scholarly journals Effect of tripterine on Notch signaling pathway in IgA nephropathy rats

2018 ◽  
Vol 2 (6) ◽  
Author(s):  
Dan Liu
Keyword(s):  
Notch Signaling ◽  
Iga Nephropathy ◽  
Signaling Pathway ◽  
Intervention Group ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Notch Signaling Pathway ◽  
Male Rats ◽  
Control Group ◽  
Model Group

Abstract: Objective: To investigate the effect of tripterine on Notch signaling pathway in renal tissue of IgA nephropathy rats. Methods: SD male rats were divided into the control group, IgAN nephropathy model group, benazepril group, 1mg/kg/d tripterine intervention group and 10mg/kg/d tripterine intervention group according to the random number table method, with 10 rats in each group. The urinary sediment and 24-hour urinary protein quantity were detected by conventional methods. The expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats were detected by real-time fluorescent quantitative PCR. Results: IgA nephropathy model was successfully established. The hematuria and proteinuria in model group were higher than those of control group (P<0.05). The expressions of Notch1, Jagged1, Hes1 and hey1 in kidney tissue of IgA nephropathy rats were significantly increased (P<0.05). Compared with the model group, hematuria and proteinuria in tripterine intervention group were alleviated. The expressions of Notch1, Jagged1, Hes1 and Hey1 in rat renal tissue were decreased (P<0.05). Moreover, the expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats in 10mg/kg/d tripterine intervention group were decreased (P<0.05). Conclusion: Tripterine can decrease the levels of hematuria and proteinuria in IgA nephropathy rats. The expression of Notch signaling pathway in IgA nephropathy rats is increased by the down-regulation of tripterine, suggesting that tripterine has a certain therapeutic effect on IgA nephropathy rat. And its role may be realized through this signal pathway so as to provide the new mentality for the diagnosis and treatment of IgA nephropathy.

Study on the Regulation of Compound siRNA Nanoparticles on the Rat Model of Kidney Injury Induced by Sepsis by Inhibiting the Expression of NF-κB and P65

2021 ◽  
Vol 21 (2) ◽  
pp. 1345-1350
Author(s):  
Ye Chen ◽  
Xiaoxia Liu ◽  
Meiling Chen ◽  
Run Yan ◽  
Wenyu Song
Keyword(s):  
Rat Model ◽  
Group Treatment ◽  
Medical Image Analysis ◽  
Intervention Group ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Control Group ◽  
Image Analysis System ◽  
Model Group ◽  
Analysis System

This article explores the pathogenesis of sepsis AKI, and seeks to protect the acute damage of sepsis tissues and organs. This study is to prepare a rat sepsis-induced AKI model by CLP, and to observe the pathological changes of kidney tissue and the function of kidney changes, and observe the effect of siRNA nanoparticles on its intervention, preliminary explore the protective effect and possible mechanism of siRNA nanoparticles on AKI in sepsis rats, and provide more information for the clinical treatment of siRNA nanoparticles in sepsis theoretical and experimental basis. We analysis the benefit and deficiency of nuclear factor-κB (NF-κB) activation in the pathogenesis of glomerulonephritis and its regulatory effect on NF-κB activation. In the rat model group, no treatment was given after injection of nephrotoxic serum, and the rats were sacrificed on the 14th day; the compound siRNA nanoparticle intervention group (treatment group) was given dexamethasone 0.125 daily on the 1st to 14th day after nephrotoxic serum injection. Immunohistochemistry and medical image analysis system were used to observe NF-κB activation of monocyte chemotactic protein-1 (MCP-1) in glomeruli and tubules, and analyze their relationship with proteinuria and glomerular cells. The results showed that the expression of NF-κB in the glomeruli and tubules of the model group was significantly up-regulated regarding to the control group, and MCP-1’s expression in the glomeruli and tubules of the model group was higher than that of the control group. The activation of NF-κB and the expression of MCP-1 in glomeruli are closely related to monocyte infiltration and proteinuria; NF-κB activation and MCP-1 expression in glomeruli and tubules of the compound siRNA nanoparticles intervention group were significantly down-regulated. It was concluded that the activation of NF-κB has great impact on the pathogenesis of glomerulonephritis, and inhibition of NF-κB activation may be one of the mechanisms of anti-nephritis effect.

scholarly journals Intervention Effect of Compatibility of Salvianolic Acid A & B on PDGF-C/PDGFR-α Signaling Pathway in Renal Fibrosis

2015 ◽  
Vol 4 (2) ◽  
pp. 13
Author(s):  
Bin Yu
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Salvianolic Acid B ◽  
Control Group ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Drug Compatibility ◽  
Renal Tubular

<strong>Objective</strong>: To explore the effect of salvianolic acid A &amp; B component molecules of drug compatibility on PDGF-c/PDGFR-α signaling pathway in renal fibrosis of rats. <strong>Methods</strong>: 40 male SPF SD rats were randomly divided into four groups: control group, salvianolic acid A group, salvianolic acid B group and salvianolic acid A + B group, with 10 rats in each group. Each group was treated for two weeks. After the intervention, samples were collected. And scores of HE and Masson was compared. The expression of PDGF-c/PDGFR-α in rental tissue in them was also tested and compared.<strong> Results</strong>: Compared with the control group, the score of HE and Masson in intervention groups was markedly decreased, and scores in salvianolic acid B group and salvianolic acid A + B group were reduced significantly (<em>p </em>&lt; 0.05); Compared with the control group, the expression of PDGF-c/PDGFR-α in rental tissue in intervention groups was lower(<em>p </em>&lt; 0.05), especially in salvianolic acid B group and salvianolic acid A + B group (<em>p </em>&lt; 0.05).<strong>Conclusion</strong>: salvianolic acid A &amp; B component molecules of drug compatibility could significantly improve the pathological changes in the kidney tissue of rats, suppress the expression of PDGF-c/PDGFR-α in renal tissue, and improve the renal function, renal tubular function and renal pathology.

scholarly journals Notch Signaling Pathway Is Involved in bFGF-Induced Corneal Lymphangiogenesis and Hemangiogenesis

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Fang Xie ◽  
Xue Zhang ◽  
Wenting Luo ◽  
Hongyan Ge ◽  
Dawei Sun ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Expression Level ◽  
Control Group ◽  
Fluorescence Signal ◽  
Mrna And Protein Expression ◽  
Corneal Lymphangiogenesis

Background. Notch/Dll4 involvement in cornea neovascularization (CRNV) and lymphangiogenesis is unclear. This study aimed to explore the role of notch signaling in basic fibroblast growth factor- (bFGF-) induced corneal lymphangiogenesis and hemangiogenesis. Methods. Corneal stroma of C57BL/6 mice was implanted with bFGF- or phosphate-buffered saline- (PBS-) soaked pellets. Corneal lymphangiogenesis and neovascularization were evaluated by immunofluorescence. Vascular endothelial growth factor-A (VEGF-A), Delta-like ligand 4 (Dll4), and Notch1 mRNA and protein expression were examined on days 1, 3, 7, and 14 by real-time polymerase chain reaction and western blot. Corneal cells were treated with ranibizumab, dexamethasone, and γ-secretase inhibitor (GSI). Microspheres were used to evaluate corneal hemangiogenesis in vivo. Results. Corneal hemangiogenesis reached its peak on day 7 after bFGF implantation, and corneal lymphangiogenesis was significantly higher on day 7 and 14, compared with PBS. mRNA and protein expression of VEGF-A, Dll4, and Notch1 were higher in bFGF-induced animal models compared with controls. Corneal hemangiogenesis and lymphangiogenesis decreased after 7 days of ranibizumab or dexamethasone treatment. After adding GSI for 24 h in bFGF-induced cells, the expression of Notch1 and Dll4 were downregulated compared with that in the control group whereas the expression level of VEGF-A was upregulated. Fluorescent particle number was higher in the GSI group. Ranibizumab and dexamethasone decreased the fluorescence signal. Conclusion. The notch signaling pathway plays a role in regulating VEGF expression, affecting corneal lymphangiogenesis and hemangiogenesis in mice. The molecular imaging probe technique can visualize the changes in the VEGF-A expression level of corneal limbus hemangiogenesis.

scholarly journals Astragalus Polysaccharide RAP Induces Macrophage Phenotype Polarization to M1 via the Notch Signaling Pathway

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 2016 ◽  
Author(s):  
Wei Wei ◽  
Zhi-Peng Li ◽  
Zhao-Xiang Bian ◽  
Quan-Bin Han
Keyword(s):  
Tumor Growth ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Macrophage Polarization ◽  
Notch Signaling Pathway ◽  
Raw264.7 Cells ◽  
Control Group ◽  
Macrophage Phenotype ◽  
Astragalus Polysaccharide ◽  
M1 Phenotype

Macrophages occur in polarized phenotypes, whose characteristics determine the role they play in tumor growth. The M1 phenotype macrophages promote tumoricidal responses and suppress tumor growth. Our previous study showed that a polysaccharide isolated from Radix Astragali, named RAP, was itself non-cytotoxic but induced RAW264.7 cells’ cytotoxicity against cancer cells. The current study was undertaken to determine its mechanism. Series studies was conducted to show that RAP is able to induce much higher gene expression of M1 markers, including iNOS, IL-6, TNF-a, and CXCL10, compared with the control group. When RAP-induced BMDMs were transplanted together with 4T1 tumor cells in BALB/c mice, both tumor volume and tumor weight decreased. Further studies indicated that RAP induces the Notch signaling pathway in RAW264.7 cells. The function of Notch signaling in macrophage polarization was confirmed by using γ-secretase inhibitor. These results suggested that Astragalus polysaccharide RAP induces macrophage’s polarization to M1 phenotype via the Notch signaling pathway.

scholarly journals Ethanolic Extract of Moringa oleifera Leaves Influences NF-κB Signaling Pathway to Restore Kidney Tissue from Cobalt-Mediated Oxidative Injury and Inflammation in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1031 ◽  
Author(s):  
Mohamed M. Abdel-Daim ◽  
Samah R. Khalil ◽  
Ashraf Awad ◽  
Ehsan H. Abu Zeid ◽  
Reda Abd El-Aziz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Moringa Oleifera ◽  
Expression Profiles ◽  
Quantitative Polymerase Chain Reaction ◽  
Kidney Tissue ◽  
Ethanolic Extract ◽  
Male Rats ◽  
Control Group ◽  
The Impact

This study aimed to describe the protective efficacy of Moringa oleifera ethanolic extract (MOEE) against the impact of cobalt chloride (CoCl2) exposure on the rat’s kidney. Fifty male rats were assigned to five equal groups: a control group, a MOEE-administered group (400 mg/kg body weight (bw), daily via gastric tube), a CoCl2-intoxicated group (300 mg/L, daily in drinking water), a protective group, and a therapeutic co-administered group that received MOEE prior to or following and concurrently with CoCl2, respectively. The antioxidant status indices (superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)), oxidative stress markers (hydrogen peroxide (H2O2), 8-hydroxy-2-deoxyguanosine (8-OHdG), and malondialdehyde (MDA)), and inflammatory response markers (nitric oxide (NO), tumor necrosis factor (TNF-α), myeloperoxidase (MPO), and C-reactive protein (CRP)) were evaluated. The expression profiles of pro-inflammatory cytokines (nuclear factor-kappa B (NF-kB) and interleukin-6 (IL-6)) were also measured by real-time quantitative polymerase chain reaction (qRT-PCR). The results showed that CoCl2 exposure was associated with significant elevations of oxidative stress and inflammatory indices with reductions in the endogenous tissue antioxidants’ concentrations. Moreover, CoCl2 enhanced the activity of the NF-κB inflammatory-signaling pathway that plays a role in the associated inflammation of the kidney. MOEE ameliorated CoCl2-induced renal oxidative damage and inflammatory injury with the suppression of the mRNA expression pattern of pro-inflammatory cytokine-encoding genes. MOEE is more effective when it is administered with CoCl2 exposure as a prophylactic regimen. In conclusion, MOEE administration exhibited protective effects in counteracting CoCl2-induced renal injury in rats.

scholarly journals Jagged2-γδT17 is Regulated by Mycobacterium Vaccae in Asthmatic Mice

2021 ◽  
Author(s):  
Yi-En Yao ◽  
Qi-Xiang Sun ◽  
Jing-Hong Zhang ◽  
Jian-Lin Huang ◽  
Si-Yue Xu ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Notch Signaling ◽  
Airway Inflammation ◽  
Signaling Pathway ◽  
Signal Transduction Pathway ◽  
Notch Signaling Pathway ◽  
Control Group ◽  
Transduction Pathway ◽  
Γδt Cells ◽  
Mycobacterium Vaccae

Abstract Background: Mycobacterium vaccae nebulization imparted protective effect against asthma in a mouse model. The Jagged2-γδT17 signal transduction pathway plays an important role in bronchial asthma. However, the effect of M. vaccae nebulization on the Jagged2-γδT17 signal transduction pathway in mouse models of asthma remains unclear. Methods: In total, 30 female C57 mice were randomized to normal control (group a), asthma control (group b), M. vaccae nebulization prevention,and M. vaccae nebulization treatment (group d) groups. Asthma mice models were created using ovalbumin (OVA). The Notch signaling pathway was blocked by DAPT inhibitors. Airway hyperreactivity (AHR) was measured by noninvasive lung function tests. Histopathological analyses using blue-periodic acid Schiff along with hematoxylin and eosin were performed. Immunohistochemistry, immunofluorescence, and a Western blotting assay allowed for the detection of lung protein expressions, while spleen expressions of IL-17+γδT+ cytokines were assessed with FLOW cytometry. One-way analysis of variance for within-group comparisons, the least significant difference t-test or Student-Newman-Keuls test for intergroup comparisons, and the nonparametric rank sum test for analysis of airway inflammation scores were used in the study. Results: Asthmatic mice models demonstrated downregulated Notch signaling pathway activation and decreased γδT cells and IL-17 cytokine secretion. There was also increased Jagged2 protein expression which correlated positively with γδT+IL-17+ secretion. In asthmatic mice, the expressions of Jagged2 and γδT17, along with airway inflammation and airway reactivity, were all decreased after M. vaccae exposure (p<0.05). Conclusion: The Notch signaling pathway contributed towards asthma initiation and progression by facilitating γδT cells and IL-17 cytokines production. Inhaled M. vaccae led to a significant decrease in Jagged2 and γδT17 expressions in asthmatic mice, indicating its utility in asthma prevention.

scholarly journals Effect of NTN and Lmx1α on the Notch Signaling Pathway during the Differentiation of Human Bone Marrow Mesenchymal Stem Cells into Dopaminergic Neuron-Like Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jinhua Zhang ◽  
Bo Yang ◽  
Lilin Luo ◽  
Linhui Li ◽  
Xuantao Yang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Dopaminergic Neuron ◽  
Notch Signaling Pathway ◽  
Control Group ◽  
Marrow Mesenchymal Stem Cells

Human bone marrow mesenchymal stem cells (h-BMSCs) have the potential to differentiate into dopaminergic neuron-like cells to treat Parkinson’s disease. The Notch signaling pathway has been implicated in the regulation of cell fate decisions such as differentiation of BMSCs. This study investigated changes in the expression of Notch-related genes in the differentiation of BMSCs in vitro into dopaminergic (DA) neuron-like cells. BMSCs transfected with empty lentiviral vectors served as the control group and those transfected with NTN and Lmx1α recombinant lentiviral vectors served as the experimental group. After induction and culture of NTN and Lmx1α-transfected h-BMSCs for 21 days, the cells exhibited features of dopaminergic neuron-like cells, which were observed by transmission and scanning electron microscopy and verified by immunofluorescence of tyrosine hydroxylase (TH) and dopamine transporter (DAT). These induced cells could secrete dopamine and had basic action potentials. Expression of the neural stem cell (NSC) markers, including octamer-binding protein (Oct4), paired box gene 6 (Pax6), and sex determining region Y-box 1 (SOX1), increased on day 14 of induction and decreased on day 21 of induction during differentiation. The human Notch signaling pathway PCR array showed a differential expression of Notch-related genes during the differentiation of h-BMSCs into DA neuron-like cells in vitro relative to that in the control group. In conclusion, h-BMSCs overexpressing NTN and Lmx1α can successfully be induced to differentiate into dopaminergic neuron-like cells with a neuronal phenotype exhibiting fundamental biological functions in vitro, and NTN and Lmx1α may affect the expression of Notch-related genes during differentiation.

scholarly journals LncRNA LINC00311 Promotes the Proliferation and Differentiation of Osteoclasts in Osteoporotic Rats Through the Notch Signaling Pathway by Targeting DLL3

2018 ◽  
Vol 47 (6) ◽  
pp. 2291-2306 ◽  
Author(s):  
Yu Wang ◽  
Tian-Bao Luo ◽  
Long Liu ◽  
Zhi-Qiang Cui
Keyword(s):  
Notch Signaling ◽  
Signaling Pathway ◽  
Cell Activity ◽  
Notch Signaling Pathway ◽  
Control Group ◽  
Expression Levels ◽  
Proliferation And Differentiation ◽  
Expression Rate ◽  
Non Coding Rnas ◽  
Sirna Group

Background/Aims: Osteoporosis is a commonly occurring condition marked by a loss of bone density. Previous evidence has highlighted the roles played by microRNAs as potential treatment tools for the disease. At present, the influence of long non-coding RNAs (lncRNAs) on the progression of osteoporosis remains largely unclear. Thus, an investigation was conducted into the target relationship between LINC00311, which has been reported to be highly expressed in osteoporosis, and delta-like 3 (DLL3), which is involved in the Notch signaling pathway, in connection with a series of bioinformatic methods. An osteoporotic rat model was established by means of ovariectomy (OVX) to evaluate the influence exerted by DLL3-binding LINC00311 on osteoclasts through the Notch signaling pathway. Methods: Osteoclasts were extracted from osteoporotic rats and transfected with the LINC00311-vector, shRNA-LINC00311, Notch activator, or a combination of the Notch activator and LINC00311-vector. Western blotting and RT-qPCR techniques were applied to determine the expression levels of LINC00311, DLL3, Notch1, Notch2, Jagged1, Hes-1 and TRAP in tissues and cells, while cell activity was detected by MTT assay. The cell cycle as well as the rate of apoptosis was detected by flow cytometry. The successfully established osteoporotic rats were designated into the OVX-siRNA, OVX-LINC00311 and OVX-control groups to observe the effects of LINC00311 on the proliferation and differentiation of osteoclasts. Results: Cells transfected with the LINC00311-vector exhibited increased expression levels of Notch2 and TRPA as well as increased cell activity, while decreased expression levels of DLL3, Notch1, Jagged1 and Hes-1, along with a decreased cell apoptosis rate, were observed. The opposite tendencies of these parameters were observed in the cells treated with shRNA-LINC00311. A key observation was made when the Notch signaling pathway was activated, in that the cell activity was decreased while the rate of apoptosis increased. In comparison with the OVX-control group, the expression levels of LINC00311, Notch2 and TRAP as well as the positive expression rate of TRAP all exhibited reductions, while those of DLL3, Jagged1 and Notch1 were elevated in the OVX-siRNA group. Compared with those in the sham group, in the OVX-control and OVX-LINC00311 groups, LINC00311 and the expression levels of Notch2 and TRAP were increased; however, decreased levels of DLL3, Jagged1 and Notch1 were noted. Conclusions: Taken together, the key findings of the present study suggest that LINC00311 induces proliferation and inhibits apoptosis of osteoclasts via the regulation of the Notch signaling pathway by inhibiting DLL3 expression, ultimately demonstrating that LINC00311 and its target gene DLL3 may serve as independent factors in cases of osteoporosis.

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