视黄素诱导的癌细胞凋亡及其对癌细胞生长抑制的相关性

以不同的受体选择性视黄素处理乳腺癌细胞，通过荧光显微术、ＴｄＴ测定和细胞生长测定，分析视黄素诱导的癌细胞凋亡及其对癌细胞生长抑制的相互关系；将受体ＲＡＲα基因转染乳腺癌ＭＢ－２３１细胞，发现受体转染与细胞凋亡诱导有关；ＲＡＲ和ＲＸＲ受体选择性视黄素联合使用，对诱导癌细胞凋亡和抑制癌细胞生长具有加强作用．结果证实，视黄素能够诱导乳腺癌细胞的细胞凋亡，并与抑制癌细胞的恶性生长相一致，这可能是视黄素抗癌作用的机制之一．     

核酸与杨梅黄素荧光体系的研究

 研究了杨梅黄素与核酸溶液的结合反应.加入核酸溶液后,杨梅黄素在436nm处的荧光强度显著地增强.在最佳实验条件下,对ctDNA和yRNA的线性范围分别为0.2～3.2μg/mL和0.18～3.2μg/mL.并讨论了干扰物质的影响,对其作用机理也进行了初步探讨.     

岩藻黄素降脂活性及其作用机制研究进展

岩藻黄素（Fucoxanthin）是海洋褐藻中主要的叶黄素类类胡萝卜素，也是褐藻中主要的降脂活性成分之一。岩藻黄素具有抗肿瘤、抗炎症、抗肥胖等多种生物活性，在代谢调节方面，岩藻黄素能促进脂肪分解和脂肪酸氧化，上调白色脂肪组织中线粒体解偶联蛋白1（UCP1）的表达，具有显著的抗肥胖功效，但其具体作用机制还需要进一步研究。本文综述近年来岩藻黄素在促进前体脂肪细胞分化、诱导白色脂肪细胞棕色化、调节胆固醇代谢等方面作用机制的研究成果，为进一步研究岩藻黄素的降脂作用机制提供理论参考。     

加工过程中褐藻岩藻黄素的特征光谱变化

以岩藻黄素特征光谱变化为指标,研究了光照、pH值、高温、高压等加工条件对岩藻黄素稳定性的影响。结果表明,岩藻黄素不仅在高温高压下会发生快速降解,光照及酸性环境也会导致其结构的缓慢破坏;但在避光及碱性环境下岩藻黄素较稳定。     

玉液汤对气阴两虚型糖尿病大鼠血糖与胰岛素受体的影响

目的：探讨玉液汤疗效及其降糖的分子机理。方法：用佐脲链菌素复制糖尿病大鼠模型,随机分为正常组、模型组、治疗组和对照组,分别给与蒸馏水、玉液汤和消渴丸,观察血糖、血脂、糖化血红蛋白、胰岛素水平和肝脏胰岛素受体、受体底物1基因表达水平。结果：注射SMZ后动物血糖、血脂、糖化血红蛋白明显升高,胰岛素水平明显降低,两组均能明显降低糖尿病大鼠血糖、血脂、糖化血红蛋白水平、提高糖尿病大鼠胰岛素的水平,与模型组比较差异有统计学意义（P<0.05）,治疗组与对照组两组间比较差异无统计学意义（P >0.05）;治疗组与对照组均能增加糖尿病大鼠肝脏IR、IRS-1m RNA水平,与模型组比较差异有统计学意义（P<0.05）,治疗组与对照组两组间比较差异无统计学意义（P >0.05）。结论：玉液汤能降低糖尿病大鼠血糖、提高胰岛素水平,其机理可能是影响胰岛素受体-受体底物实现的。     

a2及5—HT2受体与甘氨酸受体之间的对话

在新鲜分离的神经细胞模型上,运用制霉菌素（ｎｙｓｔａｔｉｎ）穿孔膜片钳方法研究ａａ２及５－ＨＴ２与甘氨酸受体之间对话的分子机理,发现：刺激ａ２受体,抑制腺苷酸环化酶,减少ｃＡＭＰ的生成,合ＰＫＡ活性降低,从而增强甘氨酸受体的功能;刺激５－ＨＴ２受体,激活磷脂酶Ｃ（ＰＬＧ）,增加甘油二酯（ＤＡＧ）的生成．ＤＡＧ增强不依赖Ｃａ＾２＋的新型ＰＫＧ（ｎＰＫＧ）的活性,从而增强甘氨酸受体的功能,ａ２及５－Ｈ     

鸢尾黄素的研究进展

鸢尾黄素是一种天然存在的异黄酮,本文从生物活性和合成两大方面对鸢尾黄素的研究状况进行了综述。     

自发曲率对受体介导的胞吞作用的影响

为研究纳米颗粒进入具有自发曲率的细胞膜的机理,在已建立的受体介导胞吞作用力学模型的基础上进行了扩展,对非零自发曲率的细胞膜上发生的受体介导的胞吞作用进行了研究。结果显示:包裹时间不仅依赖于颗粒的尺寸,而且依赖于细胞膜的自发曲率;存在最佳的颗粒半径使包裹时间最短;对于无限大尺寸的细胞膜,当细胞膜的自发曲率大于临界值时,存在最小和最大包裹半径,但当细胞膜的自发曲率小于等于临界值时,只存在最小包裹半径。     

视黄酸受体转录水平的改变与癌细胞生长的关系

用ＲＡＲ受体选择性视黄酸和ＲＸＲ受体选择性视黄酸处理乳腺癌细胞，结果表明，ＲＡＲ受体选择性视黄酸能够有效地抑制依赖激素的乳腺癌细胞的生长，而ＲＸＲ受体选择性视黄酸则有效地抑制非依赖激素的乳腺癌细胞的生长．视黄酸的作用主要由其受体ＲＡＲｓ和ＲＸＲｓ所介导，ＲＮＡ印迹表明ＲＡＲα和ＲＡＲβ可能参与介导视黄酸的作用；进一步实验表明，通过ＲＡＲａ基因的转染，可以在非依赖激素的乳腺癌细胞中诱导ＲＡＲβ高水平地表达，使ＲＡ抗性细胞变为ＲＡ敏感细胞，因此，视黄酸诱导的ＲＡＲβ表达与其抑制乳腺癌细胞生长密切相关．     

裙带菜岩藻黄素的提取分离及对人肝癌细胞HepG2的抑制作用研究

以裙带菜为原料对岩藻黄素的提取分离工艺进行改进,并对岩藻黄素体外抑制人肝癌细胞HepG2生长进行初步研究.通过对干燥温度、溶剂配比、提取剂用量和提取时间的筛选,结果显示:采用95:5(体积比)的丙酮乙醇混合提取液、1:40(质量体积比)提取剂用量、粗提冷冻干燥处理的裙带菜,抽提24 h,提取3次,1 g干燥裙带菜可提取1.201 2 mg岩藻黄素,纯化效率为28.50％;将粗提液中的色素转移至正己烷中,采用浓度为70％的乙醇溶液萃取出的岩藻黄素含量为0.847 2 mg,纯化效率为85.89％;用薄层层析进一步纯化,岩藻黄素的含量为0.593 0 mg,纯化效率为98.90％;人肝癌细胞HepG2体外培养试验表明:当岩藻黄素浓度达到50 μg·mL-1时,抑制率达到28.44％.     

Homodimer formation of retinoid X receptor induced by 9-cis retinoic acid.

Retinoid response pathways are mediated by two classes of receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs). A central question is whether distinct response pathways are regulated by these two classes of receptors. The observation that the stereoisomer 9-cis-retinoic acid binds with high affinity to RXRs suggested that this retinoid has a distinct role in controlling RXR activity, but it was almost simultaneously discovered that RXRs function as auxiliary receptors for RARs and related receptors, and are essential for DNA binding and function of those receptors. Hence, although RARs seem to operate effectively only as heterodimeric RAR/RXR complexes, RXRs themselves apparently function predominantly, if not exclusively, as auxiliary receptors. Here we report that 9-cis-retinoic acid induces RXR homodimer formation. Our results demonstrate a new mechanism for retinoid action by which a ligand-induced homodimer mediates a distinct retinoid response pathway.     

9-cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.

Vitamin A (retinol) and its natural derivatives are required for many physiological processes. The activity of retinoids is thought to be mediated by interactions with two subfamilies of nuclear retinoic acid receptors, RAR and RXR. The RARs bind all-trans retinoic acid (t-RA) with high affinity and alter gene expression as a consequence of this direct ligand interaction. RXR alpha is activated by t-RA, yet has little binding affinity for this ligand. t-RA may be converted to a more proximate ligand that directly binds and activates RXR alpha, and we have developed a method of nuclear receptor-dependent ligand trapping to test this hypothesis. Here we report the identification of a stereoisomer of retinoic acid, 9-cis retinoic acid, which directly binds and activates RXR alpha. These results suggest a new role for isomerization in the physiology of natural retinoids.     

Identification of a novel retinoic acid receptor in regenerative tissues of the newt

In urodele amphibians, the progenitor cells that regenerate amputated limbs (known as the blastema) normally replace only the missing structures. After systemic delivery of retinoic acid (RA), more proximal structures are also formed, indicating that RA can control position specification in the proximal-distal axis of the regenerating limb. According to dose and experimental context, retinoids can also re-specify the anteroposterior axis of the limb, induce deletions of skeletal elements, or block re-growth completely. To study the molecular basis of these morphogenetic effects, we screened complementary DNA libraries of newt regenerative tissues (limbs and tails) for hormone nuclear receptors activated by RA. Two functional retinoic acid receptors (RARs) were identified, one of which is the newt homologue of the human alpha-receptor (RAR alpha). The second receptor, called RAR delta, is novel. Sequence analysis suggests that the composite newt RAR previously reported is chimaeric, consisting of 5'RAR-beta-like and 3' RAR delta clones. We conclude that multiple RARs are expressed during limb regeneration in amphibians and suggest that receptor heterogeneity may underlie the different effects of retinoids on limb morphogenesis.     

Retinoids specifically enhance the number of epidermal growth factor receptors

Retinoids elicit many biological and biochemical responses from cells in vitro. One widely used criterion for the responsiveness of cells to retinoids is inhibition of growth; retinoids reduce the saturation density and/or growth rate of many normal and tumorigenic cell lines. Propagation of eukaryotic cells has been demonstrated to be dependent on the presence of macromolecular growth factors such as epidermal growth factor (EGF), which can stimulate proliferation of epithelial and fibroblastic cell lines. We now describe the effect of retinoids on the binding of EGF to its receptor. Retinoic acid enhances binding of 125I-labelled EGF to various fibroblastic and epidermal cell lines. It has no marked effect on the affinity of this growth factor for its receptor, but increases the number of EGF receptor sites. Retinoic acid has little effect on the binding of concanavalin A (Con A) and insulin, indicating the specific nature of the action of retinoids on cell-surface glycoproteins. Treatment of cells with the phorbol ester 12-o-tetradecanoyl phorbol-13-acetate (TPA) and retinoic acid shows poor antagonism between these compounds on EGF binding. It has been previously shown that retinoids induce or stimulate differentiation of embryonal carcinoma cells. EGF binding can be used as a marker to monitor differentiation of these cells.     

四株肺癌细胞系的维甲酸受体表达的研究

目的：观察来源于不同组织学类型的人肺癌细胞系（肺巨细胞癌细胞系PLA-801,肺鳞状上皮细胞癌细胞系C-57,个旧肺腺癌细胞系GLC-82和肺腺癌细胞系PC-84045）的维甲酸受体的含量和分布特征。方法：作ELISA和免疫组化显色计算机图象分析方法,对4株具有不同侵袭潜能,不同组织学类型的肺癌细胞系的维甲酸受体（RARs、RAR和RXRs）进行检测。结果：4株细胞系的RARβ的表达极少,甚至缺如;RARs主要分布在癌细胞胞浆中,但RXRs主要位于细胞核内,表达水平较高;RARs和RXRs在PLA-801细胞中表达最低。结论：肺癌中普遍存在着RAR的表达分布异常,这些改变可能与肺癌的异常分化有关,亦可能是肺癌细胞对维甲酸诱导分化不敏感的重要原因。RXRs较高水平的表达且主要位于核内,提示用9-顺式维甲酸来诱导肺癌的分化效果可能会较好。