中国病理生理杂志
Chinese Journal of Pathophysiology 중국병리생리잡지
- 主管单位： 中国科学技术协会
- 主办单位： 中国病理生理学会
- 影响因子： 1.06
- 审稿时间： 1-3个月
- 国际刊号： 1000-4718
- 国内刊号： 44-1187/R
- 论文标题 期刊级别 审稿状态
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转录因子MAZ对c1orf109基因转录表达调控的体外研究
目的:本文旨在研究转录因子Myc相关锌指蛋白(MAZ)在体外对人类1号染色体开放阅读框109(c1orf109)基因的转录表达调控.方法:体外条件下,采用凝胶电泳迁移实验筛选c1orf109基因启动子区MAZ的结合位点,并利用本室构建的由c1orf109启动子驱动的增强型绿色荧光蛋白报告载体与MAZ和转录因子特化蛋白1(Sp1)的表达质粒共转染HeLa细胞,24 h后,用激光共聚焦显微镜和流式细胞术检测c1orf109基因的转录表达情况.结果:c1orf109启动子区可与MAZ结合,且有与Sp1共享的结合位点;MAZ与Sp1皆可抑制c1orf109的转录表达,且Sp1的抑制作用大于MAZ(P<0.05).结论:MAZ与Sp1两个转录因子共同调控c1orf109基因在生理及病理条件的表达,且调控方向一致.这种冗余机制调控方式的存在提示该基因的精确表达调控对于细胞行使其生物学功能可能具有重要意义
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姜黄素对Aβ25-35诱导的PC12细胞caspase-3、caspase-8和caspase-9表达的影响
目的:探讨姜黄素对β淀粉样蛋白25-35(Aβ25-35)诱导的大鼠肾上腺嗜铬细胞瘤PC12细胞存活率、乳酸脱氢酶(LDH)释放率及凋亡的影响.方法:以Aβ25-35作用于PC12细胞,分别采用MTT法和LDH试剂盒检测细胞的存活率和LDH释放率;实验随机分为空白对照组、模型组、姜黄素10μmol/L组和姜黄素20μmol/L组,采用流式细胞术及AnnexinV-FITC/PI双染法检测凋亡情况,采用比色法和Western blot法检测凋亡相关蛋白胱天蛋白酶(caspase)-3、caspase-8和caspase-9的活性和表达.结果:与模型组比较,姜黄素可显著升高Aβ25-35诱导的PC12细胞存活率,降低LDH释放率和凋亡率(P<0.01);同时可显著降低caspase-3、caspase-8和caspase-9的活性和表达(P<0.05或P<0.01).结论:姜黄素可显著抑制caspase-3、caspase-8和caspase-9的表达,从而抑制Aβ25-35诱导的PC12细胞凋亡.
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二甲双胍联合膈下逐瘀汤对多囊卵巢综合征胰岛素抵抗大鼠TLR4/NF-κB信号通路的影响
目的:观察二甲双胍(metformin,Met)联合膈下逐瘀汤对经脱氢表雄酮诱导的多囊卵巢综合征(PCOS)胰岛素抵抗大鼠Toll样受体4(Toll-like receptor-4,TLR-4)/核因子κB(nucler factor-κB,NF-κB)信号通路的影响及其作用机制.方法:将110只经脱氢表雄酮诱导造模成功的PCOS大鼠用随机数字表法随机分为3组,分别为模型(model)组(30只)、二甲双胍治疗(Met)组(40只)和二甲双胍联合膈下逐瘀汤治疗(combination)组(40只).Model组大鼠每天灌胃相同体积的0.9％氯化钠;Met组大鼠每天给予二甲双胍(270 mg·kg-1·d-1)灌胃;combination组大鼠每天给予二甲双胍(270 mg·kg-1·d-1)+膈下逐瘀汤(34.5 mg·kg-1·d-1)灌胃.3组大鼠均连续干预28 d.干预结束后测定血糖[空腹血糖(FPG)和餐后2 h血糖(2hPBG)];用RT-PCR法分别检测3组大鼠卵泡上皮NF-κB、TLR-4及氧化型低密度脂蛋白(oxidized low-density lipoprotein,ox-LDL)的mRNA表达水平;ELISA检测外周血清炎性因子白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)和C反应蛋白(CRP)的浓度.结果:干预结束后Met和combination组大鼠FPG、2hPBG及血清IL-6、TNF-α和CRP浓度均低于model组(P<0.05),且combination组大鼠外周血清上述指标均低于Met组(P<0.05);干预结束后Met和combination组大鼠卵泡上皮NF-κB、TLR-4和ox-LDL的mRNA水平均低于model组(P<0.05),且combination组大鼠卵泡上皮NF-κB、TLR-4和ox-LDL的mRNA水平均低于Met组(P<0.05).结论:在给予二甲双胍的基础上给予膈下逐瘀汤来治疗PCOS胰岛素抵抗大鼠,能通过降低外周血清及卵巢上皮细胞炎性因子表达,以及卵巢上皮组织NF-κB、TLR-4和ox-LDL表达来改善胰岛素抵抗状态.
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DIZE对糖尿病心肌病大鼠心功能的保护作用
目的:观察研究血管紧张素转换酶2(ACE2)激动剂重氮氨苯脒乙酰甘氨酸盐(DIZE)对糖尿病心肌病(DCM)大鼠心功能的保护作用.方法:30只健康雄性Wistar大鼠随机分为正常对照组、DCM组和DIZE处理组(DIZE组),每组10只.DCM组与DIZE组一次性腹腔注射链脲佐菌素65 mg/kg,建立糖尿病模型,12周后经超声检查选出符合糖尿病心肌病的大鼠模型,分别给予DIZE 15 mg·kg-1·d-1或等体积生理盐水,皮下泵入给药4周处理.第16周末行超声检测心功能后麻醉处死大鼠.通过HE染色和Masson染色观察大鼠心肌组织形态学变化,Wsetern blot、ELISA和免疫组化等方法观察ACE2、血管紧张素(Ang)Ⅱ、Ang-(1-7)、白细胞介素(IL)-1、IL-6和结缔组织生长因子(CTGF)等指标的变化.结果:DIZE显著提高了糖尿病大鼠心肌中ACE2的表达,DIZE组较DCM组心肌组织中胶原含量明显降低,IL-1和IL-6蛋白表达水平明显下降,心功能得到明显改善(P<0.05).结论:ACE2内源性激动剂DIZE显著提高了ACE2的水平,降低了炎症水平,从而对DCM大鼠心功能起到保护作用.
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利用TCGA数据库分析miR-196b在结直肠癌患者中的临床表达特征并探索miR-196b的体外抗5-FU作用
目的:研究微小RNA(miR)-196b在结直肠癌患者中的表达及其临床意义,探讨过表达miR-196b的结直肠癌细胞对5-氟尿嘧啶(5-FU)的敏感性.方法:在癌症基因组图谱(The Cancer Genome Atlas,TCGA)公共数据库下载结直肠癌患者miRNA测序数据及其对应的临床病理资料,运用SPSS 17.0分析miR-196b在结直肠癌患者中的表达水平以及临床特征;采用瞬时转染的方法在人结直肠癌HCT116细胞中过表达miR-196b,并用MTS法分析过表达miR-196b的细胞对5-FU药物敏感性的变化.结果:miR-196b高表达与结直肠癌患者淋巴结转移及TNM分期相关(P<0.05),与年龄和性别等无相关性.淋巴结转移和远处转移是直肠癌患者生存的独立影响因子(P<0.05),miR-196b的表达水平与患者生存状况无关.过表达miR-196b的HCT116细胞在不同浓度的5-FU作用下,细胞存活率均明显高于对照组(P<0.05).结论:miR-196b可能是结直肠癌患者肿瘤分期和淋巴结转移的分子标志物,并可降低结直肠癌细胞对5-FU的敏感性.
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人参皂苷Rh1对哮喘模型小鼠炎症因子表达的抑制作用
目的:观察和探讨人参皂苷Rh1对哮喘模型小鼠的血清和支气管肺泡冲洗液(bronchoalveolar lav-age fluid,BALF)中炎症因子的表达和肺组织形态学变化的影响.方法:雄性BALB/c小鼠40只,分为正常对照组、哮喘模型组、人参皂苷Rh1小剂量(40 mg·kg-1·d-1)治疗组和人参皂苷Rh1大剂量(80 mg·kg-1·d-1)治疗组,并利用卵清蛋白致敏和雾化吸入激发方法制作哮喘模型;人参皂苷Rh1小剂量治疗组和大剂量治疗组分别在每次激发攻击前30 min灌胃,每天一次,共2周.在末次激发24 h后收集BALF,计数嗜酸性粒细胞(eosinophil,EOS)数目;利用ELISA测定BALF中白细胞介素(IL)-4、IL-5和干扰素γ(IFN-γ)的水平;收集血液并测定血清中IgG和IgE的水平;用Western blot检测肺组织中转化生长因子(TGF)-β1蛋白表达的变化;用HE染色观察肺组织的病理学变化.结果:人参皂苷Rh1可抑制小鼠哮喘模型BLAF中EOS数目(P<0.01);降低BLAF中IL-4、IL-5和IFN-γ的表达(P<0.01);减少血清中IgE的含量(P<0.01);减少肺组织中TGF-β1蛋白表达(P<0.01),并改善哮喘小鼠肺组织病理学变化.结论:人参皂苷Rh1对哮喘小鼠具有抑制炎症因子表达、调节免疫反应和改善肺组织病理变化的作用.
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SerpinE2在细胞外基质代谢中作用的研究进展
Serpin peptidase inhibitor clade E member 2(SerpinE2),a member of serine peptidase inhibitor super family,regulates multiple serine proteases.Extracellular matrix(ECM)plays an important role in stem cell differen-tiation,signal transduction,tumor metastasis,osteoarthritis physiological and pathological processes and so on.SerpinE2 regulates the protein of extracellular matrix by serine protease system and matrix metalloproteinase(MMP)system.In this paper,we elaborate the effect of SerpinE2 on metabolism of extracellular matrix,and it will provide new ideas to find new therapeutic targets.
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透明细胞肾细胞癌的表观遗传学研究进展
The epigenetic changes of clear cell renal cell carcinoma(ccRCC )are considered to be the main molecular mechanisms of its pathogenesis ,including DNA methylation ,histone modification ,microRNA change ,and so on.DNA methyltransferases(DNMTs)catalyze the occurrence of DNA methylation.DNA methylation changes are mani-fested in the overall low methylation of the genome and the high methylation of specific sites ,which were involved in the de-velopment of ccRCC by affecting the expression of tumor suppressor genes.Due to histone-modified enzyme involvement ,histone modification is shown as possible genetic reversal.MicroRNA plays an important role in the abnormal expression of ccRCC genes.With the studies of epigenetic mechanism and molecular pathology ,it is important to explore the mechanisms and to seek effective early diagnosis ,treatment and prognosis intervention of ccRCC.
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细胞内的氧化还原感受器蛋白与氧化还原信号转导
Many signaling proteins in mammalian cells are sensitive to the changes of redox environment ,which may specifically affect functions of these proteins ,thereby modulating their downstream effects.These signaling pro-teins are thought to be intracellular redox sensors.Redox-sensing functions have been observed in a variety of transcription factors,kinases,phosphatases,ion channels,and cytoskeletal/structural proteins,while the list is still expanding.We propose that many proteins with redox-sensing functions remain to be identified ,and our understanding on the complexity of the redox signaling network in cells is incomplete.In this article ,we provide an overview of some established mammalian intracellular redox sensors.It is suggested that ,when we study pathophysiological mechanisms of disease ,we should keep it in mind that oxidative damage to macromolecules is not the only consequence of increased reactive oxygen production. Rather,changes in redox balance may be linked to multiple specific pathways that are capable of transducing redox signals and regulating various fundamental cellular functions.Aberrant activation or inactivation of these redox signaling mecha-nisms may have significant contributions to the pathogenesis of diseases.
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基质蛋白CCN1与肺部疾病的研究进展
Cysteine-rich angiogenic inducer 61(Cyr61/CCN1)is an extracellular matrix-associated signaling protein consisting of 381 amino-acid residues ,which has the regulatory function for a multitude of cellular responses.The pleiotropic effects of CCN 1 on the initiation and resolution of inflammation as well as oncogenesis and development of tumor were reported.According to the numerous data from experimental and clinical studies ,this article provides an overview on CCN1 and summarizes the latest understanding of the role of CCN 1 in pulmonary diseases.
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| 1985 | 01 02 03 04 z1 |
