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AIM: To observe the inhibitory effect of recombinant human endostatin (rhES) on plaque angiogenesis, and to explore the regulatory mechanism of Dll4/Notch pathway in the anti-angiogenic effect of rhES. METHODS: Male Wistar rats were randomized into 3 groups:normal control group (N group), atherosclerotic model group (AS group), and rhES treated group (AS+rhES group). The rats in N group were fed a normal diet, while the remaining 2 groups were established to atherosclerotic rat model via high-cholesterol diet, intraperitoneal injection of vitamin D3 and aortic balloon injury. The rats in AS+rhES group received intraperitoneal injection of rhES. The blood total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), C-reactive protein (CRP), interleukin-1 (IL-1) and troponin I (TnI) were measured. The atherosclerotic abdominal aortas were taken for pathological observation. Immunohistochemical staining was used to measure the density of neovessels in the plaques, which were marked by CD31. The protein levels of Dll4 and Notch1 in the aortas were analyzed by Western blot. RESULTS: The levels of blood TC, TG, LDL-C, CRP and IL-1 in AS group and AS+rhES group were much higher than those in N group (P<0.05), and no statistical difference between AS group and AS+rhES group was observed. The expression of CD31 in AS group was the highest among all groups. Compared with AS group, the density of neovessels in the plaques of AS+rhES group decreased significantly (P<0.05). The protein expression of Dll4 and Notch1 in AS group was lower than that in N group (P<0.05). Compared with AS group, the protein expression of Dll4 and Notch1 increased significantly (P<0.05). CONCLUSION: rhES has the ability to inhibit plaque angiogenesis in rats. The activation of Dll4/Notch pathway may be the mechanism of rhES in inhibiting plaque angiogenesis. 相似文献
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LIU Tao YAO Xing-zhang HE Zhi-jun SONG Yuan LI Yan LI Jin-peng CHEN Wen WANG Hai-gang HE Yuan-xu 《园艺学报》2021,37(1):119-127
AIM To observe the effect of Xiaozhongzhitong （detumescence and relieving pain） mixture on vascular regeneration and vascular endothelial growth factor （VEGF）-Dll4/Notch signaling pathway of random flap in rats. METHODS A total of 240 SD rats were randomly divided into 6 groups： blank group, sham group, model group, Xiaozhongzhitong mixture group （detumescence group）, Xiaozhongzhitong mixture+Notch blocker MK-0752 group （detumescence+MK group） and Xiaozhongzhitong mixture+VEGF receptor inhibitor axitinib group （detumescence+AXI group）. The capillary filling time, the number of new capillaries, the microvascular density, the microvascular diameter and the vascular survival area were observed by HE staining. The serum level of VEGF was measured by ELISA, and the mRNA expression of VEGFA, Notch and Dll4 in rat flap tissues was detected by RT-qPCR. RESULTS On the 10th day, compared with model group, the capillary filling time in detumescence group was decreased （P <0.05）. The capillary filling time in detumescence+AXI group was increased compared with detumescence group （P <0.05）. The flap tissue cells inmodel group were disordered and the nucleus was sparse, which showed obvious edema. Compared with model group, the number, diameter and area of microvessels, the serum content of VEGF, and the mRNA expression of VEGFA, Notch and Dll4 were significantly increased in detumescence group （P <0.05）. Compared with detumescence group, the number, density and area of microvessels, the serum content of VEGF, and the mRNA expression of VEGFA, notch and Dll4 was significantly decreased in detumescence+AXI group （P <0.05）. After the intervention with Notch blocker, the mRNA expression of VEGFA was increased, and the mRNA expression of Notch and Dll4 was inhibited （P <0.05）. CONCLUSION Xiaozhongzhitong mixture promotes the regeneration of blood vessels and enhances the survival rate of random flap, which may be related to the regulation of VEGF-Dll4/Notch signaling pathways. 相似文献
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AIM: To investigate the effect of astragaloside IV on neurological function and the protein expression of neuron-specific enolase (NSE), Notch1 and NF-κB in acute cerebral hemorrhage (ACH) rats.METHODS: ACH model in rats was established via injection of autologous blood, and the rats were divided into 4 groups:sham, ACH, ACH+astragaloside IV (100 mg/kg) and ACH+astragaloside IV (200 mg/kg) groups. The impairment of neurological function in each group was graded, and the brain coefficient and water content were calculated. The serum level of NSE was measured by ELISA. Additionally, the expression of Notch1 and NF-κB was determined by Western blot.RESULTS: Astragaloside IV improved the neurological function and decreased the brain coefficient and water content in ACH rats. Moreover, the ACH-induced increase in NSE was inhibited after astragaloside IV treatment. Similarly, astragaloside IV also significantly attenuated the expression of Notch1 and NF-κB in ACH rats.CONCLUSION: Astragaloside IV attenuates the impairment of neurological function in ACH rats, which may be through decreasing the NSE level and down-regulating the expression of Notch1 and NF-κB. 相似文献
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The prognosis of nasopharyngeal carcinoma (NPC) is still poor. Trichosanthin (TCS) has abortifacient, anti-virus, immunoregulation and various anti-tumor pharmacological activities, but there are no reports about its effect on NPC and the exact mechanisms that TCS inhibits tumor are not well known. In this study, the proliferation, apoptosis and soft agar colony formation abilities of CNE2 cells were examined with various assays in vitro followed by treatment with TCS. Furthermore, the activation status of Notch signaling pathway in TCS and control cells also was examined. The results revealed that TCS could inhibit NPC cell line CNE2 in vitro, reduce clone formation ability and induce apoptosis of CNE2 cells. Down-regulation of Notch signaling may be one of the mechanisms that TCS inhibits NPC. 相似文献
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AIM: To study the effect of epigallocatechin-3-gallate(EGCG) on the proliferation of human nasopharyngeal carcinoma(NPC) cells, and to explore its mechanism by targeting miR-34a.METHODS: Nasopharyngeal carcinoma CNE-2Z cells were treated with various concentrations of EGCG. The ability of cell proliferation was detected by CCK-8 assay, 5-ethynyl-2-deoxyuridine(EdU) incorporation assay and colony-forming assay. The cell cycle distributions were analyzed by flow cytometry. The protein levels of P53 and Notch1 were detected by Western blot. The expression of miR-34a and Notch1 mRNA was measured by real-time PCR.RESULTS: EGCG effectively inhibited the proliferation and colony formation of CNE-2Z cells in a dose-dependent manner, which was related to its induction of cell cycle arrest at G0/G1 phase. The expression of P53 and miR-34a in CNE-2Z cells was significantly increased after treated with EGCG, while the expression of Notch1 at mRNA and protein levels was markedly suppressed.CONCLUSION: EGCG induces cell cycle arrest and suppresses cell proliferation by regulating the P53/miR-34a/Notch1 pathway in NPC cells. 相似文献
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基于转录组454 GS FLX测序结果,利用RACE和RT-PCR技术克隆了海蜇(Rhopilema esculentum) Notch基因的cDNA全长,并分析了其mRNA在海蜇不同发育阶段的表达差异,以探讨Notch基因对海蜇无性生殖的影响.结果显示,海蜇Notch基因的cDNA全长为6768 bp,包括90 bp的5'非编码区、6066 bp的开放阅读框及612 bp包含AATAAA加尾信号的3'非翻译区.SMART分析表明,海蜇Notch为分泌蛋白,其信号肽由21个氨基酸组成.成熟肽由2000个氨基酸组成,包括37个结构域、26个表皮生长因子样结构域、3个富含半胱氨酸的Notch/Lin-12(NL)结构域、1个NOD结构域、1个NODP结构域、1个跨膜结构域和6个锚蛋白结构域ANK,并含有25个N-糖基化位点.同源分析表明,海蜇Notch与来自刺胞动物门的海葵(Nematostella vectensis)的Notch相似性为39％,与无脊椎动物和脊椎动物的氨基酸相似度分别为35％-37％和34％-38％.RT-PCR分析表明,Notch基因在海蜇无性繁殖的4个发育时期均有表达,螅状体阶段的表达量最高,横裂体阶段表达量最低,螅状体的表达量是横裂体的1.85倍.这些研究结果为进一步研究Notch信号通路在海蜇无性繁殖中的调控作用奠定了基础. 相似文献
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鸡的体内器官表现出明显的左右不对称性,这些不对称性的确立发生在胚胎发育的早期,并且要求多种机制共同筹划和有序进行。对于从亨氏节(Hensen’s node)到机体原基的左右信息传递的基因网络已经有了较清楚的阐述。有助于我们对这种机制的理解。以鸡胚为模式动物进行不对称性发生和发育的研究具有多种优点,文章以鸡胚为发育模式,对器官不对称性发育的分子机理,研究方法和未来的研究趋势进行了较为详细的介绍和论述,以期丰富我们对器官不对称发育的理解。 相似文献
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AIM To investigate the effects of local perfusion of Mailuoning on Wnt/β-catenin and Notch signaling pathway in crush injury syndrome model pigs. METHODS A total of 24 Bama mini pigs were randomly divided into normal control group， model group， normal perfusion group and Mailuoning perfusion group， with 6 in each group. Except for normal control group， the other groups were established crush injury model. After modeling， the blood supply of the pigs in model group was immediately restored. The normal perfusion group and Mailuoning perfusion group were pre-processed for modeling， and were given normal perfusion and Mailuoning perfusion for 1 h to restore their blood supply. After the recovery of blood supply for 4 h， the skeletal muscle morphology was detected by hematoxylin-eosin （HE） staining. The ultrastructure of the skeletal muscle was observed under transmission electron microscope. The serum levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） were measured by ELISA. The mRNA levels of vascular endothelial growth factor （VEGF） and matrix metalloproteinase-2 （MMP-2） were detected by RT-qPCR， and the protein levels of β-catenin， Delta-like ligand 4 （Dll4） and Notch in skeletal muscular tissue were observed by Western blot. RESULTS The HE results of model group showed disordered arrangement of skeletal muscle fibers， swollen or obviously constricted nucleus， shrunken sarcolemma， ruptured and swollen blood vessels， edematous interstitium， obvious infiltrating inflammatory cells. The results of electron microscopy in model group showed disorderly arranged and dissolved myofilaments， partial loss of I-band， A-line and Z-line muscle fibers， obviously swollen endoplasmic reticulum， mitochondria and nuclei， and a large number of aggregated and internally shifted nuclei. The above indexes in normal perfusion group were slightly lighter than those in model group. In Mailuoning perfusion group， the results of HE staining observation showed almost normal skeletal muscle， neatly arranged muscle fibers， almost invisible shrinkage or swelling muscle membrane， and basically returned to normal blood vessels； the results of electron microscopy showed clearly visible and regular muscle fiber I-band， A-line， Z-line and neatly arranged nuclei. Compared with normal control group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of IL-1β and TNF-α， the mRNA expression of VEGF and MMP-2， the protein levels of nucleoprotein/total β-catenin， Dll4 and Notch in skeletal muscular tissue in model group were increased （P <0.05）. Compared with model group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of IL-1β and TNF-α， the mRNA expression of MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in normal perfusion group， and the serum levels of IL-1β and TNF-α， the mRNA expression of VEGF and MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in Mailuoning perfusion group were decreased （P <0.05）. Compared with normal perfusion group， the proportion of tissue swelling and vascular damage， the percentage of abnormal Z-line， the serum levels of TNF-α， the mRNA expression of MMP-2， the protein levels of nuclear/total β-catenin， Dll4 and Notch in skeletal muscular tissue in Mailuoning perfusion group were decreased （P <0.05）. CONCLUSION Mailuoning local perfusion suppresses Wnt/β-catenin and Notch signaling pathways， attenuates inflammation and vascular damage， thus realizing the protection of crush injury syndrome. 相似文献
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AIM: To investigate whether Notch1 changes stemness and chemotherapeutic sensitivity in human glioma U251 cells. METHODS: The lentiviral vectors, which expressed Notch1-shRNA or Notch1 intracellular domain (NICD), were transfected into U251 cells. Western blot and immunofluorescence staining were applied to monitor the validity of the cells, down-regulation of Notch1 expression or over-expression of NICD. The proportion of CD133+ cells was analyzed by flow cytometry. The expression of nestin and GFAP was identified by immunofluorescence staining. The formation rate of tumor cell spheres and the implanted tumor growth in SCID mice were observed. MTT assay was performed to evaluate the chemotherapeutic sensitivity to VM-26 and BCNU of the cells with different treatments. RESULTS: Stemness was significantly enhanced in the cells over-expressing NICD. For example, the proportion of CD133+ cells was increased, the expression of nestin was up-regulated, the expression of GFAP was down-regulated, and the formation rate of tumor cell spheres and implanted tumor growth were increased. The chemotherapeutic sensitivity to VM-26 and BCNU of the cells was decreased. In the cells with Notch1 gene down-regulation by RNAi, the stemness was inhibited and chemotherapeutic sensitivity was increased. CONCLUSION: Notch1, which leads to the change of stemness and chemotherapeutic sensitivity in human glioma U251 cells, is likely to be a potential molecular target for treatment of glioma. 相似文献