排序方式: 共有84条查询结果,搜索用时 15 毫秒
51.
Objective: To explore the mechanism of Danggui Buxue Decoction (DGBXD) in regulating Atherosclerosis (AS) network based on integrated pharmacological methods.Methods: The active ingredients and targets of DGBXD are obtained from TCMSP database and ETCM. AS-related targets were collected from the Genecards and OMIM databases. The drug–disease protein interaction (PPI) networks were constructed by Cytoscape. Meanwhile, it was used to screen out densely interacting regions, namely clusters. Finally, Gene Ontology (GO) annotations are performed on the targets and genes in the cluster to obtain biological processes, and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotations are performed on the targets of the PPI network to obtain signaling pathways.Results: A total of 212 known targets, 265 potential targets and 229 AS genes were obtained. The ‘DGBXD known-AS PPI network’ and ‘DGBXD-AS PPI Network’ were constructed and analyzed. DGBXD can regulate inflammation, platelet activation, endothelial cell apoptosis, oxidative stress, lipid metabolism, vascular smooth muscle proliferation, angiogenesis, TNF, HIF-1, FoxO signaling pathway, etc. The experimental data showed that compared with the model group, the expressions of ICAM-1, VCAM-1, and interleukin (IL)-1β protein and mRNA in the DGBXD group decreased (P<0.05). However, plasma IL-1β, TNF-α, and MCP-1 in the DGBXD group were not significantly different from the model group (P>0.05).Conclusion: The mechanism of DGBXD in the treatment of AS may be related to the improvement of extracellular matrix (ECM) deposition in the blood vessel wall and the anti-vascular local inflammatory response, which may provide a reference for the study of the mechanism of DGBXD. 相似文献
52.
朱鹮(Nipponia nippon)种群生存力分析 总被引:3,自引:1,他引:3
到目前为止,只有一个野生朱鹮群体幸存下来,而且它的种群大小自1981年重新发现以来,一直在20只以下波动。本文应用种群生存力分析的方法,借助漩涡模型,根据朱鹮14年的种群数据,总结和预测了其种群动态,并着重研究了朱鹮的濒危程度。结果显示,按过去10余年的生存状况,朱鹮在50年内绝灭的可能性是98.5%,平均绝灭时间为15.72 年。现存种群数量很低,所以种群统计随机性对其命运有很大影响。灵敏度分析表明,当前的朱鹮种群对意外死亡和生存环境的波动较为敏感。保护工作的优先项目是对猎杀和天敌的控制以及从各个方面提高朱鹮的生活质量。 相似文献
54.
Ang Guo Duane Hall Caimei Zhang Tianqing Peng Jordan D. Miller William Kutschke Chad E. Grueter Frances L. Johnson Richard Z. Lin Long-Sheng Song 《The Journal of biological chemistry》2015,290(29):17946-17955
Junctophilin-2 (JP2), a membrane-binding protein that provides a structural bridge between the plasmalemma and sarcoplasmic reticulum, is essential for precise Ca2+-induced Ca2+ release during excitation-contraction coupling in cardiomyocytes. In animal and human failing hearts, expression of JP2 is decreased markedly, but the molecular mechanisms underlying JP2 down-regulation remain incompletely defined. In mouse hearts, ischemia/reperfusion injury resulted in acute JP2 down-regulation, which was attenuated by pretreatment with the calpain inhibitor MDL-28170 or by transgenic overexpression of calpastatin, an endogenous calpain inhibitor. Using a combination of computational analysis to predict calpain cleavage sites and in vitro calpain proteolysis reactions, we identified four putative calpain cleavage sites within JP2 with three N-terminal and one C-terminal cleavage sites. Mutagenesis defined the C-terminal region of JP2 as the predominant calpain cleavage site. Exogenous expression of putative JP2 cleavage fragments was not sufficient to rescue Ca2+ handling in JP2-deficient cardiomyocytes, indicating that cleaved JP2 is non-functional for normal Ca2+-induced Ca2+ release. These data provide new molecular insights into the posttranslational regulatory mechanisms of JP2 in cardiac diseases. 相似文献
55.
Xie C Guo Y Zhu T Zhang J Ma PX Chen YE 《The Journal of biological chemistry》2012,287(18):14598-14605
The Hippo-Yap (Yes-associated protein) signaling pathway has emerged as one of the critical pathways regulating cell proliferation, differentiation, and apoptosis in response to environmental and developmental cues. However, Yap1 roles in vascular smooth muscle cell (VSMC) biology have not been investigated. VSMCs undergo phenotypic switch, a process characterized by decreased gene expression of VSMC contractile markers and increased proliferation, migration, and matrix synthesis. The goals of the present studies were to investigate the relationship between Yap1 and VSMC phenotypic switch and to determine the molecular mechanisms by which Yap1 affects this essential process in VSMC biology. Results demonstrated that the expression of Yap1 was rapidly up-regulated by stimulation with PDGF-BB (a known inducer of phenotypic switch in VSMCs) and in the injured vessel wall. Knockdown of Yap1 impaired VSMC proliferation in vitro and enhanced the expression of VSMC contractile genes as well by increasing serum response factor binding to CArG-containing regions of VSMC-specific contractile genes within intact chromatin. Conversely, the interaction between serum response factor and its co-activator myocardin was reduced by overexpression of Yap1 in a dose-dependent manner. Taken together, these results indicate that down-regulation of Yap1 promotes VSMC contractile phenotype by both up-regulating myocardin expression and promoting the association of the serum response factor-myocardin complex with VSMC contractile gene promoters and suggest that the Yap1 signaling pathway is a central regulator of phenotypic switch of VSMCs. 相似文献
56.
57.
58.
Wenteng He Qingran Kong Yongqian Shi Bingteng Xie Mingxia Jiao Tianqing Huang Shimeng Guo Kui Hu Zhonghua Liu 《基因组蛋白质组与生物信息学报(英文版)》2013,11(5):327-333
The aim of this study was to optimize electrofusion conditions for generating porcine tetraploid(4n)embryos and produce tetraploid/diploid(4n/2n)chimeric embryos.Different electric feld intensities were tested and 2 direct current(DC)pulses of 0.9 kV/cm for 30 ls was selected as the optimum condition for electrofusion of 2-cell embryos to produce 4n embryos.The fusion rate of 2-cell embryos and the development rate to blastocyst of presumably 4n embryos,reached85.4%and 28.5%,respectively.68.18%of the fused embryos were found to be 4n as demonstrated by fluorescent in situ hybridization(FISH).Although the number of blastomeres in 4n blastocysts was signifcantly lower than in 2n blastocysts(P<0.05),there was no signifcant difference in developmental rates of blastocysts between 2n and 4n embryos(P>0.05),suggesting that the blastocyst forming capacity in 4n embryos is similar to those in 2n embryos.Moreover,4n/2n chimeric embryos were obtained by aggregation of 4n and 2n embryos.We found that the developmental rate and cell number of blastocysts of 4-cell(4n)/4-cell(2n)chimeric embryos were signifcantly higher than those of 2-cell(4n)/4-cell(2n),4-cell(4n)/8-cell(2n),4-cell(4n)/2-cell(2n)chimeric embryos(P<0.05).Consistent with mouse chimeras,the majority of 4n cells contribute to the trophectoderm(TE),while the 2n cells are mainly present in the inner cell mass(ICM)of porcine4n/2n chimeric embryos.Our study established a feasible and effcient approach to produce porcine4n embryos and 4n/2n chimeric embryos. 相似文献
59.
Tianqing Chu Jiajun TengLiyan Jiang Hua ZhongBaohui Han 《Biochemical and biophysical research communications》2014
Wnt/β-catenin signaling and Dickkopf1 (DKK1) play important roles in the progression of lung cancer, which preferably metastasizes to skeleton. But the role of them in bone dissemination is poorly understood. This study aims to define the role of DKK1 in lung cancer bone metastases and investigate the underlying mechanism. Our results demonstrated that DKK1 over-expression was a frequent event in non-small-cell lung cancer (NSCLC) blood samples, and serous DKK1 level was much higher in bone metastatic NSCLC compared to non-bone metastatic NSCLC. We also found that conditioned medium from DKK1 over-expressing lung cancer cells inhibited the differentiation of osteoblast, determined by alkaline phosphatase activity and osteocalcin secretion, whereas the conditioned medium from DKK1 silencing lung cancer cells exhibited the opposite effects. Mechanistically, DKK1 reduced the level of β-catenin and RUNX2, as well as inhibiting the nuclear translocation of β-catenin. Taken together, these results suggested that lung cancer-produced DKK1 may be an important mechanistic link between NSCLC and bone metastases, and targeting DKK1 may be an effective method to treat bone metastase of NSCLC. 相似文献
60.
Changhui Li Jiaqi Zhang Xiaohua Yang Cheng Hu Tianqing Chu Runbo Zhong Yinchen Shen Fang Hu Feng Pan Jianlin Xu Jun Lu Xiaoxuan Zheng Hai Zhang Wei Nie Baohui Han Xueyan Zhang 《Cell death & disease》2021,12(9)
The relationship between circular RNA (circRNA) and cancer stem cells (CSCs) is uncertain. We have investigated the combined influence of CSCs, circRNA (hsa_circ_0003222), and immune checkpoint inhibitors in NSCLC progression and therapy resistance. We constructed lung CSCs (LCSCs; PC9 and A549). The effects of hsa_circ_0003222 in vitro were determined by cell counting, colony and sphere formation, and Transwell assays. A tumor xenograft model of metastasis and orthotopic model were built for in vivo analysis. We found that hsa_circ_0003222 was highly expressed in NSCLC tissues and LCSCs. Higher levels of hsa_circ_0003222 were associated with the stage, metastasis, and survival rate of patients with NSCLC. Reduced levels of hsa_circ_0003222 decreased tumor cell proliferation, migration, invasion, stemness-like properties, and chemoresistance. The silencing of hsa_circ_0003222 was found to downregulate PHF21B expression and its downstream, β-catenin by relieving the sponging effect of miR-527. Moreover, silencing hsa_circ_0003222 alleviated NSCLC resistance to anti-programmed cell death-ligand 1 (PD-L1)-based therapy in vivo. Our data demonstrate the significant role of hsa_circ_0003222 in NSCLC cell stemness-like properties. The manipulation of circRNAs in combination with anti-PD-L1 therapy may alleviate NSCLC stemness and progression.Subject terms: Cancer microenvironment, Cancer stem cells 相似文献