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miR-181a-5p调控LIF的表达调节胰腺腺泡细胞凋亡的分子机制 被引量:1
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作者 龚倩倩 陈铁江 《世界华人消化杂志》 CAS 2019年第8期494-502,共9页
背景急性胰腺炎(acute pancreatitis, AP)发病迅速,并发全身感染,因此早期的高效治疗对控制病情起到关键作用.微小RNA(microRNA, miRNA)在AP中的作用机制及临床应用的研究成为近几年的热点.其在AP发生发展及转归中的作用有助于为AP的诊... 背景急性胰腺炎(acute pancreatitis, AP)发病迅速,并发全身感染,因此早期的高效治疗对控制病情起到关键作用.微小RNA(microRNA, miRNA)在AP中的作用机制及临床应用的研究成为近几年的热点.其在AP发生发展及转归中的作用有助于为AP的诊断和治疗提供新思路.目的探讨miR-181a-5p对雨蛙素诱导的大鼠胰腺腺泡细胞AR42J凋亡的影响及机制.方法运用ELISA法检测雨蛙素诱导的大鼠胰腺腺泡细胞中AMY、肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)、白介素-6(interleukin-6,IL-6)的表达;将Cerulein+anti-miR-con组(转染anti-miR-con)、Cerulein+anti-miR-181a-5p组(转染anti-miR-181a-5p)、Cerulein+si-con组(转染si-con)、Cerulein+si-白血病抑制因子(leukemia inhibitory factor, LIF)组(转染si-LIF),均用脂质体法转染至AR42J细胞,再用15 nmol/L的雨蛙素处理8h;流式细胞术法检测各组细胞的凋亡; qRT-PCR检测各组细胞中miR-181a-5p mRNA和LIF mRNA的表达; Western blot检测各组细胞中LIF、caspase-3的蛋白表达;双荧光素酶报告基因检测实验检测各组细胞的荧光活性.结果与对照组相比,雨蛙素处理8 h是AMY、TNF-α和IL-6的含量均升高的时间点,且细胞凋亡率显著降低(P <0.05);与Control组相比,Cerulein组AR42J细胞中miR-181a-5p mRNA表达显著下调, LIF mRNA和蛋白表达显著上调(P<0.05);过表达miR-181a-5p、敲减LIF均可抑制雨蛙素诱导的AR42J细胞凋亡的促进作用; miR-181a-5p可抑制野生型LIF细胞的荧光活性,且可负向调控LIF的蛋白表达.结论 miR-181a-5p可抑制雨蛙素诱导的AR42J细胞的凋亡,其机制可能与靶向LIF有关,将可为AP的治疗提供新方向. 展开更多
关键词 miR-181a-5p 白血病抑制因子 凋亡 急性胰腺炎
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High-quality CdS quantum dots sensitized ZnO nanotube array films for superior photoelectrochemical performance
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作者 qian-qian gong Yun-Long Zhao +5 位作者 Qi Zhang Chun-Yong Hu Teng-Fei Liu Hai-Feng Zhang Guang-Chao Yin Mei-Ling Sun 《Chinese Physics B》 SCIE EI CAS CSCD 2022年第9期561-569,共9页
The surface characteristics of ZnO were synthetically optimized by a self-designed simultaneous etching and W-doping hydrothermal method utilizing as-prepared ZnO nanorod(NR)array films as the template.Benefiting from... The surface characteristics of ZnO were synthetically optimized by a self-designed simultaneous etching and W-doping hydrothermal method utilizing as-prepared ZnO nanorod(NR)array films as the template.Benefiting from the etching and regrowth process and the different structural stabilities of the various faces of ZnO NRs,the uniquely etched and W-doped ZnO(EWZ)nanotube(NT)array films with larger surface area,more active sites and better energy band structure were used to improve the photoelectrochemical(PEC)performance and the loading quality of CdS quantum dots(QDs).On the basis of their better surface characteristics,the CdS QDs were uniformly loaded on EWZ NT array film with a good coverage ratio and interface connection;this effectively improved the light-harvesting ability,charge transportation and separation as well as charge injection efficiency during the PEC reaction.Therefore,all the CdS QD-sensitized EWZ NT array films exhibited significantly enhanced PEC performance.The CdS/EWZ-7 composite films exhibited the optimal photocurrent density with a value of 12 mA·cm^(-2),2.5 times higher than that of conventional CdS/ZnO-7 composite films under the same sensitization times with CdS QDs.The corresponding etching and optimizing mechanisms were also discussed. 展开更多
关键词 ZnO nanotubes W-doping CdS quantum dots
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A disputed evidence on obesity:comparison of the effects of Rcan2^(-/-) and Rps6kb1^(-/-) mutations on growth and body weight in C57BL/6J mice 被引量:1
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作者 Jing ZHAO Shi-wei LI +5 位作者 qian-qian gong Ling-cui DING Ye-cheng JIN Jian ZHANG Jian-gang GAO Xiao-yang SUN 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2016年第9期657-671,共15页
It is widely accepted that body weight and adipose mass are tightly regulated by homeostatic mechanisms, in which leptin plays a critical role through hypothalamic pathways, and obesity is a result of homeostatic diso... It is widely accepted that body weight and adipose mass are tightly regulated by homeostatic mechanisms, in which leptin plays a critical role through hypothalamic pathways, and obesity is a result of homeostatic disorder. However, in C57BL/6J mice, we found that Rcan2 increases food intake and plays an important role in the develop- ment of age- and diet-induced obesity through a leptin-independent mechanism. RCAN2 was initially identified as a thyroid hormone (T3)-responsive gene in human fibroblasts. Expression of RCAN2 is regulated by T3 through the PI3K-Akt/PKB-mTOR-Rps6kbl signaling pathway. Intriguingly, both Rcan2-/- and Rps6kb1-/- mutations were re- ported to result in lean phenotypes in mice. In this study we compared the effects of these two mutations on growth and body weight in C57BL/6J mice. We observed reduced body weight and lower fat mass in both Rcan2-/- and Rps6kb1-/- mice compared to the wild-type mice, and we reported other differences unique to either the Rcan2-/- or Rps6kb1-/- mice. Firstly, loss of Rcan2 does not directly alter body length; however, Rcan2-/- mice exhibit reduced food intake. In contrast, Rps6kb1-/- mice exhibit abnormal embryonic development, which leads to smaller body size and reduced food intake in adulthood. Secondly, when fed a normal chow diet, Rcan2-/- mice weigh significantly more than Rps6kb1-/- mice, but both Rcan2-/- and Rps6kbl-/- mice develop similar amounts of epididymal fat. On a high-fat diet, Rcan2-/- mice gain body weight and fat mass at slower rates than Rps6kb1-/- mice. Finally, using the double-knockout mice (Rcan2-/- Rps6kb1-/-), we demonstrate that concurrent loss of Rcan2and Rps6kbl has an additive effect on body weight reduction in C57BL/6J mice. Our data suggest that Rcan2 and Rps6kbl mutations both affect growth and body weight of mice, though likely through different mechanisms. 展开更多
关键词 Rcan2 gene Rps6kbl gene GROWTH Body weight regulation OBESITY
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