Search results for: Glucose Assay Kit
#28921392 2017/09/18 Save this To Up
Resveratrol attenuates high glucose-induced endothelial cell apoptosis via mediation of store-operated calcium entry.The aim of this study was to evaluate the influence of resveratrol on HG-induced calcium entry in islet microvascular (MS-1) endothelial cells. MS-1 cells were pretreated with resveratrol or 2-APB (an inhibitor of store-operated calcium entry) and then incubated with high glucose. Cell viability was determined using the cell counting kit-8 method. Reactive oxygen species, endothelial apoptosis, and NO production were detected by DHE probe, TUNEL detection, and nitrate reductase assay kit. Protein levels of SOCE were detected by western blotting. Pretreatment with resveratrol significantly attenuated HG-induced endothelial apoptosis and improved cell viability. However, pretreatment with resveratrol and 2-APB abolished this effect, suggesting that the attenuation of HG-induced apoptosis by resveratrol may be associated with SOCE. Subsequent analyses indicated that HG induced the SOCE-related proteins, including TRPC1, Orai1, and Stim1. These results suggest that resveratrol pretreatment is associated with relieved HG-induced endothelial apoptosis at least partly via inhibition of SOCE-related proteins.
1838 related Products with: Resveratrol attenuates high glucose-induced endothelial cell apoptosis via mediation of store-operated calcium entry.CD31, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; CD34, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Cell Meter™ Cell Viabil Cell Meter™ Cell Viabil
#28915418 2017/09/15 Save this To Up
Purification, identification and molecular mechanism of two dipeptidyl peptidase IV (DPP-IV) inhibitory peptides from Antarctic krill (Euphausia superba) protein hydrolysate.Dipeptidyl peptidase IV (DPP-IV) played an important role in blood glucose regulation. Inhibition of DPP-IV may improve glycemic control in diabetics by preventing the rapid breakdown of incretin hormones and prolonging their physiological action. In this study, Antarctic krill (Euphausia superba) protein was hydrolyzed using animal proteolytic enzymes. The hydrolysate was purified sequentially by ultrafiltration, gel filtration chromatography and reversed phase high-performance liquid chromatography (RP-HPLC). DPP-IV inhibitory activity of the fractions achieved from Antarctic krill protein was determined by DPP-IV screening reagent kit. Two purified peptides were identified by Xevo G2-XS QTof mass spectrometer (QTOF-MS). One peptide purified was Ala-Pro (AP) with IC50 values of 0.0530mg/mL, the other Ile-Pro-Ala (IPA) with IC50 values of 0.0370mg/mL. They both exhibited strong DPP-IV inhibitory activity. The molecular docking analysis revealed that DPP-IV inhibition by AP and IPA was mainly due to formation of a strong interaction surface force with the 91-96 and 101-105 amino acids of the DPP-IV. Our results suggested that the protein hydrolysate from Antarctic krill can be considered as a promising natural source of DPP-IV inhibitory peptides in the management of diabetes.
1031 related Products with: Purification, identification and molecular mechanism of two dipeptidyl peptidase IV (DPP-IV) inhibitory peptides from Antarctic krill (Euphausia superba) protein hydrolysate.Dipeptidyl Peptidase IV, ELISA Human , Dipeptidyl Native Influenza HA (A Ca Native Influenza HA (A Ca Native Influenza HA (A Ca Recombinant Human Regener Recombinant Human Regener Recombinant Human REG1-IV Native Human Collagen IV Peroxiredoxin IV, Human , Bovine Collagen Type IV P Rabbit Anti-Bovine Collag
#28903386 2017/09/14 Save this To Up
Synergistic inhibition of colon cancer growth by the combination of methylglyoxal and silencing of glyoxalase I mediated by the STAT1 pathway.Methylglyoxal (MG), an extremely reactive glucose metabolite, exhibits antitumor activity. Glyoxalase I (GLOI), which catalyzes MG metabolism, is associated with the progression of human malignancies. While the roles of MG or GLOI have been demonstrated in some types of cancer, their effects in colon cancer and the mechanisms underlying these effects remain largely unknown. For this study, MG and GLOI levels were manipulated in colon cancer cells and the effects on their viability, proliferation, apoptosis, migration, and invasion in vitro were quantified by Cell Counting Kit-8, colony formation assay, flow cytometry, and transwell assays. The expression levels of STAT1 pathway-associated proteins and mRNAs in these cells were quantified by western blot and qRT-PCR, respectively. The antitumor effects of MG and silencing of GLOI were investigated in vivo in a SW620 colon cancer xenograft model in BALB/c nude mice. Our findings demonstrate that MG in combination with silencing of GLOI synergistically inhibited the cancer cells' proliferation, colony formation, migration, and invasion and induced apoptosis in vitro compared with the controls. Furthermore, these treatments up-regulated STAT1 and Bax while down-regulating Bcl-2 in vitro. MG treatment alone or in combination with silencing of GLOI also reduced the growth of the SW620 tumors in mice by up-regulation of STAT1 and Bax and down-regulation of Bcl-2. Taken together, our findings suggest that MG in combination with silencing of GLOI merits further evaluation as a targeted therapeutic strategy for colon cancer.
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#28902344 2017/09/13 Save this To Up
Insulin-like growth factor-1 promotes the proliferation and odontoblastic differentiation of human dental pulp cells under high glucose conditions.Insulin-like growth factor-1 (IGF-1) promotes human dental pulp stem cell proliferation and osteogenic differentiation. However, the effects of IGF-1 on the proliferation, apoptosis and odontoblastic differentiation (mineralization) of dental pulp cells (DPCs) under high glucose (GLU) conditions remain unclear. In this study, isolated primary human DPCs were treated with various concentrations of high GLU. Cell proliferation and apoptosis were determined by Cell Counting Kit-8 and Annexin V-FITC/PI assays, respectively. The cells were cultured in odontoblastic induction medium containing various concentrations of high GLU. Odontoblastic differentiation was determined by alkaline phosphatase (ALP) activity assay. Mineralization formation was evaluated by von Kossa staining. The expression levels of IGF family members were measured by western blot analysis and RT-qPCR during proliferation and differentiation. The cells were then exposed to 25 mM GLU and various concentrations of IGF-1. Cell proliferation, apoptosis, ALP activity, mineralization formation and the levels of mineralization-related proteins were then evaluated. Our results revealed that high GLU significantly inhibited cell proliferation and promoted cell apoptosis. GLU (25 and 50 mM) markedly reduced ALP activity and mineralization on days 7 and 14 after differentiation. The levels of IGF family members were markedly decreased by high GLU during proliferation and differentiation. However, IGF-1 significantly reversed the effects of high GLU on cell proliferation and apoptosis. Additionally, IGF-1 markedly restored the reduction of ALP activity and mineralization induced by high GLU. Our findings thus indicate that IGF-1 attenuates the high GLU-induced inhibition of DPC proliferation, differentiation and mineralization.
1828 related Products with: Insulin-like growth factor-1 promotes the proliferation and odontoblastic differentiation of human dental pulp cells under high glucose conditions.Epidermal Growth Factor ( Epidermal Growth Factor ( Growth Differentiation Fa Growth Differentiation Fa Human Insulin-like Growth Human Growth and Differen Human Growth and Differen Human Growth and Differen IGF-1R Signaling Phospho- Fibroblast Growth Factor Fibroblast Growth Factor Human Vascular Endothelia
#28893745 2017/09/12 Save this To Up
A new risk locus in CHCHD5 for hypertension and obesity in a Chinese child population: a cohort study.Coiled-coil-helix-coiled-coil-helix domain containing 5 (CHCHD5), a mitochondrial protein, is involved in the oxidative folding process in the mitochondrial intermembrane space. A previous study identified a hypertension-related single nucleotide polymorphism (SNP), rs3748024, in CHCHD5 in adults, but there are no reports regarding the association between CHCHD5 and obesity, which is a known risk factor for hypertension. The aim of the present study is to investigate the associations of the SNP rs3748024 with hypertension and obesity.
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#28870477 2017/09/05 Save this To Up
A low-protein, high-carbohydrate diet increases browning in perirenal adipose tissue but not in inguinal adipose tissue.The aim of this study was to evaluate the browning and origin of fatty acids (FAs) in the maintenance of triacylglycerol (TG) storage and/or as fuel for thermogenesis in perirenal adipose tissue (periWAT) and inguinal adipose tissue (ingWAT) of rats fed a low-protein, high-carbohydrate (LPHC) diet.
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#28858844 2017/08/31 Save this To Up
Can regular moderate exercise lead to changes in miRNA-146a and its adapter proteins in the kidney of streptozotocin-induced diabetic male rats?The aim of this study was to assess whether microRNA-146a and its adapter proteins TNF receptor associated factor6 (TRAF6) and interleukin-1 receptor-associated kinase-1 (IRAK1) may be changed in the kidney of streptozotocin-induced diabetic rats, following regular moderate exercise.
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#28854426 2017/08/30 Save this To Up
Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages.Type 2 diabetes is a persistent inflammatory response that impairs the healing process. We hypothesized that stimulation with high glucose following a pro-inflammatory signal would lead to autophagy inhibition, reactive oxygen species (ROS) production and eventually to the activation of the Nod-like receptor protein (NLRP) -3.
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#28848152 2017/08/29 Save this To Up
Effect of the Diabetic Environment On the Expression of MiRNAs in Endothelial Cells: Mir-149-5p Restoration Ameliorates the High Glucose-Induced Expression of TNF-α and ER Stress Markers.This study aimed to screen microRNAs and their corresponding target genes that are associated with vascular injury in type two diabetes mellitus (T2DM), investigate the effects of differentially expressed miRNAs and their target genes on high glucose-induced vascular injury and establish the mechanism underlying these effects.
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#28843827 2017/08/27 Save this To Up
PTPN21 protects PC12 cell against oxygen-glucose deprivation by activating cdk5 through ERK1/2 signaling pathway.PTPN21, a cytosolic non-receptor tyrosine phosphatase isolated from human skeletal muscle, was reported to promote neuronal survival. Nevertheless, it is not clear whether PTPN21 plays a role in hypoxia ischemia-induced neuronal injury. A proper understanding of the PTPN21 mechanism in neuron growth regulation is limited. In this study, we investigated the neuroprotective effects and potential mechanism of PTPN21 on oxygen glucose deprivation (OGD)-injured PC12 cells. The ischemic stroke model of PC12 cells was made by OGD for 2h, after transfection of the PTPN21 siRNA and pcDNA 3.1 PTPN21(+). Cell viability was tested using the MTT and CCK-8 assay. Apoptotic cells were estimated by Annexin V-FITC/PI staining and caspase-3 activity using the Caspase-3 Assay Kit; the PTPN21, cdk5, ERK1/2 and p-ERK1/2 levels were estimated by qRT-PCR and Western blot. We found that the PTPN21 markedly increased cell viability, inhibited apoptosis. We also found that PTPN21 inhibited caspase-3 activity and down-regulating the Bax/Bcl-2 ratio. Furthermore, the expression of cdk5 protein was up-regulated by PTPN21 by activating ERK1/2 signaling pathway. Finally, our results showed that cdk5 siRNA or ERK1/2 signaling inhibitor PD98059 attenuated the accelerative effect of pcDNA3.1 PTPN21(+) on cell proliferation and apoptosis in PC12 cells. In short, it appears that PTPN21 may protect the PC12 from ischemia injury by upregulating cdk5 via ERK1/2 signaling pathway.
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