scholarly journals Proanthocyanidins Attenuation of H2O2-Induced Oxidative Damage in Tendon-Derived Stem Cells via Upregulating Nrf-2 Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Wenshuang Sun ◽  
Jia Meng ◽  
Zhenheng Wang ◽  
Tao Yuan ◽  
Hong Qian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Oxidative Damage ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Cell Counting ◽  
Sprague Dawley ◽  
Isolated Cells ◽  
Flow Cytometry Assay ◽  
Significant Difference ◽  
Protein Expressions

Proanthocyanidins (PCs) have shown inhibition of oxidative damage by improving Nrf-2 expression in many tissues. However, the cytoprotective effects of PCs on H2O2-induced tendon damage have not been verified. The current study was aimed at assessing the cytoprotection of PCs on the oxidative cellular toxicity of tendon-derived stem cells (TDSCs) induced by H2O2. The TDSCs were isolated from patellar tendons of Sprague Dawley (SD) rats, and the cells after third passage were used for subsequent experiments. The isolated cells were identified by flow cytometry assay and multidifferentiation potential assay. Cell Counting Kit-8 assay was performed to examine cell viability. Real-Time PCR and Western Blot were employed to, respectively, assess the mRNA and protein expressions of Nrf-2, GCLM, NQO-1, and HO-1. PCs significantly improved the cell viability of TDSCs. Furthermore, H2O2 upregulated Nrf-2, GCLM, NQO-1, and HO-1 without significant difference, while the proteins expressions were increased with significant difference in PCs group and PCs + H2O2 cotreated group. All the findings indicated that PCs could protect against the oxidative damage induced by H2O2 in TDSCs, and the cytoprotective effects might be due to the ability of PCs to activate the expressions of GCLM, HO-1, and NQO-1 via upregulating Nrf-2 signaling pathway.

ALK7 Inhibition Protects Osteoblast Cells Against High Glucose-induced ROS Production via Nrf2/HO-1 Signaling Pathway

2021 ◽  
Vol 21 ◽  
Author(s):  
Zhen Zhao ◽  
Yu Lu ◽  
Huan Wang ◽  
Xiang Gu ◽  
Luting Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Signaling Pathway ◽  
High Glucose ◽  
Collagen I ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
Ros Production ◽  
Alizarin Red

Background: Some studies demonstrated that under high-glucose (HG) condition, osteoblasts develop oxidative stress, which will impair their normal functions. The effects of activin receptor-like kinase 7 (ALK7) silencing on HG-induced osteoblasts remained unclear. Objective: The aim of this study was to explore the effect of ALK7 on HG-induced osteoblasts. Methods: MC3T3-E1 cells were treated with different concentrations of HG (0, 50, 100, 200 and 300mg/dL), and the cell viability was detected using cell counting kit-8 (CCK-8). HG-treated MC3T3-E1 cells were transfected with siALK7 or ALK7 overexpression plasmid or siNrf2, and then the viability and apoptosis were detected by CCK-8 and flow cytometry. The levels of reactive oxygen species (ROS), collagen I and calcification nodule were determined by oxidative stress kits, Enzyme-linked immunosorbent assay and Alizarin red staining. The expressions of NF-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and osteoblast-associated genes were determined by quantitative real-time PCR (qRT-PCR) and Western blot. Results: Cell viability was reduced with HG treatment. Silencing ALK7 inhibited the effect of HG on increasing cell apoptosis and ROS production, reduced cell viability, mineralized nodules, and downregulated collagen I and osteoblast-associated genes expression in MC3T3-E1 cells. ALK7 silencing activated the Nrf2/HO-1 signaling pathway by affecting expressions of HO-1 and Nrf2. ALK7 overexpression had the opposite effects. In addition, siNrf2 partially reversed the effects of ALK7 silencing on HG-induced MC3T3-E1 cells. Conclusion: ALK7 silencing protected osteoblasts under HG condition possibly through activating the Nrf2/HO-1 pathway.

scholarly journals Yunnan Baiyao Conditioned Medium Promotes the Odonto/Osteogenic Capacity of Stem Cells from Apical Papilla via Nuclear Factor Kappa B Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xiyao Pang ◽  
Yanqiu Wang ◽  
Jintao Wu ◽  
Zhou Zhou ◽  
Tao Xu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Alkaline Phosphatase ◽  
Osteogenic Differentiation ◽  
Conditioned Medium ◽  
Signaling Pathway ◽  
Cell Counting ◽  
Dependent Manner ◽  
Alizarin Red ◽  
Apical Papilla ◽  
Yunnan Baiyao

Yunnan Baiyao is a traditional Chinese herbal remedy that has long been used for its characteristics of wound healing, bone regeneration, and anti-inflammation. However, the effects of Yunnan Baiyao on the odonto/osteogenic differentiation of stem cells from apical papilla (SCAPs) and the potential mechanisms remain unclear. The aim of this study was to investigate the odonto/osteogenic differentiation effects of Yunnan Baiyao on SCAPs and the underlying mechanisms involved. SCAPs were isolated and cocultured with Yunnan Baiyao conditioned media. The proliferation ability was determined by cell counting kit 8 and flow cytometry. The differentiation capacity and the involvement of NF-κB pathway were investigated by alkaline phosphatase assay, alizarin red staining, immunofluorescence assay, real-time RT-PCR, and western blot analyses. Yunnan Baiyao conditioned medium at the concentration of 50 μg/mL upregulated alkaline phosphatase activity, induced more mineralized nodules, and increased the expression of odonto/osteogenic genes/proteins (e.g., OCN/OCN, OPN/OPN, OSX/OSX, RUNX2/RUNX2, ALP/ALP, COL-I/COL-I, DMP1, DSP/DSPP) of SCAPs. In addition, the expression of cytoplasmic phos-IκBα, phos-P65, and nuclear P65 was significantly increased in Yunnan Baiyao conditioned medium treated SCAPs in a time-dependent manner. Conversely, the differentiation of Yunnan Baiyao conditioned medium treated SCAPs was obviously inhibited when these stem cells were cocultured with the specific NF-κB inhibitor BMS345541. Yunnan Baiyao can promote the odonto/osteogenic differentiation of SCAPs via the NF-κB signaling pathway.

scholarly journals Effect of Manitoba-Grown Red-Osier Dogwood Extracts on Recovering Caco-2 Cells from H2O2-Induced Oxidative Damage

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 250 ◽  
Author(s):  
Runqiang Yang ◽  
Qianru Hui ◽  
Qian Jiang ◽  
Shangxi Liu ◽  
Hua Zhang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Cell Viability ◽  
Native Species ◽  
Mrna Level ◽  
Damage Model ◽  
Fluorescein Isothiocyanate ◽  
Flowering Plant ◽  
Feed Additive ◽  
Protein Expressions ◽  
Antioxidative Effects

Red-osier dogwood, a native species of flowering plant in North America, has been reported to have anti-oxidative properties because of abundant phenolic compounds; this could be promising as a functional food or a feed additive. In the present study, an oxidative damage model using 1.0 mM hydrogen peroxide (H2O2) in Caco-2 cells was established to evaluate the antioxidative effects of red-osier dogwood extracts (RDE). The results showed that 1.0 mM H2O2 pre-exposure for 3 h significantly decreased cell viability, and increased interleukin 8 (IL-8) secretion and the intracellular reactive oxygen species (ROS) level. Caco-2 cells were treated with 100 µg/mL RDE for 24 h after pre-exposure to H2O2. It was found that the decreased cell viability caused by H2O2 was significantly restored by a subsequent 100 µg/mL RDE treatment. Furthermore, the IL-8 secretion and ROS level were significantly blocked by RDE, accompanied by the enhanced gene expression of hemeoxygenase-1 (HO-1), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), and the enhanced protein expression of the nuclear factor (erythroid-derived 2)-like 2 (Nrf-2). Moreover, RDE improved barrier functions in Caco-2 cells. Using RDE reduced the diffusion of fluorescein isothiocyanate (FITC)-dextran and increased the transepithelial resistance (TEER) value. The relative mRNA level of tight junction claudin-1, claudin-3, and occludin was elevated by RDE. These extracts also repaired the integrity of zonula occludens-1 (ZO-1) damaged by H2O2 and increased the protein expressions of ZO-1 and claudin-3 in the H2O2-pretreated cells. These results illustrated that RDE reduced the ROS level and enhanced the barrier function in oxidative-damaged epithelial cells.

Normoxic ventilatory resuscitation following controlled cortical impact reduces peroxynitrite-mediated protein nitration in the hippocampus

2008 ◽  
Vol 108 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Edward S. Ahn ◽  
Courtney L. Robertson ◽  
Viktoria Vereczki ◽  
Gloria E. Hoffman ◽  
Gary Fiskum
Keyword(s):  
Oxidative Damage ◽  
Sprague Dawley ◽  
Controlled Cortical Impact ◽  
Neuronal Nuclei ◽  
Ca1 Region ◽  
Significant Difference ◽  
Cortical Impact ◽  
Fraction Of Inspired Oxygen ◽  
Oxidative Damage To Proteins ◽  
Hyperoxic Ventilation

Object Ventilatory resuscitation with 100% O2 after severe traumatic brain injury (TBI) raises concerns about the increased production of reactive oxygen species (ROS). The product of peroxynitrite-meditated tyrosine residue nitration, 3-nitrotyrosine (3-NT), is a marker for oxidative damage to proteins. The authors hypothesized that posttraumatic resuscitation with hyperoxia (100% fraction of inspired oxygen [FiO2] concentration) results in increased ROS-induced damage to proteins compared with resuscitation using normoxia (21% FiO2 concentration). Methods Male Sprague–Dawley rats underwent controlled cortical impact (CCI) injury and resuscitation with either normoxic or hyperoxic ventilation for 1 hour (5 rats per group). Twenty-four hours after injury, rat hippocampi were evaluated using 3-NT immunostaining. In a second experiment, animals similarly underwent CCI injury and normoxic or hyperoxic ventilation for 1 hour (4 rats per group). One week after injury, neuronal counts were performed after neuronal nuclei immunostaining. Results The 3-NT staining was significantly increased in the hippocampi of the hyperoxic group. The normoxic group showed a 51.0% reduction of staining in the CA1 region compared with the hyperoxic group and a 50.8% reduction in the CA3 region (p < 0.05, both regions). There was no significant difference in staining between the injured normoxic group and sham-operated control groups. In the delayed analysis of neuronal survival (neuronal counts), there was no significant difference between the hyperoxic and normoxic groups. Conclusions In this clinically relevant model of TBI, normoxic resuscitation significantly reduced oxidative damage to proteins compared with hyperoxic resuscitation. Neuronal counts showed no benefit from hyperoxic resuscitation. These findings indicate that hyperoxic ventilation in the early stages after severe TBI may exacerbate oxidative damage to proteins.

scholarly journals Implantation of Autologous Stem Cells Derived from Adipose Tissue in Rat Bone Fractures

2018 ◽  
Vol 1 (2) ◽  
pp. 105-115
Author(s):  
Carolina Smok ◽  
Manuel Meruane ◽  
Mariana Rojas
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Bone Regeneration ◽  
Bone Fractures ◽  
Control Group ◽  
Vascular Density ◽  
Major Advance ◽  
Sprague Dawley ◽  
Angiogenic Growth Factors ◽  
Significant Difference

Stem cells derived from adipose tissue (ASCs) correspond to a major advance with respect to the bone regenerative medicine, as they have the ability for self-renewal, differentiation and paracrine stimulation to various types of tissues including bone and cartilage. The hypothesis of this study considers that fractures treated with ASCs, time decreases bone regeneration and vascularization increases, aiming to histologically evaluate bone regeneration and vascularization in these fractures. To accomplish this, 24 young male Sprague Dawley rats were used. The specimens were divided into two groups: Group A (treated) and group B (control). In both groups, the rats were euthanized at 11 and 21 days post-fracture. Statistically significant difference was observed in the number of newly formed trabeculae and vascular density in the treated group compared to control group concluded that rats treated with ASCs have a higher rate and better angiogenic bone regeneration, especially given the ability to synthesize components of the extracellular matrix of these cell, and the production of angiogenic growth factors.

scholarly journals Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy through inhibiting NF-κB activation

2020 ◽  
Author(s):  
Min Han ◽  
Xiao-Cui Chen ◽  
Ming-Hui Sun ◽  
Min-Tao Gai ◽  
Yi-Ning Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Western Blot ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Neonatal Rat ◽  
Cell Counting ◽  
Pyrrolidine Dithiocarbamate ◽  
Induced Apoptosis

Abstract Background: Inflammation and oxidative stress play a predominant role in the initiation and progression of ischemia/reperfusion (I/R) injury, of which nuclear factor kappa B (NF-κB) is a crucial mediator. Overexpression of the inhibitor of κB alpha (IκBα) gene is hypothesized to have protective effects against apoptosis and autophagy in cardiomyocytes subjected to hydrogen peroxide (H2O2) through inhibiting the NF-κB pathway.Methods: The IκBαS32A, S36A gene was transfected via adeno-associated virus serotype 9 (AAV9) delivery into neonatal rat ventricular cardiomyocytes (NRVMs) prior to H2O2 treatment. NRVMs were divided into control, H2O2, GFP +H2O2, IκBα+H2O2, and pyrrolidine dithiocarbamate (PDTC)+H2O2 groups. Nuclear translocation of NF-κB p65 subunit was evaluated by immunofluorescence and Western blot. Cell viability was assessed by Cell Counting Kit-8 assay. Supernatant lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA) were measured to identify H2O2-stimulated cytotoxicity. Apoptosis was determined by Annexin V-PE/7-AAD staining, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. Western blot was used to detect apoptosis- and autophagy-related proteins.Results: IκBα transfection significantly increased cell viability and ΔΨm, but decreased the supernatant LDH and cellular MDA levels in cardiomyocytes exposed to H2O2. Meanwhile, IκBα overexpression decreased H2O2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-Ⅱ/LC3-Ⅰ ratio. These effects partly accounted for the ability of IκBα to inhibit the NF-κB signaling pathway, as evidenced by decreases in p65 phosphorylation and nuclear translocation. Indeed, the effects of inactivation of NF-κB signaling with the specific inhibitor, PDTC, resembled the cardioprotective effects of IκBα during H2O2 stimulation.Conclusion: IκBα overexpression can ameliorate H2O2-induced apoptosis, autophagy, oxidative injury, and ΔΨm loss through inhibition of the NF-κB signaling pathway. These findings suggest that IκBα transfection can successfully resist oxidative stress-induced damage through inhibiting NF-κB activation, which may provide a potential therapeutic target for prevention of myocardial I/R injury.

Kaempferol reversals retinal ischemia/reperfusion (IR) injury through activating of PI3K/Akt/mTOR signaling pathway

2021 ◽  
Author(s):  
Da Sun ◽  
Fusheng Shang ◽  
Dagui Chen ◽  
Wenwen Wang ◽  
lili lin
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Ischemia Reperfusion ◽  
Retinal Ischemia ◽  
Mtor Signaling ◽  
Cell Counting ◽  
Mtor Signaling Pathway ◽  
Autophagy Gene ◽  
Retinal Vascular Occlusion

Abstract Purpose Retinal ischemia/reperfusion (IR) injury is associated with many ocular diseases, including acute glaucoma, diabetic retinopathy, and retinal vascular occlusion. However, currently there are no effective medications to prevent the development ofretinal IR injury.Kaempferol is a kind of plant extract which has showed an excellent ability to inhibit the inflammation.. Materials and Methods In this study, both in vitro and in vivo retinaloxidative damage models were established.Cell viability was assessed by Cell Counting Kit-8 assay. Apoptosis was examined using flow cytometry analysis.Atherosclerotic lesion analysis was performed using hematoxylin-eosin staining,The expressions of Inflammatory cytokines were detected by quantitative real-time PCR and ELISA respectively.The effect of expression of apoptosis、utophagy and the PI3K/Akt/mTOR signaling pathway related pathway was evaluated by Western blot. Results We found kaempferol was able to protect the viability of ARPE-19 cells against oxidative damage by reducing its apoptosis. In addition, it also kept structurally complete epithelium, stroma and endothelium of cornea after oxidative damage. Moreover, it also able to reduce the expression of inflammatory cytokines and increased the expression of anti-inflammatory cytokines.Kaempferol was able to enhanced the expression of anti-apoptotic genes BCL-2, and reduced the expression of autophagy gene Beclin 1 and increased the expression of anti-autophagy gene LC-3,was also able to enhance the expression PI3K and the phosphorylation ofAkt andmTOR. Conclusion Kaempferolreversals retinal ischemia/reperfusion (IR) injury through activating of PI3K/Akt/mTOR signaling pathway.

scholarly journals Cannabinoid receptor 2 deletion deteriorates myocardial infarction through the down-regulation of AMPK-mTOR-p70S6K signaling-mediated autophagy

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Yao Hu ◽  
Yu Tao ◽  
Jing Hu
Keyword(s):  
Myocardial Infarction ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Cannabinoid Receptor ◽  
Cell Counting ◽  
Protective Effects ◽  
Cannabinoid Receptor 2 ◽  
Related Proteins

AbstractCannabinoid receptor 2 (CB2R) has been reported to play an important role in the regulation of pathogenesis and progression of myocardial infarction (MI). Here we tried to investigate its potential mechanisms. The ratio of infarct size in heart issue was detected by TTC staining, and cardiac functions were calculated according to echocardiographic evaluation. Cell viability in cardiomyocytes was investigated by Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays. Western blot was used to detect autophagy-related proteins including Beclin-1, LC3, p62, adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK)-mammalian target of rapamycin rabbit (mTOR)-p70 ribosomal protein S6 kinase (p70S6K) signaling-related proteins including AMPK, mTOR, p70S6K, and their phosphorylation formation. Rapamycin was used for the induction of autophagy. Cleaved caspase-3 and Bax were detected for analyzing apoptosis. TEM was used for the detection of autophagosomes. We found that CB2R deletion (CB2R KO) largely deteriorated the severity of MI and the cardiac function as well as cell viability of cardiomyocytes. Knocking out CB2R decreased the level of autophagy in heart issues from MI mice as well as cardiomyocytes under oxygen-glucose deprivation (OGD). Furthermore, CB2R dysfunction significantly attenuated the cardiac protective effects of rapamycin both in vivo and in vitro. Finally, we found that CB2R-mediated autophagy was induced by AMPK-mTOR-p70S6K signaling pathway. Our current study demonstrated for the first time that CB2R deletion led to a detrimental effect of MI through the dysfunction of AMPK-mTOR-p70S6K signaling pathway, which might provide a novel insight in the treatment of MI.

scholarly journals NELL-1 Increased the Osteogenic Differentiation and mRNA Expression of Spheroids Composed of Stem Cells

Medicina ◽  
2021 ◽  
Vol 57 (6) ◽  
pp. 586
Author(s):  
Jong-Ho Lee ◽  
Young-Min Song ◽  
Sae-Kyung Min ◽  
Hyun-Jin Lee ◽  
Hye-Lim Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
Alkaline Phosphatase ◽  
Stem Cell ◽  
Cell Viability ◽  
Osteogenic Differentiation ◽  
Mrna Expression ◽  
Cell Counting ◽  
Calcium Deposition ◽  
Anthraquinone Dye ◽  
Cell Spheroids

Background and objectives: NELL-1 is a competent growth factor and it reported to target cells committed to the osteochondral lineage. The secreted, osteoinductive glycoproteins are reported to rheostatically control skeletal ossification. This study was performed to determine the effects of NELL-1 on spheroid morphology and cell viability and the promotion of osteogenic differentiation of stem cell spheroids. Materials and Methods: Cultures of stem cell spheroids of gingiva-derived stem cells were grown in the presence of NELL-1 at concentrations of 1, 10, 100, and 500 ng/mL. Evaluations of cell morphology were performed using a microscope, and cell viability was assessed using a two-color assay and Cell Counting Kit-8. Evaluation of the activity of alkaline phosphatase and calcium deposition assays involved anthraquinone dye assay to determine the level of osteogenic differentiation of cell spheroids treated with NELL-1. Real-time quantitative polymerase chain reaction (qPCR) was used to evaluate the expressions of RUNX2, BSP, OCN, COL1A1, and β-actin mRNAs. Results: The applied stem cells produced well-formed spheroids, and the addition of NELL-1 at tested concentrations did not show any apparent changes in spheroid shape. There were no significant changes in diameter with addition of NELL-1 at 0, 1, 10, 100, and 500 ng/mL concentrations. The quantitative cell viability results derived on Days 1, 3, and 7 did not show significant disparities among groups (p > 0.05). There was statistically higher alkaline phosphatase activity in the 10 ng/mL group compared with the unloaded control on Day 7 (p < 0.05). A significant increase in anthraquinone dye staining was observed with the addition of NELL-1, and the highest value was noted at 10 ng/mL (p < 0.05). qPCR results demonstrated that the mRNA expression levels of RUNX2 and BSP were significantly increased when NELL-1 was added to the culture. Conclusions: Based on these findings, we conclude that NELL-1 can be applied for increased osteogenic differentiation of stem cell spheroids.

scholarly journals Suppressive Effect of α-mangostin for Cancer Stem Cells in Colorectal Cancer via the Notch Pathway

2021 ◽  
Author(s):  
Min Kyoung Jo ◽  
Chang Mo Moon ◽  
Eun Ju Kim ◽  
Jee Hee Kwan ◽  
Xiang Fei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Flow Cytometry ◽  
Cancer Stem Cells ◽  
Cell Viability ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Suppressive Effect ◽  
Notch Signaling Pathway ◽  
Dependent Manner

Abstract Background: Since colon cancer stem cells (CSCs) play an important role in chemoresistance and in tumor recurrence and metastasis, targeting of CSCs has emerged as a sophisticated strategy for cancer therapy. α-mangostin (αM) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of αM on CSCs in colorectal cancer (CRC) and the suppressive effect on 5-fluorouracil (5-FU)-induced CSCs. Methods: The cell viability assay was performed to determine the optimal concentration of αM. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the αM-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of αM on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of αM in combination with 5-FU was investigated using a xenograft mouse model. Results: αM inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. αM treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. αM markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, αM attenuated CSC markers CD44 and CD133, in a manner similar to that upon DAPT treatment, in HT29 cells. In xenograft mice, the tumor and CSC makers were suppressed in the αM group and in the αM group with 5-FU treatment. Conclusion: This study shows that low-dose αM inhibits CSCs in CRC and suppresses 5-FU–induced augmentation of CSCs via the Notch signaling pathway.

Sign in / Sign up

Export Citation Format

Share Document