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1.
利用还原型烟酰胺腺嘌呤二核苷酸NADPH黄递酶组织化学方法,对硕螽雄性生殖系统中一氧化氮合酶的分布进行了定位研究.结果表明,一氧化氮合酶阳性反应发生在硕螽精子发生中各级生精细胞的胞质中,由精原细胞群包围着的端胞呈一氧化氮合酶强阳性反应,精原细胞呈强阳性反应,胞质着色为深蓝色.精母细胞呈一氧化氮合酶阳性,精子呈阳性,胞质着色为浅蓝色.输精管细胞呈一氧化氮合酶阳性反应,附腺管壁细胞呈阳性反应.提示一氧化氮不仅参与了硕螽精子发生,还参与了精子的输送.  相似文献   

2.
一氧化碳(CO)是与一氧化氮(NO)相似的信使分子,在人体内广泛存在。它可以通过酶解血红素氧合酶(HO)而在多种细胞产生,是一种鸟苷酸环化酶(sGC)的激活剂。近来研究表明,CO对呼吸系统,心血管系统、神经系统等均发挥调节作用。  相似文献   

3.
将雄性SD大鼠30只随机分三组,其中正常对照组10只,20只通过高脂饲料喂养建立高脂血症大鼠模型后随机分为高脂模型组和高脂运动组.喂养6周后,测定总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、一氧化氮(NO)、一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)、丙二醛(MDA)等相关指标,并进行比较分析.结果显示:对于患高脂血症的大鼠,运动有明显调节血脂、降低过氧化物以及改善血管内皮功能的作用.  相似文献   

4.
一氧化氮是一种气体性细胞间信息分子,在肠缺血再灌注损伤中具有重要的作用。文章介绍一氧化氮合酶的生物学特性、在肠道的分布和一氧化氮的作用等方面的研究进展。  相似文献   

5.
一氧化氮在生物体内的化学过程   总被引:1,自引:0,他引:1  
传统的观念认为,一氧化氮(NO)是极不受欢迎的化合物,因为它污染大气、形成酸雨等而危害人类。只是到了20世纪80年代后期,由于分子生物学的研究进展,才发现和证实NO是生物体内具有重要作用的信使分子。它分布在脑、血管、外周神经及肺、肝、生殖器官中,参与生理、病理等多种效能。本文仅对NO在人体中的化学过程及主要效能简述如下:1NO的生物合成1.1酶合成途径系以左旋精氨酸(L-Arg)和氧分子(O2)为底物,经一氧化氮合酶NOS)催化,使在内皮细胞、神经细胞及巨噬细胞等中生成NO。该途径以烟酞胺腺嘌呤…  相似文献   

6.
对PPAR-γ的激动剂及其在动脉粥样硬化中对血管细胞的影响等方面进行综述。过氧化物酶体增殖物激活受体-γ(peroxisome proliferator—activatedreceptor-γ,PPAR-γ)几乎对参与动脉粥样硬化的所有血管细胞均有影响,在调节动脉粥样硬化的发生中起重要的作用。PPAR-γ与特异性激动剂结合后,调节靶基因的转录活性,抑制血管细胞的增殖与迁移,降低炎症反应,阻止动脉粥样硬化的发生。  相似文献   

7.
目的:观察九龙虫对血管痴呆型(VD)小鼠脑组织一氧化氮(NO)、一氧化氮合酶(NOS)和海马形态学的影响。方法:采用双侧颈总动脉结扎法制造VD小鼠模型,给药后,测定小鼠脑组织中NO含量和NOS活性,并观察海马细胞形态学的变化。结果:模型组NO含量和NOS活性明显高于都可喜组和九龙虫各给药组,从形态学观察,都可喜组和九龙虫各给药组小鼠海马组织神经细胞损伤明显小于模型组。结论:九龙虫治疗VD的作用机制可能与降低脑组织中NO含量及NOS活性,从而减轻对脑组织的损伤有关。  相似文献   

8.
研究跑台过度训练对大鼠骨骼肌组织与血液中自由基代谢水平及主要代谢酶的活性的影响,揭示黄柳菇总黄酮对过度运动后大鼠骨骼肌组织的氧化防御效果,并探讨其可能性机制。研究结果显示过度训练组与安静组相比,大鼠骨骼肌中抗氧化酶超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、总抗氧化能力(T-AOC)显著下降,丙二醛(MDA)含量显著增加,血清中肌酸激酶(CK)、一氧化氮合酶(NOS)水平明显升高,表明骨骼肌组织脂质过氧化水平升高,肌细胞损伤效果明显;而过度训练+黄柳菇总黄酮组大鼠骨骼肌组织有良好改善。表明黄柳菇总黄酮可以改善过度运动大鼠的自由基代谢水平,使组织中抗氧化酶活性增强,有利于保护骨骼肌组织结构和功能的完整性,可作为天然抗氧化剂和微生态制剂进一步研究和开发的真菌资源。  相似文献   

9.
硫化氢(hydrogen sulfide,H2S)是继一氧化氮(nitric oxide,NO)和一氧化碳(carbon monoxide,CO)之后的第三种气体信号分子,其在体内由特殊的酶倦化产生,有其特殊的代谢过程.其在中枢神经系统中发挥着重要的作用,在生理状态下参与海马长时程增强、神经胶质细胞作用的发挥,通过影响下丘脑-垂体-肾上腺轴而影响神经内分泌过程,参与神经元氧化应激反应和脑血管功能的调节;H2S还参与多种中枢神经系统疾病如阿尔茨海默病、热性惊厥、唐氏综合症、脑缺血、脑缺血再灌注等的病理生理过程.该文就H2S在中枢神经系统的研究概况做了综述.  相似文献   

10.
目的:研究心肌缺血预处理(IP)延迟性保护作用终末阶段(IP后48h至72h)的机制,以及神经型一氧化氮合酶(nNOS)、诱生型一氧化氮合酶(iNOS)是否中介了此过程。方法:采用在体家兔冠状动脉阻断的缺血/复灌损伤模型,测定心肌梗死面积、冠脉流出液中乳酸脱氢酶(LDH)和肌酸激酶(CK)含量及各项心室力学指标。结果:与单纯缺血/复灌组相比,IP后72h,明显降低心脏缺血/复灌后的梗死面积和血浆中乳酸脱氢酶(LDH)、肌酸激酶(CK)的含量,促进左室收缩压(LVSP)、最大左室收缩速率(+dP/dtmax)和最大左室舒张速率(-dP/dtmax)的恢复。使用iNOS的特异性抑制剂S-methylisothiourea sulfate(SMT)不能阻断IP后72h心肌保护作用。而nNOS的特异性抑制剂N-propyl-L-arginine(NPA)、NOS的非特异性抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)阻断了IP后72h心肌保护作用。结论:IP后72h心肌保护作用依然存在,nNOS介导了心肌缺血预处理延迟性保护作用终末阶段,而与iNOS无关。  相似文献   

11.
文章以清洁级纯系雄性SD大鼠为实验模型,应用组织病理学、RT—PCR技术,研究高脂饮食诱发动脉粥样硬化过程中血管内膜细胞大电导钙激活的钾通道(large conductance Ca—activated K+ channels,BKCa)、中电导钙激活的钾通道(Intermediate condutance Ca—activated K+ channels,IKCa)基因表达的动态改变情况,从基因表达水平探讨高脂饮食诱发动脉粥样硬化的作用机制。同时指出,IKCa可能为动脉粥样硬化的早期启动因子,此观点有助于动脉粥样硬化的早期检测与防治。  相似文献   

12.
Background:The adhesion of monocytes to the endothelium following accumulation oflow-density lipoprotein(LDL) in subendothelial spaces is an important step in the development of intimal hyperplasia in arterially implanted vein grafts and atherosclerosis in both animals and humans.However.it iS not well known how serum factors affect the adhesion of monocytes.Methods:We have studied the efrect of fetal calf serum(FCS).which we considered a source of LDL.on the adhesion of monocytes to endothelial cells(Ecs)by using human monocytic THP-1 cells and both a monolayer of cultured bovine aortic endothelial cells(EC monoculture)and a co-culture with bovine aortic smooth muscle cells(EC-SMC co-culture).Results:It was found that the addition of FCS to the medium greatly affected the adhesion of THP-1 cells,and the higher the concentration of FCS in the medium,the greater the adhesion of THP-1 cells to endothelial cells.Adhesion of THP-1 cells to an EC-SMC co-culture Was approximately twofold greater than that to an EC monoculture,and after adhering to endothelial cells,many THP-1 cells transmigrated into the layer of smooth muscle cells.Conclusion:The results suggest that the elevation of the LDL(cholesterol)level in blood provides a favorable condition for the development of intimal hyperplasia and atherosclerosis by promoting the adhesion of monocytcs to the endothelium and their subsequent migration into subendothelial spaces.  相似文献   

13.
血管紧张素-(1—7)是AngII的内源性拮抗因子,具有保护血管内皮细胞抗血管平滑肌细胞增殖与迁移等作用,从而发挥抗动脉粥样硬化效应。探讨血管紧张素-(1—7)的生理功能及其在抗动脉粥样硬化中的作用,有助于进一步揭示ACEI及ATl受体阻断剂的抗动脉粥样硬化机制,并有可能为防治动脉粥样硬化等疾病提供新的有效思路。  相似文献   

14.
High blood pressure (hypertension) is implicated in the development of atherosclerosis. Blood vessels are constantly subjected to stretch due to blood pressure and changes in stretch usually instigate adaptive vascular remodeling, including abnormal growth and proliferation of vascular smooth muscle cells (VSMCs) as well as extracellular matrix (ECM). In this experiment, we used bovine aortic endothelial cells and smooth muscle cells (EC-SMC) co-cultured ePTFE vascular grafts subjected to normal atmospheric pressure (as a control), and 100 mmHg hydrostatic pressure for 7 d. The increase of cell layer thickness was observed. When measured, the cell layer thickness increased by 116.2%. The increase of collagen (Type IV) synthesis was also observed in the immunohistochemistry assay. When stained with toluidine blue, the cells showed metachromatic phenomenon.  相似文献   

15.
心血管疾病是危害人类健康的主要因素,其中动脉粥状硬化又是致死和致残的主要因子,它可以发生在多种动脉中并导致许多疾病,导致动脉粥状硬化的因素有几种,在此仅介绍血管内皮细胞损伤。  相似文献   

16.
研究血浆中不对称二甲基精氨酸(ADMA)浓度与蛛网膜下腔出血(SAH)的关系。蛛网膜下腔出血患者血浆ADMA平均水平,第3、7和14天分别为2.3±0.8μmol/L、6.4±1.5μmol/L和14.1±0.9μmol/L,对照组平均为1.1±0.3μmol/L,两组间比较差异显著(P〈0.01)。ADMA参与了蛛网膜下腔出血病理生理过程,水平与脑血管痉挛关系密切。  相似文献   

17.
Homoharringtonine (HHT) has currently been used successfully in the treatment of acute and chronic myeloid leukemias and has been shown to induce apoptosis of different types of leukemic cells in vitro. Emerging evidence suggests that angiogenesis may play an important role in hematological malignancies, such as leukemia. How ever, whether HHT can relieve leukemia by anti-angiogenesis is still unknown. We investigated the anti-angiogenesis potential of HHT with the human umbilical vein endothelial cell line (ECV304) and leukemic cell line (K562) in vitro. Cellular proliferation was determined by MTT assay and apoptosis was analyzed by flow cytometry. The mRNA expression of vascular endothelial growth factor (VEGF) was assessed by RT-PCR and VEGF protein production was detected by Western blot. Inhibition of cell proliferation and induction of apoptosis by HHT were discovered in ECV304 cells, and appeared in a dose- and time-dependent manner. Also, treatment with HHT caused down-regulation of VEGF mRNA expression in K562 cells in similar dose- and time-dependent manner and inhibition of VEGF protein production in K562 cells in response to the enhancing concentration of HHT. The results demonstrated that HHT could also induce apoptosis in endothelium and down-regulate VEGF expression in K562 cells. In conclusion, we believe HHT has anti-angiogenesis potential and speculate that HHT might exert its anti-leukemia effects via reduction of angiogenesis.  相似文献   

18.
INTRODUCTION Homoharringtonine (HHT) is a cephalotoxin alkaloid with anti-leukemic activity and had been used successfully in the treatment of acute and chronic myeloid leukemias (O払rien et al., 1995; 1999; Feldman et al., 1992). The principal mecha-nism of action by HHT is the inhibition of protein synthesis in a dose- and time-dependent manner by binding to ribosome and inhibiting polypeptide chain elongation (Tujebajeva et al., 1989; Zhou et al., 1995). HHT had been shown to indu…  相似文献   

19.
阿魏酸钠对高脂饮食致动脉粥样硬化的作用   总被引:2,自引:0,他引:2  
目的:探讨阿魏酸钠(SF)抗动脉粥样硬化(AS)的作用及其机理.方法:18只家兔随机分为三组:对照组、高脂组、SF组.分别给予普通饲料、高脂饲料、高脂饲料加SF.10周末颈动脉放血取血样后,处死动物,检查血脂、观察主动脉粥样硬化斑块变化、主动脉超微结构.结果:⑴高脂组和SF组血脂含量显著高于对照组,SF组甘油三脂(TG)含量显著低于高脂组(P<0.05);⑵SF组AS斑块显著低于高脂组(P<0.01);⑶电镜结果显示SF组主动脉损伤明显减轻.结论:SF具有明显的抗AS形成的作用,其机制是:降低血中TG含量,保护内皮细胞.  相似文献   

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