水通道蛋白1与肿瘤

<正>水通道蛋白家族是位于生物膜上具有快速水转运及离子转运功能的一族蛋白质。水通道蛋白1(Aquapor-in-1,AQP1)是第一个被发现的水通道蛋白,研究发现其不仅能介导水及离子转运,还对细胞内外气体交换、肿瘤血管的生成及细胞迁移产生重要影响     

钙离子信号通路及相关蛋白激酶对弓形虫的作用

弓形虫是世界范围分布的专性细胞内寄生原虫,可感染人类和所有温血动物的有核细胞。由于宿主的广泛性,弓形虫病已经成为一个全球性的、严重的公共卫生问题,不但危害人类健康,而且成为影响畜牧业发展的重要机会性病原体[1]。     

菟丝子提取物对衰老小鼠心肌细胞凋亡的抑制作用

目的研究菟丝子水煎剂对D-半乳糖所致衰老模型小鼠细胞凋亡的抑制作用。方法 30只小鼠按体重随机分为青年对照组、模型组、菟丝子给药组。激光共聚焦显微镜测定细胞内钙、免疫组化法检测bcl-2和bax表达、流式细胞仪检测心肌细胞凋亡。结果菟丝子组与衰老模型相比细胞内钙显著降低(P<0.05),bcl-2/bax比值高于模型组,心肌细胞凋亡指数减少(P<0.05)。结论菟丝子对D-半乳糖致衰老小鼠的心肌细胞凋亡有抑制作用。     

β_3肾上腺能受体通过逆转一种氧化性修饰刺激心脏Na~+-K~+泵

<正>β3肾上腺能受体与β1及β2受体在结构上,配体亲和力和与细胞内信号转导径路等方面均不相同。心力衰竭时它在心肌的表达上调,因为它介导正常心脏的一种负性变力性效应。曾有人一度认为是适应不良。因而提     

硫化氢对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡的影响

目的探讨硫化氢对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡的影响及有关机制。方法人脐静脉内皮细胞分别经不同浓度(25、50、100、200μmol/L)和不同时间(6、12、24 h)硫氢化钠预孵育24 h后加入100 mg/L氧化型低密度脂蛋白处理24 h,Hoechst 33258荧光染色和流式细胞术检测细胞凋亡,罗丹明123染色检测细胞线粒体膜电位变化,双氢罗丹明123染色检测细胞内活性氧的含量变化。结果硫氢化钠预处理能以时间和浓度依赖性的方式抑制氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡(均P<0.01),硫氢化钠或N-乙酰半胱氨酸预先处理能显著阻断氧化型低密度脂蛋白引起的人脐静脉内皮细胞线粒体膜电位降低、活性氧生成增多(均P<0.05)。结论硫化氢能显著抑制氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡,其机制与减少细胞线粒体膜电位及降低活性氧生成有关。     

Effects of prostaglandin F_（2α） on small intestinal interstitial cells of Cajal

AIM: To explore the role of prostaglandin F_2α (PGF_2α)) on pacemaker activity in interstitial cells of Cajal (ICC) from mouse small intestine.METHODS: In this study, effects of PGF_2α in the cultured ICC cells were investigated with patch clamp technology combined with Ca²⁺ image analysis.RESULTS: Externally applied PGF_2α (10 μmol/L) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The application of flufenamic acid (a non-selective cation channel inhibitor) or niflumic acid (a Cl^- channel inhibitor) abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF_2α-induced tonic inward currents. In addition, the tonic inward currents induced by PGF_2α were not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt. Pretreatment with Ca²⁺ free solution, U-73122, an active phospholipase C inhibitor, and thapsigargin, a Ca²⁺-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the PGF_2α-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the PGF_2α-induced effects on pacemaker currents. When recording intracellular Ca²⁺ ([Ca²⁺]_i) concentration using fluo-3/AM, PGF_2α broadly increased the spontaneous [Ca²⁺]_i oscillations.CONCLUSION: These results suggest that PGF_2α can modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via [Ca²⁺]i regulation     

SPIO标记影响干细胞内IRPs/IREs系统的研究进展

铁是人体内含量最多的一种必须微量元素,它广泛参与机体内的代谢过程,在细胞生命活动中起着至关重要的作用。人体内的铁主要用于血红素蛋白及非血红素蛋白的合成,包括血红蛋白、肌红蛋白、呼吸链的主要复合体、细胞色素酶和过氧化物酶等,在人体内参与氧的运输、细胞内电子传递及能量代谢等过程[1]。     

脑源性神经生长因子功能及细胞内信号传导通路

<正>神经营养因子包括神经生长因子(nerve groth factoe,NGF),脑源性神经生长因子(brain-derived neurotrophic factor,BDNF),神经营养因子-3(neurotrophin-3,NT-3),神经营养因子-4/5(neurotrophin-4/5,NT-4/5)等。这些因子可以作为信号传导通路的配体与其受体酪氨酸蛋白激酶(Trk)高亲和力结合,也可以与分子量为75KDNT受体(75KDNT receptor,p75)以低亲和力结合。Trk包括TrkA、TrkB、TrkC等3种,神经营养因子与其Trk结合具有明显的选择性,其中NGF可与TrkA特异性结合,     

Protective role of mitochondrial K-ATP channel and mitochondrial membrane transport pore in rat kidney ischemic postconditioning

Background  Previous studies suggested that mechanical intervention during early reperfusion, or ischemia postconditioning (IPo), could protect kidneys against renal ischemia reperfusion injury (RIRI). However, the mechanisms responsible for this protection remain unclear. This study therefore investigated the protection afforded by IPo in rat kidneys in vivo, and the roles of mitochondrial K_ATP channels (mitoK_ATP) and mitochondrial permeability transition pores (MPTPs), by inhibiting mitoK_ATP with 5-hydroxydecanoate (5-HD), and by directly detecting open MPTPs using calcein-AM and CoCl₂.

Methods  Thirty-five male Sprague-Dawley rats were randomly assigned to sham-operation (S), ischemia-reperfusion (I/R), IPo, ischemia reperfusion with 5-HD (I/R+5-HD), or IPo with 5-HD (IPo +5-HD) groups. Rats in each group were sacrificed after 6 hours of reperfusion by heart exsanguination or cervical dislocation under anesthesia. RIRI was assessed by determination of creatinine and blood urea nitrogen (BUN), and by examination of histologic sections. The roles of mitoK_ATP and MPTP were investigated by analyzing fluorescence intensities of mitochondria, mitochondrial membrane potential, intracellular reactive oxygen species (ROS) and intracellular calcium, using appropriate fluorescent markers. The relationship between apoptosis and RIRI was assessed by determining the apoptotic index (AI) of kidney tubular epithelial cells.

Results  The RIRI model was shown to be successful. Significantly higher levels of creatinine and BUN, and abnormal pathology of histologic sections, were observed in group I/R, compared with group S. 5-HD eliminated the renoprotective effects of IPo. Mitochondrial and mitochondrial membrane potential fluorescence intensities increased, and intracellular calcium, ROS fluorescence intensities and AI decreased in group IPo, compared with group I/R. However, mitochondrial and mitochondrial membrane potential fluorescence intensities decreased, and intracellular calcium and ROS fluorescence intensities and AI increased in group IPo+5-HD, compared with group IPo.

Conclusions  mitoK_ATP and MPTPs participated in IPo-induced renoprotective mechanisms in rat kidneys subjected to RIRI, possibly through decreased renal tubular epithelial cell apoptosis. 

     

核因子C(Nfic)与牙根发育

牙根发育在牙冠发育完成之后,但是和牙冠发育有着不同的机制.核因子C(Nfic)存在于牙冠和牙根的间充质细胞内,但是它只对牙根的发育起到重要的作用,却并不影响牙冠的形成.本文总结了近几年国内外关于牙根发育的研究和作者近几年的工作,阐述Nfic和牙根发育在形态学上的关系和分子机制.