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991.
目的:观察红芪、黄芪及配伍当归对环磷酰胺(CTX)所致血虚模型小鼠的干预作用。方法:昆明种小鼠随机分为7组,每组10只。采用CTX复制小鼠血虚模型,正常组与模型组小鼠用生理盐水灌胃,阳性对照组小鼠给予驴胶补血颗粒,四个给药组分别灌胃红芪、黄芪、红芪-当归组(5:1)及黄芪-当归组(5:1),连续灌胃7 d后,采用血细胞分析仪测定各组小鼠外周红细胞(RBC)、淋巴细胞(LYM)、红细胞压积(HCT)、白细胞(WBC)、血小板(PLT),取脾脏、胸腺、股骨,计算脾脏指数(SI)、胸腺指数(TI)的变化,进行网织红细胞计数(RC)、骨髓有核细胞计数,并对股骨进行病理切片观察。结果:与正常组比较,模型组小鼠RBC、WBC、HCT、PLT、LYM等含量均降低(P<0.05),与模型组比较,红芪及不同配伍各组小鼠中SI、TI均显著升高(P<0.05),红芪-当归组及黄芪-当归组可显著提高外周RBC、HCT、WBC、PLT、LYM的含量(P<0.05),可升高RC及骨髓有核细胞数量(P<0.05),股骨病理切片显示有所改善。结论:红芪-当归(5:1)与黄芪-当归(5:1)配伍对血虚模型小鼠的改善作用及补血作用优于红芪、黄芪的单独作用,黄芪-当归(5:1)效果更佳。 相似文献
992.
A highly selective colorimetric and long‐wavelength fluorescent probe for the detection of Hg2+ 下载免费PDF全文
Jing Xu Zuokai Wang Caiyun Liu Zhenghe Xu Ning Wang Xin Cong Baocun Zhu 《Luminescence》2018,33(6):1122-1127
Currently, the fluorescent probe is an important method for detecting heavy metal ions, especially mercury ion (Hg2+), which is harmful to the health of humans and the environment due to its toxicity and extensive use. In this paper, we designed and synthesized a colorimetric and long‐wavelength fluorescent probe Hg‐P with high sensitivity and excellent selectivity, which could detect Hg2+ by the changes of visual color, fluorescence and absorption spectroscopy. With the addition of Hg2+ to probe Hg‐P solution, its color changed from yellow to pink, and showed a 171 nm red‐shifted absorption spectrum. Probe Hg‐P was used in real water and soil solution samples to detect Hg2+, and the result is satisfactory. Therefore, this new probe shows great value and application in detecting Hg2+ in the environment. 相似文献
993.
Jiaxiang Hu Xiaoxue Wang Yanling Xing Enguang Rong Mengfei Ning Jacqueline Smith Yinhua Huang 《BMC evolutionary biology》2018,18(1):201
Background
Oligoadenylate synthetases (OASs) are widely distributed in Metazoa including sponges, fish, reptiles, birds and mammals and show large variation, with one to twelve members in any given species. Upon double-stranded RNA (dsRNA) binding, avian and mammalian OASs generate the second messenger 2'-5'-linked oligoadenylate (2-5A), which activates ribonuclease L (RNaseL) and blocks viral replication. However, how Metazoa shape their OAS repertoires to keep evolutionary balance to virus infection is largely unknown. We performed comprehensive phylogenetic and functional analyses of OAS genes from evolutionarily lower to higher Metazoa to demonstrate how the OAS repertoires have developed anti-viral activity and diversified their functions.Results
Ancient Metazoa harbor OAS genes, but lack both upstream and downstream genes of the OAS-related pathways, indicating that ancient OASs are not interferon-induced genes involved in the innate immune system. Compared to OASs of ancient Metazoa (i.e. sponge), the corresponding ones of higher Metazoa present an increasing number of basic residues on the OAS/dsRNA interaction interface. Such an increase of basic residues might improve their binding affinity to dsRNA. Moreover, mutations of functional residues in the active pocket might lead to the fact that higher Metazoan OASs lose the ability to produce 3'-5'-linked oligoadenylate (3-5A) and turn into specific 2-5A synthetases. In addition, we found that multiple rounds of gene duplication and domain coupling events occurred in the OAS family and mutations at functionally critical sites were observed in most new OAS members.Conclusions
We propose a model for the expansion of OAS members and provide comprehensive evidence of subsequent neo-functionalization and sub-functionalization. Our observations lay the foundation for interrogating the evolutionary transition of ancient OAS genes to host defense genes and provide important information for exploring the unknown function of the OAS gene family.994.
Vascular smooth muscle cells direct extracellular dysregulation in aortic stiffening of hypertensive rats 下载免费PDF全文
Aortic stiffening is an independent risk factor that underlies cardiovascular morbidity in the elderly. We have previously shown that intrinsic mechanical properties of vascular smooth muscle cells (VSMCs) play a key role in aortic stiffening in both aging and hypertension. Here, we test the hypothesis that VSMCs also contribute to aortic stiffening through their extracellular effects. Aortic stiffening was confirmed in spontaneously hypertensive rats (SHRs) vs. Wistar‐Kyoto (WKY) rats in vivo by echocardiography and ex vivo by isometric force measurements in isolated de‐endothelized aortic vessel segments. Vascular smooth muscle cells were isolated from thoracic aorta and embedded in a collagen I matrix in an in vitro 3D model to form reconstituted vessels. Reconstituted vessel segments made with SHR VSMCs were significantly stiffer than vessels made with WKY VSMCs. SHR VSMCs in the reconstituted vessels exhibited different morphologies and diminished adaptability to stretch compared to WKY VSMCs, implying dual effects on both static and dynamic stiffness. SHR VSMCs increased the synthesis of collagen and induced collagen fibril disorganization in reconstituted vessels. Mechanistically, compared to WKY VSMCs, SHR VSMCs exhibited an increase in the levels of active integrin β1‐ and bone morphogenetic protein 1 (BMP1)‐mediated proteolytic cleavage of lysyl oxidase (LOX). These VSMC‐induced alterations in the SHR were attenuated by an inhibitor of serum response factor (SRF)/myocardin. Therefore, SHR VSMCs exhibit extracellular dysregulation through modulating integrin β1 and BMP1/LOX via SRF/myocardin signaling in aortic stiffening. 相似文献
995.
996.
Yuhang Yuan Daokui Ding Ning Zhang Jiaxiang Wang Heying Yang 《Cell cycle (Georgetown, Tex.)》2018,17(11):1390-1402
Necrotizing enterocolitis (NEC) is a potentially fatal illness in premature neonates. Tumor necrosis factor-α (TNF-α) and autophagy are associated with the pathogenesis of NEC. This study aimed to explore whether TNF-α might regulate apoptosis in neonatal NEC model cells IEC-6 via regulation of autophagy. NEC rat model was induced by hand feeding and exposure to asphyxia/cold-stress for histologic examination. The NEC in vitro model (IEC-6/NEC cells) was established by stimulating the intestinal epithelial cell line IEC-6 with lipopolysaccharide (LPS, 100 μg/mL) for 3 h to investigate the effects of TNF-α on IEC-6 proliferation and apoptosis. In this study, NEC rats showed decreased proliferating cell nuclear antigen (PCNA) expression, increased TUNEL-positive cells, higher expression of TNF-α, p-ERK1/2, and autophagy-related proteins in rat small intestine compared with their controls. Additionally, the LPS-stimulated IEC-6/NEC cells showed a significantly decreased proliferation and increased apoptosis compared with the control cells. Furthermore, the LPS-stimulated IEC-6/NEC cells exhibited enhanced autophagy level, as evidenced by a dose-dependent increase in Beclin-1 protein expression, LC3II/LC3I ratio and accumulation of MDC-positive autophagic vacuoles. Moreover, inhibition of autophagy by wortmannin or LY294002 significantly abolished the LPS-mediated decreased proliferation and increased apoptosis of IEC-6/NEC cells. Results also showed that inhibition of ERK1/2 pathway using U0126 significantly inhibited TNF-α-induced autophagy. Furthermore, the TNF-α-mediated inhibition of IEC-6 proliferation and promotion of IEC-6 apoptosis was abolished by U0126. Our findings demonstrated that TNF-α might induce autophagy through ERK1/2 pathway to regulate apoptosis in neonatal NEC cells IEC-6. Our study enhances our understanding of neonatal NEC pathogenesis. 相似文献
997.
Xin Liu Gensheng Liu Juan Liu Peng Zhu Jiahui Wang Yanwei Wang Wenting Wang Ning Li Xuebo Wang Chenglin Zhang Xiaofang Shen Fujun Liu 《Clinical proteomics》2018,15(1):27
Background
In the assisted reproduction, the infertile molecules of spermatozoa from normozoospermic men who underwent the unexplained failure of in vitro fertilization (IVF) due to the lack of sperm binding to the normal zona pellucida, and then achieved pregnancy with the rescue intracytoplasmic sperm injection (R-ICSI) remain unclear. More works are still necessary to explore this male infertile mechanism.Methods
Normozoospermicmen with the IVF pregnancy and normozoospermic men with the R-ICSI pregnancy after the conventional IVF failure were collected. iTRAQ-based proteomic approach were performed to reveal the new infertile causes between the IVF pregnancy men and the R-ICSI pregnancy men. To validate the confidence of proteome data, the individual samples were analyzed by western blot and immunofluorescence. Further, the spontaneous acrosome reactions were measured to evaluate the sperm quality.Results
Compared with IVF pregnancy group, 56 sperm proteins were differentially expressed in the R-ICSI pregnancy group. Bioinformatic analyses (PANTHER, DAVID, PubMed and STRING) indicated these altered sperm proteins were involved in various molecular functions: reproduction, chromosome organization, and sperm-oocyte interaction. Moreover, the confidence of proteome data was confirmed by western blot and immunofluorescence using the individual samples, which were consistent with our proteomic data. Additionally, an increased rate of the spontaneous acrosome reaction rate was found in the R-ICSI pregnancy group.Conclusions
The sealtered sperm proteins and the increased spontaneous acrosome reaction rate might account for this unexplained male infertility in the R-ICSI pregnancy patients. The present proteomic results will throw light on the better understanding of the unexplained infertile mechanisms underlying these normozoospermic man who achieved R-ICSI pregnancy after IVF failure.998.
Stathmin inhibits proliferation and differentiation of dental pulp stem cells via sonic hedgehog/Gli 下载免费PDF全文
Dandan Ma Haiyue Yu Shuaimei Xu He Wang Xiaoyi Zhang Tingting Ning Buling Wu 《Journal of cellular and molecular medicine》2018,22(7):3442-3451
The mineralization of dental pulp stem cells is an important factor in the tissue engineering of teeth, but the mechanism is not yet obvious. This study aimed to identify the effect of Stathmin on the proliferation and osteogenic/odontoblastic differentiation of human dental pulp stem cells (hDPSCs) and to explore whether the Shh signalling pathway was involved in this regulation. First, Stathmin was expressed in the cytoplasm and on the cell membranes of hDPSCs by cell immunofluorescence. Then, by constructing a lentiviral vector, the expression of Stathmin in hDPSCs was inhibited. Treatment with Stathmin shRNA (shRNA‐Stathmin group) inhibited the ability of hDPSCs to proliferate, as demonstrated by a CCK8 assay and flow cytometry analysis, and suppressed the osteogenic/odontoblastic differentiation ability, as demonstrated by alizarin red S staining and osteogenic/odontoblastic differentiation‐related gene (ALP, BSP, OCN, DSPP) activity, compared to that of hDPSCs from the control shRNA group. Molecular analyses showed that the Shh/GLI1 signalling pathway was inhibited when Stathmin was silenced, and purmorphamine, the Shh signalling pathway activator, was added to hDPSCs in the shRNA‐Stathmin group, real‐time PCR and Western blotting confirmed that expression of Shh and its downstream signalling molecules PTCH1, SMO and GLI1 increased significantly. After activating the Shh signalling pathway, the proliferation of hDPSCs increased markedly, as demonstrated by a CCK8 assay and flow cytometry analysis; osteogenic/odontoblastic differentiation‐related gene (ALP, BSP, OCN, DSPP) expression also increased significantly. Collectively, these findings firstly revealed that Stathmin‐Shh/GLI1 signalling pathway plays a positive role in hDPSC proliferation and osteogenic/odontoblastic differentiation. 相似文献
999.
Ectodysplasin A regulates epithelial barrier function through sonic hedgehog signalling pathway 下载免费PDF全文
Sanming Li Jing Zhou Liying Zhang Juan Li Jingwen Yu Ke Ning Yangluowa Qu Hui He Yongxiong Chen Peter S. Reinach Chia‐Yang Liu Zuguo Liu Wei Li 《Journal of cellular and molecular medicine》2018,22(1):230-240
Ectodysplasin A (Eda), a member of the tumour necrosis factor superfamily, plays an important role in ectodermal organ development. An EDA mutation underlies the most common of ectodermal dysplasias, that is X‐linked hypohidrotic ectodermal dysplasia (XLHED) in humans. Even though it lacks a developmental function, the role of Eda during the postnatal stage remains elusive. In this study, we found tight junctional proteins ZO‐1 and claudin‐1 expression is largely reduced in epidermal, corneal and lung epithelia in Eda mutant Tabby mice at different postnatal ages. These declines are associated with tail ulceration, corneal pannus formation and lung infection. Furthermore, topical application of recombinant Eda protein markedly mitigated corneal barrier dysfunction. Using cultures of a human corneal epithelial cell line and Tabby mouse skin tissue explants, Eda up‐regulated expression of ZO‐1 and claudin‐1 through activation of the sonic hedgehog signalling pathway. We conclude that EDA gene expression contributes to the maintenance of epithelial barrier function. Such insight may help efforts to identify novel strategies for improving management of XLHED disease manifestations in a clinical setting. 相似文献
1000.