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101.
102.
Xu Zhao Ying Yang Bao-Fa Sun Yue Shi Xin Yang Wen Xiao Ya-Juan Hao Xiao-Li Ping Yu-Sheng Chen Wen-Jia Wang Kang-Xuan Jin Xing Wang Chun-Min Huang Yu Fu Xiao-Meng Ge Shu-Hui Song Hyun Seok Jeong Hiroyuki Yanagisawa Yamei Niu Gui-Fang Jia Wei Wu Wei-Min Tong Akimitsu Okamoto Chuan He Jannie M Rendtlew Danielsen Xiu-Jie Wang Yun-Gui Yang 《Cell research》2014,24(12):1403-1419
103.
人尾加压素Ⅱ对大鼠脑微循环的影响 总被引:2,自引:0,他引:2
目的:探讨尾加压素Ⅱ(UII)对于大鼠软脑膜微循环的影响.方法:健康成年SD大鼠随机分为对照组、生理盐水(NS)、UII(10-7mol/L)、去甲肾上腺素(NA,10-6mol/L)、UII(10-7mol/L) NA(10-6mol/L)等五组,采用活体微循环观测技术观察大鼠软脑膜微血管内径、血流速度等微循环参数,采用激光多普勒血流量仪测定软脑膜血流量的变化.结果:正常对照组软脑膜细动脉和细静脉血管内径分别为(35.4±3.6)μm和(40.6±8.5)μm,UII组于滴加UII(10-7mol/L)后即刻细动脉和细静脉出现收缩,1 min时细动脉和细静脉收缩达到高峰,血管内径分别为(25.6±3.4)μm和(23.4±3.3)μm (与正常对照组比较,P均<0.05);细动、静脉内血流速度无明显变化(与正常对照组比较P均>0.05);软脑膜血流量于滴加UII(10-7mol/L)后1 min开始升高,5 min达到高峰(3.5±0.4 )PU 值,正常对照组(2.3±0.6)PU值(P<0.05).结论:UII可以使大鼠软脑膜微血管收缩,血流量增加. 相似文献
104.
105.
IntroductionSkin is susceptible to senescence‐associated secretory phenotype (SASP) and inflamm‐ageing partly owing to the degeneration of mitochondria. AdipoRon (AR) has protective effects on mitochondria in metabolic diseases such as diabetes. We explored the role of AR on mitochondria damage induced by skin inflamm‐ageing and its underlying mechanism.MethodsWestern blot, immunofluorescence and TUNEL staining were used to detect inflammatory factors and apoptosis during skin ageing. Transmission electron microscopy, ATP determination kit, CellLight Mitochondria GFP (Mito‐GFP), mitochondrial stress test, MitoSOX and JC‐1 staining were used to detect mitochondrial changes. Western blot was applied to explore the underlying mechanism. Flow cytometry, scratch test, Sulforhodamine B assay and wound healing test were used to detect the effects of AR on cell apoptosis, migration and proliferation.ResultsAR attenuated inflammatory factors and apoptosis that increased in aged skin, and improved mitochondrial morphology and function. This process at least partly depended on the suppression of dynamin‐related protein 1 (Drp1)‐mediated excessive mitochondrial division. More specifically, AR up‐regulated the phosphorylation of Drp1 at Serine 637 by activating AMP‐activated protein kinase (AMPK), thereby inhibiting the mitochondrial translocation of Drp1. Moreover, AR reduced mitochondrial fragmentation and the production of superoxide, preserved the membrane potential and permeability of mitochondria and accelerated wound healing in aged skin.ConclusionAR rescues the mitochondria in aged skin by suppressing its excessive division mediated by Drp1. 相似文献
106.
Inês BoalCarvalho Bryl MazelSanchez Filo Silva Laure Garnier Soner Yildiz Joao PPL Bonifacio Chengyue Niu Nathalia Williams Patrice Francois Nicolaus Schwerk Jennifer Schning Julia Carlens Dorothee Viemann Stephanie Hugues Mirco Schmolke 《EMBO reports》2020,21(12)
Pyroptosis is a fulminant form of macrophage cell death, contributing to release of pro‐inflammatory cytokines. In humans, it depends on caspase 1/4‐activation of gasdermin D and is characterized by the release of cytoplasmic content. Pathogens apply strategies to avoid or antagonize this host response. We demonstrate here that a small accessory protein (PB1‐F2) of contemporary H5N1 and H3N2 influenza A viruses (IAV) curtails fulminant cell death of infected human macrophages. Infection of macrophages with a PB1‐F2‐deficient mutant of a contemporary IAV resulted in higher levels of caspase‐1 activation, cleavage of gasdermin D, and release of LDH and IL‐1β. Mechanistically, PB1‐F2 limits transition of NLRP3 from its auto‐repressed and closed confirmation into its active state. Consequently, interaction of a recently identified licensing kinase NEK7 with NLRP3 is diminished, which is required to initiate inflammasome assembly. 相似文献
107.
八肽胆囊收缩素对内毒素休克时海马损伤的影响及其机制初探 总被引:2,自引:0,他引:2
目的:观察八肽胆囊收缩素(CCK-8)对内毒素休克(ES)时海马损伤的影响,并探讨其可能的作用机制。方法:将日本大耳白兔经静脉注入内毒素的主要活性成分脂多糖(LPS,8mg/kg)复制ES模型。动物(32只)随机分为对照组、LPS组、CCK-8+LPS组和非特异性CCK受体拮抗剂丙谷胺(Pro)+LPS组(n=8)。监测平均动脉压(MAP)的变化,光、电镜观察海马的组织形态学改变,比色法检测海马NOS和SOD活性、N0和MDA含量的改变.用SD大鼠(12只,同上复制模型及分组)以免疫组织化学染色法观察海马iNOS和nNOS表达的变化。结果:与对照组相比,注入LPS后出现MAP显著而持续下降(P〈0.01);海马部位神经元损伤明显;iNOS和nNOS表达增强,NOS活性、NO和MDA含量显著升高(P〈0.05、P〈0.01和P〈0.01),SOD活性则降低(P〈0.01)。预先注入CCK-8可明显减轻上述变化,预先注入Pro则加剧以上变化。结论:CCK-8可减轻ES时脑内海马部位的损伤。其机制可能与其抗氧化作用和抑制NO的过量生成有关。 相似文献
108.
Mingming Zhang Xiaolin Niu Jianqiang Hu Yuan Yuan Shuhong Sun Jiaxing Wang Wenjun Yu Chen Wang Dongdong Sun Haichang Wang 《PloS one》2014,9(10)
Aim
The aim of the present study was to investigate the role of Lin28a in protecting against hypoxia/reoxygenation (H/R)-induced cardiomyocytes apoptosis under high glucose/high fat (HG/HF) conditions.Methods
Primary cardiomyocytes which were isolated from neonatal mouse were randomized to be treated with lentivirus carrying Lin28a siRNA, Lin28acDNA 72 h before H/R (9 h/2 h). Cardiomyocytes biomarkers release (LDH and CK), cardiomyocytes apoptosis, mitochondria biogenesis and morphology, intracellular reactive oxygen species (ROS) production, ATP content and inflammatory cytokines levels after H/R injury in high glucose/high fat conditions were compared between groups. The target proteins of Lin28a were examined by western blot analysis.Results
Our results revealed that Lin28a cDNA transfection (overexpression) significantly inhibited cardiomyocyte apoptotic index, improved mitochondria biogenesis, increased ATP production and reduced ROS production as compared with the H/R group in HG/HF conditions. Lin28a siRNA transfection (knockdown) rendered the cardiomyocytes more susceptible to H/R injury as evidenced by increased apoptotic index, impaired mitochondrial biogenesis, decreased ATP production and increased ROS level. Interestingly, these effects of Lin28a were blocked by pretreatment with the PI3K inhibitor wortmannin. Lin28a overexpression increased, while Lin28a knockdown inhibited IGF1R, Nrf-1, Tfam, p-IRS-1, p-Akt, p-mTOR, p-p70s6k, p-AMPK expression levels after H/R injury in HG/HF conditions. Moreover, pretreatment with wortmannin abolished the effects of Lin28a on the expression levels of p-AKT, p-mTOR, p-p70s6k, p-AMPK.Conclusions
The present results suggest that Lin28a inhibits cardiomyocytes apoptosis by enhancing mitochondrial biogenesis and function under high glucose/high fat conditions. The mechanism responsible for the effects of Lin28a is associated with the PI3K/Akt dependent pathway. 相似文献109.
白茆塘和戚浦塘位于苏州市辖区,水生维管植物十分丰富.对其流域水生维管束植物资源进行了调查,发现共有水生植物99种,隶属于36科76属.同时对水生维管束植物的资源及群落进行了分析探讨,以期为水生植物资源的保护和合理利用等方面提供科学建议. 相似文献
110.
Niu Yuan Wang Fang Liu Le Zhang Guoliang Qi Bo Liu Xinhai Zhao Hongliang Huang Zhiwei Fan Song Zhang Linqing 《Journal of Plant Growth Regulation》2023,42(1):154-167
Journal of Plant Growth Regulation - 1,2,4-trichlorobenzene (1,2,4-TCB) pollution in fields has become a potential threat to rice growth, yet little is known about the different response of many... 相似文献