,而PGE_2为1.8～66毫微克;PGF_(2α)/PGE_2的比值为1.5～200。但在离体的支气管中,PGE_2的浓度为PGF_(2α)的2～3倍。实验证明,肺过度膨胀、过敏反应、肺的空气栓塞以及某些药物如组织胺、色胺、五羟色胺、缓激肽、和磷酸酯酶A等均可作为刺激而促使肺释放前列腺素。某些非类固醇性抗炎药物(如消炎痛等)能抑制前列腺素的合成。前列腺素在体循环中较为稳定,但当通过一次肺循环后,95％的PGE和PGF经代谢而灭活。前列腺素合成和代谢紊乱与某些肺部疾病的发生和发展有一定关系。近年来,前列腺素又试用于治疗     

妊娠期牙周病与早产低体重儿的关系

目的:探讨牙周疾病与早产的关系。方法:合并牙周炎孕妇78例作为牙周炎组,选取同期无牙周炎孕妇80例作为非牙周炎组,分析两组患者早产、流产的发生率。收集孕妇妊娠20周～24周时的龈沟液及分娩后羊水,测定羊水中及龈沟液中肿瘤坏死因子a、白介素6和前列腺素E2的水平。比较两组早产发生率,早产妇与足月产妇牙龈液和羊水中的肿瘤坏死因子a、白介素6和前列腺素E2的质量浓度。结果:牙周病组中的早产发生率为31.1%,非牙周病组的早产发生率为6.3%,两组差异有统计学意义(P<0.01)。早产妇龈沟液与羊水中的肿瘤坏死因子a、白介素6和前列腺素E2高于足月产妇,差异有统计学意义(P<0.05)。结论:孕妇牙周感染可能是导致早产低体重儿的原因之一。     

黄芪总苷对大鼠脑缺血机制与前列腺素的关系

目的:研究黄芪总苷(astragalosides,AST)预处理的脑保护作用机制及其与前列腺素E2的关系.方法:采用间断静脉推注AST模拟预适应的实验方法,观察大鼠大脑中动脉栓塞再灌致脑梗死体积、血清中前列腺素E2(prostaglandin E2,PGE2)的含量的变化.结果:AST(20,40,80mg.kg-1)预处理明显减少脑梗塞体积、并可明显降低血清中PGE2含量.结论:黄芪总苷预处理对大鼠脑缺血再灌注损伤具有明显的保护作用,其机制与脑组织中减少PGE2的产生有密切的关系.     

环氧化酶-2及表达产物与肿瘤的关系研究进展

环氧化酶-2是花生四烯酸代谢产生前列腺素过程的重要限速酶。研究表明环氧化酶-2和前列腺素参与了肿瘤的发生、发展,非甾体类抗炎药(NSAIDS)可通过抑制环氧化酶-2和前列腺素而抑制肿瘤细胞增殖。本文对环氧化酶-2和前列腺素的生物学特性、两者与肿瘤及预防的关系加以综述。1环氧化酶(cyclooxygenase,COX)COX是与膜结构相连的糖蛋白复合物,有三种异构形式:COX-1、COX-2和COX-3。COX-2为诱导型酶,即静息状态下不表达,当细胞受到刺激时COX-2基因迅速被激活,合成COX-2蛋白。COX-2与炎症及肿瘤的发生、发展密切相关。人的COX-2基…     

环氧合酶-2与膀胱移行细胞癌的关系

环氧化酶-2(COX-2)是一种诱导型前列腺素内源性过氧化物酶,在多种肿瘤中有不同程度的表达.近期研究表明COX-2表达与膀胱移行细胞癌(BTCC)有密切关系,其作用机制可能涉及多个方面.     

前列腺素E_2及其受体在卵泡发育中的作用

前列腺素E_2(PGE_2)作为传递黄体生成激素(LH)信号的关键旁分泌因子,主要由颗粒细胞合成,其分泌至胞外后结合至卵丘细胞上的前列腺素E_2受体2和前列腺素E_2受体4(PTGER2、PTGER4),这两种受体都通过活化胞内偶联的Gas蛋白,进而激活腺苷酸环化酶,增加胞内环磷酸腺苷(c AMP)含量并促进透明质酸合酶2(HAS2)和肿瘤坏死因子α介导蛋白6的合成,引起卵丘细胞扩展。此外PGE_2还通过调控颗粒细胞芳香酶(CYP19)和孕酮表达,从而在排卵后调节黄体的功能。PGE_2的调控异常与多种生殖相关疾病有关,如未破裂卵泡黄素化综合征(LUFS)和受精障碍等。     

前列腺液中PGE2水平与慢性非细菌性前列腺炎的相关性研究

目的 探讨前列腺液中PGE2水平与慢性非细菌性前列腺炎的相关性.方法 选择因慢性非细菌性前列腺炎在某院就诊的患者90例为实验组,症状表现为尿频、尿急、尿痛、排尿困难,持续3个月以上.同时选择在该院体检的人群87例为对照组,对照组任何人无尿频、尿急、尿痛、排尿困难等症状.结果 实验组的白细胞为(21.4±3.4)个/hpf,明显高于对照组(4.3±3.1)个/hpf,差异有统计学意义(P/0.05).实验组的PGE2浓度为(263.5±23.7) pg/ml,高于对照组(121.4±20.5)pg/ml,差异有统计学意义(P＜0.05).实验组前列腺液中PGE2水平与NIH-CPSI中的疼痛不适症状评分呈正相关(r=0.063,P＜ 0.01).实验组前列腺液中PGE2水平与NIH-CPSI中的排尿症状、生活质量无明显相关性.实验组前列腺液中PGE2水平与NIH-CPSI症状总评分呈正相关(r=0.534,P＜0.01).结论 前列腺液中PGE2水平与慢性非细菌性前列腺炎的发病有一定的相关性.     

镉对免疫系统的影响及与前列腺素的关系

应用心得安和前列腺素动物模型观察了镉对免疫系统的影响及与前列腺素Ｅ２（ＰＧＥ２）的关系。结果表明：整体动物实验时，ＰＧＥ２和淋巴细胞ｃＡＭＰ在镉单独作用各组均有升高趋势。淋巴细胞ｃＡＭＰ在心得安单独作用时，５ｍｇ／ｋｇ组低于对照组（Ｐ＜０．０５）；１５ｍｇ／ｋｇ组高于对照组（Ｐ＜０．０５）。还见心得安高剂量组的ＰＧＥ２显著低于镉中剂量组和消炎痛＋镉组（Ｐ均＜０．０５）。体外培养人外周血淋巴细胞时见镉组及消炎痛＋镉组的ＡＣ酶活性和ｃＡＭＰ含量均显著升高；心得安＋镉组的ＡＣ酶活性与对照组比较无显著性差异，ｃＡＭＰ含量在两作用组中有一组无显著变化。此外，消炎痛可阻断巨噬细胞分泌ＰＣＥ２，且能缓解镉对巨噬细胞的抑制。结果提示：心得安的作用较消炎痛明显，即在镉的免疫毒性作用机制中，β肾上素能受体机制存在的可能性大于ＰＧＥｃＡＭＰ机制。     

牙周疾病与早产关系的研究

目的:探讨牙周疾病与早产的关系。方法:测定130例孕产妇的牙龈液与羊水中肿瘤坏死因子α(TNFα)、基质金属蛋白酶8、9(MMP-8、9)和前列腺素E2(PGE2)的水平。结果:早产儿组牙龈液与羊水中TNFα、MMP-8、9、和PGE2高于足月儿组(P<0.01)。结论:牙周疾病与早产有一定的联系,是引起早产的原因之一。     

煤工尘肺与血液中前列腺素E_2水平的关系

用放射免疫方法检测不同期别的煤工尘肺（ＣＷＰ）患者血浆中前列腺素Ｅ２（ＰＧＥ２）的水平，同时用体外细胞培养方法将煤尘作用于肺泡巨噬细胞（ＡＭ）后对其分泌ＰＧＥ２的情况进行比较。结果表明：ＣＷＰ患者血浆中ＰＧＥ２的水平明显高于对照组；不同期别的病人血浆中ＰＧＥ２含量不一样．表现为Ⅰ＞Ⅱ＞Ⅲ，经统计分析．Ｐ＜０．０１．体外实验显示随着煤尘对ＡＭ作用浓度增加．培养时间延长，ＡＭ培养上清液中ＰＧＥ２含量升高。体内、体外的研究结果均证实煤尘作用于ＡＭ后，可以改变ＡＭ的分泌功能，使其分泌大量的ＰＧＥ２．提示：ＣＷＰ的发生发展与血浆中ＰＧＥ２的水平有一定的关系。     

Effects of Obesity on the Regulation of Macrophage Population in the Prostate Tumor Microenvironment

Obesity is associated with a greater risk of prostate cancer mortality. However, the mechanisms connecting obesity to the progression of prostate cancer remain unknown. This study determined the impact of obesity on macrophage recruitment and tumor-associated macrophage (TAM) polarization in the prostate tumor microenvironment, since a high concentration of TAMs in tumors has been linked to progression in prostate cancer. We utilized an in vitro model in which pre-adipocytes, prostate cancer cells, and macrophages were exposed to sera from obese or nonobese men, or conditioned media generated under obese or nonobese conditions. Matrigel invasion chambers were used to assess macrophage recruitment in vitro, and immunohistochemical analysis evaluated recruitment in a PTEN knockout mouse model. qPCR was used to measure mRNA levels of CCL2, COX-2, IL-10, TGF-beta, VEGF-A, arginase-1, and MMP-9. PGE2 production was measured by ELISA. Obesity increased macrophage and TAM recruitment, and increased mRNA levels of TAM markers in macrophages. Similarly, obese conditions increased CCL2 and COX-2 expression, as well as PGE2 levels in prostate cancer cells. COX-2 inhibition resulted in lower expression of obesity-induced TAM markers. Our data suggest that obesity promotes macrophage infiltration into the prostate tumor microenvironment, and induces TAM polarization through the COX-2/PGE2 pathway.     

Dose-dependent effect of dietary conjugated linoleic acid on the growth of rat hepatoma dRLh-84 cells in vivo

In this study, the effect of varying doses of conjugated linoleic acid (CLA) on the growth of transplanted hepatoma dRLh-84 cells and the relationship between tumor growth and prostaglandin (PG) E2 production or cyclooxygenase (COX)-2 expression were examined. Donryu rats were fed an experimental diet containing 0, 0.1, 0.5, or 2 wt.% CLA for 3 wk, and then dRLh-84 cells were transplanted into the liver. Results show that dietary CLA (0.5 and 2 wt.%) significantly enhanced the growth of the transplanted hepatoma cells compared to the non-CLA diet group at 20 d after cell transplantation. Tumor weight at 10 d after transplantation was also significantly higher in the 2 wt.% CLA group than in non-CLA fed rats. Ten days after transplantation, the PGE2 level in the tumor tissue was shown to be depressed in a CLA dose-dependent manner. Cyclooxygenase-2 (COX-2) mRNA expression in the tumor also tended to be lower in the CLA group than in the non-CLA diet group 10 d after transplantation. Dietary CLA did not affect the tumor phospholipid arachidonic acid level, which is a substrate for PG synthesis. These results indicate that dietary CLA of at least 0.5 wt.% enhances the growth of transplanted dRLh-84 cells in vivo. It is believed that growth promotion of dRLh-84 cells in vivo by CLA cannot be clarified by the PG synthesis dependent mechanism.     

Effect of dietary conjugated linoleic acid on phorbol ester-induced PGE2 production and hyperplasia in mouse epidermis.

Conjugated linoleic acid (CLA) is a chemoprotective fatty acid that inhibits phorbol ester-induced skin tumor promotion in mice. The goal of the present study was to determine potential chemoprotective mechanisms through which CLA may be acting. Mice were fed diets containing 0.0%, 0.5%, 1.0%, or 1.5% CLA (by wt) for six weeks. The epidermis was evaluated for fatty acid composition, vascular permeability, prostaglandin E2 (PGE2) production, hyperplasia, ornithine decarboxylase activity, and c-myc mRNA accumulation. Fatty acid analysis of mouse epidermis demonstrated a dose-dependent increase of CLA incorporation into phospholipids and neutral lipids. In mice topically treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), dietary CLA (1.5%) significantly (p < 0.05) reduced PGE2 synthesis (2-fold). Additionally, CLA lowered accumulation of c-myc mRNA, a gene commonly associated with regulating cell cycle components involved in cellular proliferation, although this trend was not significant. Vascular permeability was unaffected by dietary CLA. These data suggest that dietary CLA modulates TPA-induced tumor promotion through a mechanism involving PGE2 production; however, dietary CLA had a moderate effect on c-myc mRNA levels and little effect on TPA-induced hyperplasia and ornithine decarboxylase activity.     

Fish oil and tocopherol-induced changes in natural killer cell-mediated cytotoxicity and PGE2 synthesis in young and old mice

Natural killer cell (NK) activity decreases and prostaglandin E2 (PGE2) level increases in aged mice. Because PGE2 is involved in control of NK activity this study was conducted to investigate whether or not decreasing PGE2 level by changing the type of dietary fat or increasing the level of vitamin E (vit. E) modulates NK activity of young and old mice. Mice were fed either a corn oil (CO) or a fish oil (FO) diet supplemented with 30 or 500 mg/kg diet of vit. E for 6 wk. To study the effect of vit. E during active immune response and oxidative stress, groups of old mice fed CO and either 30 or 500 mg/kg diet of vit. E were injected with sheep red blood cells (SRBC) prior to assessment of their NK activity. As reported by others regarding mice fed a nonpurified diet, the old mice in all dietary groups had significantly less NK activity and tended to synthesize more PGE2 than young mice. FO-fed mice synthesized less PGE2 than CO-fed mice; however, their NK activity was not higher than that of CO-fed mice. By contrast young mice fed FO had a moderately lower NK activity than those fed CO. Vit. E supplementation did not change NK activity in nonimmunized mice but was effective in preventing SRBC-induced decrease in NK activity of old mice.