Search results for: CellQuanti-MTT™ Cell Viability Assay Kits
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Angiopoietin-like protein 2 is an important facilitator of tumor proliferation, metastasis, angiogenesis and glycolysis in osteosarcoma.Solid tumors are often exposed to hypoxia. Hypoxia inducible factor (HIF-1α) upregulates numerous target genes associated with the malignant behavior of hypoxic cancer cells. Angiopoietin-like protein 2 (Angptl2), a member of the angiopoietin family, is a hypoxia-inducible gene. However, the role and potential mechanism of Angptl2, and the relationship between Angptl2 and hypoxia in osteosarcoma (OS) remain unclear. In this study, quantitative RT-PCR was performed to detect the levels of Angptl2 and HIF-1α, and western blot assay was performed to measure the expression of Angptl2, HIF-1α, CDK2, cyclin E1, P21, MMP2, MMP9, VEGFA, Ang II and HK2 in osteosarcoma cells and tissue. Subsequently, cell viability and cycle were analyzed using CCK-8 and flow cytometer assays. Cell migration, invasion and glycolysis were analyzed with Transwell, Scratch Test and glucose/lactic acid detection kits, respectively. Experiments were performed to value the effects of Angptl2 on the growth of osteosarcoma xenografts in mice. Immunofluorescent and immunohistochemistry staining were conducted to detect the expression of Ki-67 and Angptl2, respectively. The results demonstrated that Angptl2 was highly expressed in OS cells, which was induced by hypoxia (HIF-1α). Additionally, Angptl2 overexpression regulated cell proliferation, invasion, migration and G1 phase arrest in OS cells. Moreover, Angptl2 promoted OS tumor growth in vivo tumor xenografts. Angptl2 might enhance angiogenesis and glycolysis by promoting VEGFA, Ang II and HK2 both in vitro and in vivo. In conclusion, the present findings indicated that hypoxia-induced Angptl2 expression was independent of HIF-1α in hypoxic OS cells. Angptl2 might promote OS cell proliferation, metastasis, angiogenesis and glycolysis, which could be regarded as a favorable marker for predicting a long survival time in patients with OS.
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Selectively monitoring glutathione in human serum and growth-associated living cells using gold nanoclusters.Glutathione (GSH) plays a variety of vital functions in biological systems. Growth-associated change of GSH level in cells might be critical for cell survival and monitoring of GSH in living cells are of great significance for understanding the dynamic link between GSH and some diseases. In this work, chitason micelles templated gold nanoclusters (CM-Au NCs) emitting red fluorescence were prepared with a simple and rapid method, which shows interesting phenomenon of aggregation induced emission (AIE) affected by the size of the chitosan micelles. The unique CM-Au NCs can be used to develop turn-off fluorescent probe for detecting GSH in human serum and living cells based on the reverse process of AIE of CM-Au NCs, completely different from the principle of aggregation caused quenching (ACQ) effect, which can distinguish GSH from other biothiols (cysteine and homocysteine) and quantitatively detect GSH concentration of human serum in healthy people and cancer patients with high sensitivity. The practical application of fluorescent CM-Au NCs for cellular imaging and detecting GSH level indicates ultra-trace changes of GSH levels in normal and cancer cells could be monitored at different growth stages, which reveals that the levels of GSH in cancer cells was always higher than that of normal cells. Compared with commercial GSH assay kits for detection GSH in human serum and living cells, the proposed method was verified to be accuracy and precision. The results not only reflect the changes of GSH during cell growth at different stages, but also demonstrate the feasibility of reverse process of AIE of CM-Au NCs for detection GSH. This strategy would provide a platform to understand the dynamic link between GSH and disease to clarify the disease mechanism.
1089 related Products with: Selectively monitoring glutathione in human serum and growth-associated living cells using gold nanoclusters.Human Small Intestine Mic Epidermal Growth Factor ( Sterile filtered human se Human Insulin-like Growth Human Internal Mammary Ar Epidermal Growth Factor ( Goat Anti-Human Glutathio Human Insulin-like Growth Human interleukin 2(IL-2) Goat Anti-Human Fibroblas ELISA Human Serum Growth Human Large Intestine Mic
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Neuroprotection of miR-214 against isoflurane-induced neurotoxicity involves the PTEN/PI3K/Akt pathway in human neuroblastoma cell line SH-SY5Y.Isoflurane, one of the commonly used inhalation anesthetics worldwide in clinical practice, may generate substantial risks of neurotoxicity in the developing brains. The present study aimed to illustrate the effects and underlying mechanisms of miR-214 on isoflurane-induced neurotoxicity in human neuroblastoma cell line SH-SY5Y. SH-SY5Y cells were transfected with miR-214 or miR-con alone or in combination with pcDNA empty vector or pcDNA-PTEN in the presence of 3% isoflurane and incubated for 48 h. Cell viability, lactate dehydrogenase (LDH) release, apoptosis, and caspase-3/7 activity were evaluated using CCK-8, LDH release assay, flow cytometry analysis, and caspase-3/7 activity assay, respectively. The superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) activities were measured using commercial kits. miR-214 expression and alterations of the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway were detected by qRT-PCR and Western blot, respectively. The interaction between miR-214 and PTEN was explored by luciferase reporter assay. We found that isoflurane exposure induced neurotoxicity in SH-SY5Y cells, as evidenced by the reduced cell viability, increased LDH release, apoptotic rate, caspase-3/7 activity, and oxidative stress levels. Moreover, isoflurane exposure decreased the expression of miR-214 and affected the PTEN/PI3K/Akt pathway in SH-SY5Y cells. miR-214 overexpression significantly suppressed isoflurane-induced viability reduction, LDH release, apoptosis and oxidative stress, as well as inactivation of the PI3K/Akt pathway in SH-SY5Y cells. Interestingly, PTEN was identified as a target of miR-214. Moreover, PTEN upregulation blocked the effects of miR-214 on isoflurane-induced neurotoxicity in SH-SY5Y cells. In conclusion, miR-214 protected against isoflurane-induced neurotoxicity in SH-SY5Y cells via regulation of PI3K/Akt pathway by targeting PTEN, contributing to better understanding the underlying mechanisms of anesthetics-induce neurotoxicity.
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PINK1 depletion sensitizes non-small cell lung cancer to glycolytic inhibitor 3-bromopyruvate: Involvement of ROS and mitophagy.Despite significant strides in understanding the pathophysiology of non-small cell lung cancer (NSCLC), these neoplasms typically present with intrinsic chemo- and radiotherapeutic resistance. Transcriptomic analyses of patient NSCLC tumors stratified by survival times have identified the PTEN-induced putative kinase 1 (PINK1) as a molecular governor of tumor aggressiveness and patient survival time. PINK1 has been shown to confer neuroprotection in models of Parkinson Disease by ensuring proper mitochondrial turnover (mitophagy), the upkeep of ATP production and sequestering of reactive oxygen species (ROS).
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Protective mechanism of artemisinin on rat bone marrow-derived mesenchymal stem cells against apoptosis induced by hydrogen peroxide via activation of c-Raf-Erk1/2-p90-CREB pathway.Bone marrow-derived mesenchymal stem cell (BMSC) transplantation is one of the new therapeutic strategies for treating ischemic brain and heart tissues. However, the poor survival rate of transplanted BMSCs in ischemic tissue, due to high levels of reactive oxygen species (ROS), limits the therapeutic efficacy of this approach. Considering that BMSC survival may greatly enhance the effectiveness of transplantation therapy, development of effective therapeutics capable of mitigating oxidative stress-induced BMSC apoptosis is an important unmet clinical need.
1832 related Products with: Protective mechanism of artemisinin on rat bone marrow-derived mesenchymal stem cells against apoptosis induced by hydrogen peroxide via activation of c-Raf-Erk1/2-p90-CREB pathway.Rat Mesenchymal Stem Cell Rat Mesenchymal Cells 129 Mouse Embryonic Stem Stemez hN2 Human Neuron D ReadiUse™ hydrogen pero Multiple myeloma test tis Amplite™ Fluorimetric H Wnt Signaling Pathway TCF Normal bone marrow tissue ECOS™ 9-5 Competent Cel AP-1 Reporter – HEK293 Hydrogen peroxide 30% CAS
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Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88.Tetramethylpyrazine (TMP) has been reported to play a significant role in the cardiovascular and neuronal diseases. But, the functions of TMP in osteoarthritis (OA) remain unclear. In this investigation, we intended to probe the protective effectiveness of TMP in lipopolysaccharide (LPS)-caused damage in ATDC5 cells.
2018 related Products with: Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88.OxiSelect™ Cellular UV- Human Large Intestine Mic anti HSV (II) gB IgG1 (mo anti Transferrin receptor Jurkat Cell Extract (Indu GLP 1 ELISA Kit, Rat Gluc MarkerGeneTM in vivo lacZ Nile Red, A lipophilic dy Anti AGO2 Mouse, Monoclon Cold Fusion Cloning Kit w Human Epstein-Barr Virus superSf9-2 insect cells
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Fisetin, via CKIP-1/REGγ, limits oxidized LDL-induced lipid accumulation and senescence in RAW264.7 macrophage-derived foam cells.To test the hypothesis that the flavonoid compound, fisetin, protects macrophages from lipid accumulation and senescence through regulation of casein kinase 2-interacting protein-1 (CKIP-1)/REGγ (11S regulatory particles, 28 kDa proteasome activator, proteasome activator subunit 3) signaling. RAW264.7 macrophage cells were exposed to 100 μg/ml oxidized low-density lipoprotein (ox-LDL) with or without 20 μg/ml fisetin for 24 h. Cell viability was detected by CCK-8 after 1 h. Intracellular lipid accumulation was measured using Oil Red O staining. Total cholesterol (TC) and free cholesterol (FC) contents were measured using assay kits, and cell senescence was inferred by β-gal staining. Protein expression levels of CKIP-1, REGγ, organic cation transporter 1 (Oct-1), lectin-like oxidized LDL receptor-1 (LOX-1), tumor suppressor protein p53 (p53), cell cycle regulatory protein p21 (p21), and multiple tumor suppressor-1 (p16) were detected by immunofluorescence and confirmed by Western blot. Stimulating RAW264.7 macrophage cells with 100 μg/ml ox-LDL for 24 h induced the formation of foam cells, increased intracellular lipid accumulation, increased TC and FC content, and promoted cell senescence. Furthermore, cells induced with 100 μg/ml ox-LDL for 24 h showed decreased CKIP-1 and REGγ protein, while the expressions of Oct-1, LOX-1, p53, p21 and p16 were increased. In contrast, treatment with 20 μg/ml fisetin reversed 100 μg/ml ox-LDL effects to increase cell viability, and decrease β-gal staining, intracellular lipid levels and TC and FC levels. These beneficial effects were associated with increased CKIP-1 and REGγ and decreased Oct-1, LOX-1, p53, p21, and p16 protein expression. Results indicated that fisetin limited ox-LDL-mediated lipid accumulation and senescence in RAW264.7 macrophage-derived foam cells. The mechanism underlying these effects may involve regulation of CKIP-1/REGγ signaling.
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Targeted RNA-sequencing assays: a step forward compared to FISH and IHC techniques?ALK and ROS1 rearrangements are molecular targets of several tyrosine kinase inhibitors. RNA-sequencing approaches are regarded as the new standard for fusion gene detection, representing an alternative to standard immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) techniques.
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Curcumin attenuates hypoxia/reoxygenation‑induced myocardial injury.Curcumin (Cur) has been reported to function as an antioxidant and anti‑inflammatory agent and to play a role in anti‑atherosclerosis. The present study aimed to explore the protective effect of Cur on hypoxia/reoxygenation (H/R) injury. The morphological changes in H9c2 cardiomyocytes were observed under an inverted microscope. Cell viability was determined by Cell Counting Kit‑8 (CCK‑8). Lactate dehydrogenase (LDH) level, malondialdehyde (MDA) level and the antioxidant superoxide dismutase (SOD) activity were determined by corresponding kits. Apoptosis and reactive oxygen species (ROS) levels were determined by flow cytometry. Endoplasmic reticulum (ER) stress‑related factors, which were examined by quantitative real‑time polymerase chain reaction (qPCR) and western blot analysis, included 78‑kDa glucose‑regulated protein (GRP78) and C/EBP homologous protein (CHOP). Extracellular signal regulating kinase 1/2 (ERK1/2), p38, c‑Jun NH2‑terminal kinase (JNK) and the phosphorylation levels of key proteins in the mitogen‑activated protein kinase (MAPK) signaling pathway were all determined by western blot analysis. Compared to the control group, the cell morphology of the H9c2 cells was obviously altered upon H/R. Cell viability was significantly decreased, while apoptosis was significantly increased by H/R. We also observed that the levels of LDH and MDA were elevated and the activity of SOD was decreased in the H/R group. Notably, LDH, MDA and SOD levels were reversed following treatment with Cur; while apoptosis and ROS levels in the H/R injury group were decreased by Cur. H/R injury‑triggered ER stress and the MAPK signaling pathway were suppressed by Cur. These results demonstrated that Cur has a protective effect on cardiomyocytes via suppression of ER stress and the MAPK pathway.
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LncRNA ROR is involved in cerebral hypoxia/reoxygenation-induced injury in PC12 cells via regulating miR-135a-5p/ROCK1/2.Ischemic stroke is a common cerebrovascular disease with high morbidity, disability and mortality. LncRNAs were involved in ischemia/reperfusion injury. The present study aims to investigate whether lncRNA ROR can promote the cerebral hypoxia/reoxygenation (H/R) injury in vitro, a cellular model of cerebral ischemia/reperfusion injury, through inhibiting the expression of miR-135a-5p or upregulating the expression of ROCK1 and ROCK2. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the lncRNA ROR expression in PC12 cells induced by H/R and verify the transfection effect. ROS, LDH, SOD and MDA levels were detected by respective kits. CCK-8 assay and flow cytometry analysis respectively detected the cell viability and cell apoptosis. Western blot analysis was to analyze the expression of apoptosis-related proteins (Bcl-2, Bax and cleaved caspase3). Immunofluorescent staining detected the ROCK1/2 expression. As a result, lncRNA ROR expression was increased in the PC12 cells induced by H/R. LncRNA ROR overexpression could aggravate injury of PC12 cells induced by H/R. And, lncRNA ROR overexpression could decrease viability and promote apoptosis of PC12 cells induced by H/R. In addition, miR-135a-5p was demonstrated to be a target of lncRNA ROR and lncRNA ROR improved H/R injury in PC12 cells by up-regulating the expression of miR-135a-5p via down-regulating ROCK1/2 expression. In conclusion, this study indicated that lncRNA ROR could promote the cerebral H/R injury by inhibiting the expression of miR-135a-5p or upregulating the expression of ROCK1/2. And, miR-135a-5p overexpression could improve the cerebral H/R injury by inhibiting the expression of ROCK1/2.
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