Effects of drinking desalinated seawater on cell viability and proliferation

Desalination of seawater is becoming an important means to address the increasing scarcity of freshwater resources in the world. Seawater has been used as drinking water in the health, food, and medical fields and various beneficial effects have been suggested, although not confirmed. Given the presence of 63 minerals and trace elements in drinking desalinated seawater (63 DSW), we evaluated their effects on the behavior of tumorigenic and nontumorigenic cells through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and annexin-V-fluorescein isothiocyanate/propidium iodide staining. Our results showed that cell viability and proliferation in the presence of 63 DSW were significantly greater than in mineral water and in the presence of fetal bovine serum in a dose-dependent manner. Furthermore, 63 DSW showed no toxic effect on murine embryonic fibroblast (NIH-3T3) and murine melanoma (B16-F10) cells. In another assay, we also showed that pre-treatment of non-adherent THP-1 cells with 63 DSW reduces apoptosis incidence, suggesting a protective effect against cell death. We conclude that cell viability and proliferation were improved by the mineral components of 63 DSW and this effect can guide further studies on health effects associated with DSW consumption.

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The Olive Leaves Extract Has Anti-Tumor Effects against Neuroblastoma through Inhibition of Cell Proliferation and Induction of Apoptosis

Nutrients ◽

10.3390/nu13072178 ◽

2021 ◽

Vol 13 (7) ◽

pp. 2178

Author(s):

Fabio Morandi ◽

Veronica Bensa ◽

Enzo Calarco ◽

Fabio Pastorino ◽

Patrizia Perri ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Cell Viability ◽

Cell Cycle Progression ◽

Treatment Strategies ◽

Annexin V ◽

Dependent Manner ◽

Induction Of Apoptosis ◽

Dose Dependent

Neuroblastoma (NB) is the most common extra-cranial solid tumor of pediatric age. The prognosis for high-risk NB patients remains poor, and new treatment strategies are desirable. The olive leaf extract (OLE) is constituted by phenolic compounds, whose health beneficial effects were reported. Here, the anti-tumor effects of OLE were investigated in vitro on a panel of NB cell lines in terms of (i) reduction of cell viability; (ii) inhibition of cell proliferation through cell cycle arrest; (iii) induction of apoptosis; and (iv) inhibition of cell migration. Furthermore, cytotoxicity experiments, by combining OLE with the chemotherapeutic topotecan, were also performed. OLE reduced the cell viability of NB cells in a time- and dose-dependent manner in 2D and 3D models. NB cells exposed to OLE underwent inhibition of cell proliferation, which was characterized by an arrest of the cell cycle progression in G0/G1 phase and by the accumulation of cells in the sub-G0 phase, which is peculiar of apoptotic death. This was confirmed by a dose-dependent increase of Annexin V+ cells (peculiar of apoptosis) and upregulation of caspases 3 and 7 protein levels. Moreover, OLE inhibited the migration of NB cells. Finally, the anti-tumor efficacy of the chemotherapeutic topotecan, in terms of cell viability reduction, was greatly enhanced by its combination with OLE. In conclusion, OLE has anti-tumor activity against NB by inhibiting cell proliferation and migration and by inducing apoptosis.

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SAT0363 DELPHINIDIN DOSE-DEPENDENTLY DIMINISHES PERIPHERAL IL-17 AND IFN-Γ PRODUCING LYMPHOCYTES IN PSORIATIC ARTHRITIS

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.4147 ◽

2020 ◽

Vol 79 (Suppl 1) ◽

pp. 1128.1-1129

Author(s):

A. Mavropoulos ◽

S. Tsiogkas ◽

D. Skyvalidas ◽

C. Liaskos ◽

A. Roussaki-Schulze ◽

...

Keyword(s):

Psoriatic Arthritis ◽

Cell Viability ◽

Annexin V ◽

Nkt Cells ◽

Inhibitory Effect ◽

Dependent Manner ◽

Research Support ◽

Research Activities ◽

Ifn Γ

Background:Delphinidin, a dietary anthocyanidin and powerful anti-oxidant from pigmented fruits and vegetables, has broad anti-inflammatory properties. In a human skin model of psoriasis, delphinidin reduced expression of proliferative and inflammatory markers (1).Objectives:The rationale of our study was to assess whether delphinidin can in vitro suppress IL-17 and IFN-γ production in peripheral blood mononuclear cell (PBMC) subsets from patients with psoriatic arthritis (PsA).Methods:PBMCs were obtained from 24 patients with PsA attending the outpatient clinic of the Department of Rheumatology/clinical Immunology at the University General Hospital of Larissa, Greece. 16 age- and sex-matched healthy volunteers were also included in the study. Delphinidin was supplemented at a concentration ranging from 1 to 50μg/ml, one hour prior to cell stimulation. Cell viability (Annexin V staining) and innate/adaptive lymphocyte subpopulations were assessed by flow cytometry with a panel of fluorochrome-conjugated antibodies against CD56, CD3, CD4 and CD8. Intracellular expression of IL-17 and IFN-γ was measured following PMA/ionomycin stimulation for 5 hours using standard cell permeabilization protocols and monoclonal antibodies against IL-17 and IFN-γResults:Delphinidin at concentration ≥10 μg/ml sharply diminished IL-17-production by CD4(+) T cells (Th17) and CD56(+)CD3(+) (NKT) cells from patients with psoriatic arthritis and normal controls (p≤0.05). IFN-γ producing T (CD4 and CD8) cells, as well as NK and NKT cells were also dose-dependently suppressed following delphinidin pre-incubation in both patients and healthy controls. Inhibition of IFN-γ(+) cells ranged from 27 to 69% and peaked at delphinidin concentration 20-50μg/ml. The inhibitory effect of delphinidin on IL-17 and IFN-γ producing lymphocytes was not due to compromised cell viability, as assessed by annexin V binding.Conclusion:Delphinidin exerts, in a dose-dependent manner, a profound in vitro inhibitory effect on T cell and NKT cell IL-17 and IFN-γ production in PsA, and therefore, it may be used as a dietary immunosuppressant, complementary to standard treatment.References:[1]Chamcheu JC Skin Pharmacol Physiol. 2015;28(4):177-88. doi: 10.1159/000368445Disclosure of Interests:ATHANASIOS MAVROPOULOS: None declared, Sotirios Tsiogkas: None declared, Dimitrios Skyvalidas: None declared, Christos Liaskos: None declared, Aggeliki Roussaki-Schulze Grant/research support from: Received a grant to support the educational and research activities of the department from Genesis Pharma (2018), Speakers bureau: Received honoraria from Genesis Pharma and Janssen(2017) and from Roche and Pharmaserve Lilly(2018), Efterpi Zafiriou Speakers bureau: Received honoraria from Genesis Pharma, Abbvie, Novartis, Roche, Jansses(2017) and Novartis, Abbvie(2018), Dimitrios Bogdanos: None declared, Lazaros Sakkas Grant/research support from: Received a grant to support the educational and research activities of the department from Bristol-Meyers Squib, Speakers bureau: Received honoraria from Actellion(2018), Janssen(2017), Novartis(2017), Sanofi-Aventis(2018), Abbvie(2017) and Roche(2017)

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Evaluation effects of Quercetin on streptozotocin-treated RINm5F pancreatic β-cells in vitro

Current Chemical Biology ◽

10.2174/2212796816666211223101206 ◽

2021 ◽

Vol 16 ◽

Author(s):

Maryam Mazraesefidi ◽

Maryam Mohammad Sadeghipour ◽

Hossein Khorramdelazad ◽

Mahdi Mahmoodi ◽

Alireza Khoshdel ◽

...

Keyword(s):

Cell Viability ◽

Insulin Content ◽

Β Cells ◽

Simultaneous Treatment ◽

Beneficial Effects ◽

Naturally Occurring ◽

Low Toxicity ◽

Pre Treatment ◽

Glucose Stimulated Insulin Secretion

Background and objectives: Quercetin is a naturally occurring phenolic compound abundantly present in plants as a secondary metabolite. The purpose of this study was to investigate the effect of quercetin on improving RINm5F β-insulinemia cell viability, glucose-stimulated insulin secretion (GSIS), and cell insulin content in the presence or absence of streptozotocin (STZ). Methods: This experimental study was conducted on RINm5F β-insulinemia cell line. The cell viability was evaluated by MTT assay. The necrosis was confirmed by flowcytometry and insulin ELISA kit was used to measure the GSIS level and cell insulin content. It should be noted that for testing of cells by 50μM of quercetin, simultaneous treatment and pre-treatment of quercetin were performed in the presence of STZ (20mM). Results: The quercetin was able to improve the viability of RINm5F cells in the presence of STZ and to increase the GSIS level and cell insulin content under STZ and glucotoxic conditions Conclusion: The quercetin seems to have beneficial effects on β-cells, especially the synthesis and secretion of insulin. In addition to the therapeutic effect, given the low toxicity of this flavonoid and the results of this study, the quercetin as a preventive agent may play an important role in maintaining the health of β-cells in people at risk of diabetes.

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Benzo(a)pyrene, an Active Product of Cigarette Smoke, Role in PLA2 Isoforms Activation in Colon Cancer

Journal of Global Oncology ◽

10.1200/jgo.18.79801 ◽

2018 ◽

Vol 4 (Supplement 2) ◽

pp. 193s-193s

Author(s):

S. Sharma ◽

S. Yadav ◽

S. Rana ◽

P. Avti ◽

K.L. Khanduja

Keyword(s):

Colon Cancer ◽

Cell Viability ◽

Cigarette Smoke ◽

Membrane Integrity ◽

Annexin V ◽

Cell Types ◽

Ros Generation ◽

Dependent Manner ◽

Colon Cells ◽

Ht 29

Background and aim: One of the active combustion product of cigarette smoke, Benzo[a]pyrenes, role in pulmonary cancer is clearly understood. However, its role in gastrointestinal cancer including colon cancer is not clearly understood. Methods: In this study, benzo(a)pyrenes was treated to colon cells to evaluate its role in cell viability, cellular ROS, and gene expression of various PLA2 isoforms was evaluated by FACS and PCR. The identified PLA2 was silenced at the gene level to evaluate its role in cell viability and ROS generation. Results: B(a)P treatment at 1 µg/mL for 48 h to HCT-15 male colon cells significantly reduced the cell viability without affecting HT-29 female colon cells. Higher doses and longer treatment duration with B(a)P showed that female colon cells were highly sensitive than male colon cells. Annexin-V/PI staining for preapoptotic detection showed that B(a)P treatment increased the apoptosis in both the cell types in a concentration and time-dependent manner. The cytosolic ROS (cROS) and superoxide radical (SOR) formation in the female colon cells was significantly higher than male colon cells unlike the mitochondrial ROS (mtROS) production which was significantly higher in male colon cells. Treatment with B(a)P significantly upregulated the IID and IVA PLA2 isoform groups in HCT-15 male colon cells, whereas IB was upregulated in HT-29 female colon cells among the various PLA2 isozyme gene studied (IB, IID, III, IVA, IVB, IVC, VI, X, aiPLA2 and iPLA2). Gene silencing experiments targeting PLA2 IID and IVA in the HCT-15 male colon cells and IB in HT-29 female colon cells showed no effect with B(a)P treatment on the cell proliferation, apoptosis, membrane integrity and free radicals (ROS, mtROS, and SOR) generation. Conclusion: Targeting specific PLA2 isozymes in a cell-specific manner abolished the B(a)P-induced PLA2-mediated oxidative damage–related signaling pathways.

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Antitumor Effects of Nordihydroguaiaretic Acid (NDGA) in Bladder T24 Cancer Cells are Related to Increase in ROS Production and Mitochondrial Leak Respiration

Natural Product Communications ◽

10.1177/1934578x1801301128 ◽

2018 ◽

Vol 13 (11) ◽

pp. 1934578X1801301

Author(s):

Gustavo Ignacio Vázquez-Cervantesa ◽

Karla Villaseñor-Aguayoa ◽

Jacqueline Hernández-Damiána ◽

Omar Emiliano Aparicio-Trejoa ◽

Omar Noel Medina-Camposa ◽

...

Keyword(s):

Cell Viability ◽

Annexin V ◽

Nordihydroguaiaretic Acid ◽

Mitochondrial Respiratory Chain ◽

Cellular Respiration ◽

Dependent Manner ◽

Antitumor Effects ◽

Concentration Dependent Manner ◽

T24 Cells ◽

Iodide Solution

The aim of this study was to evaluate the effect of nordihydroguaiaretic acid (NDGA) on tumor bladder T24 cells. Bladder cancer T24 cells were cultured on Dulbecco's Modified Eagle Medium in presence of NDGA. Cell viability and apoptosis were evaluated after 24, 48 and 72 h by using fluorescein diacetate (FDA) and Alexa fluor 488 annexin-V/propidium iodide solution, respectively. To determine the mitochondrial effects of NDGA (0-24 h), reactive oxygen species (ROS) levels by dihydroethidium fluorescence, mitochondrial membrane potential (ΔΨm) by 5,5’,6,6'-tetrachloro-1,1’,3,3'-tetraethyl-imidacarbocyanine iodide (JC-1) dual fluorescence and cellular respiration states by high resolution respirometry were evaluated. It was found that NDGA reduced T24 cell viability after 72 h of incubation in a concentration-dependent manner and apoptosis increased at 48 h. Furthermore, 20 μM NDGA increased ROS levels, decreased ΔΨm and promoted leak of respiration from mitochondrial respiratory chain in T24 cells which was associated to the death of tumor cells. Taken together these results suggested that antitumor effects of NDGA in T24 cells are related to its ability to induce mitochondrial alteration.

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Characterisation of the progesterone receptor on canine spermatozoa

Reproduction Fertility and Development ◽

10.1071/rd05074 ◽

2005 ◽

Vol 17 (7) ◽

pp. 733 ◽

Cited By ~ 13

Author(s):

Jui-Te Wu ◽

Pei-Shiue Tsai ◽

Shuang-Lin Lee ◽

Feng-Pang Cheng

Keyword(s):

Monoclonal Antibodies ◽

Plasma Membrane ◽

Progesterone Receptor ◽

Seminal Plasma ◽

High Capacity ◽

Fluorescein Isothiocyanate ◽

Dependent Manner ◽

Sperm Plasma Membrane ◽

Pre Treatment ◽

Dose Dependent

The present study was conducted to characterise and localise the progesterone receptor (PR) on canine spermatozoa. Using a progesterone–bovine serum albumin–fluorescein isothiocyanate conjugate (PBF) and different monoclonal antibodies (C262 and NCL-PGR against the steroid binding domain and N-terminus of intracellular PR, respectively, and h151 against the hinge domain of the intracellular oestrogen receptor), the PR was identified on the plasma membrane over the acrosomal region. Two proteins (54 kDa and 65 kDa) were detected by recognition of the three monoclonal antibodies using Western blotting. PBF labelling was observed in the majority of cauda epididymal spermatozoa (63 ± 4%), but this labelling was markedly reduced (33 ± 17%) after the addition of canine seminal plasma. Over a 7-h capacitation, the proportion of ejaculated spermatozoa exhibiting PBF labelling (indicating the presence of the PR) increased from 18 ± 10% (onset) to 59 ± 7% by 5 h, where it plateaued. Progesterone (P4) induced the acrosome reaction (AR) in a dose-dependent manner (0, 0.1, 1 and 10 µg/mL P4 corresponding to 10 ± 5%, 16 ± 9%, 23 ± 7% and 30 ± 7%). Pre-treatment of capacitated spermatozoa with canine seminal plasma reduced the incidence of the P4-induced AR (12 ± 5%). In addition, treatment with the monoclonal antibodies significantly reduced the incidence of the P4-induced AR (10 µg/mL) in capacitated ejaculated spermatozoa from 19 ± 6% to 11 ± 4% (h151, 1 : 10) and 12 ± 6% (C262, 1 : 10), respectively. A typical Scatchard plot revealed one binding with high affinity and low capacity, and another binding with low affinity and high capacity, suggesting at least two different characteristic PR. Taken together, these results demonstrate that P4 induced the AR in a dose-dependent manner via functional transmembranal receptors in the acrosomal region of the canine sperm plasma membrane. The characteristics of this membrane receptor seem similar to those of other mammalian spermatozoa, and it shows structural homology to the intracellular PR.

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Unfolded Protein Response is Involved in Trans-Platinum (II) Complex-Induced Apoptosis in Prostate Cancer Cells via ROS Accumulation

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666190409103334 ◽

2019 ◽

Vol 19 (9) ◽

pp. 1184-1195

Author(s):

Didem Karakas ◽

Buse Cevatemre ◽

Arzu Y. Oral ◽

Veysel T. Yilmaz ◽

Engin Ulukaya

Keyword(s):

Prostate Cancer ◽

Cell Death ◽

Cell Viability ◽

Er Stress ◽

Apoptotic Cell ◽

Annexin V ◽

Treatment Modalities ◽

Drug Candidate ◽

Ros Generation ◽

Dependent Manner

Background:Prostate cancer is one of the most common cancer types and it is the sixth leading cause of cancer-related death in men worldwide. Even though novel treatment modalities have been developed, it still a lifethreatening disease. Therefore novel compounds are needed to improve the overall survival.Methods:In our study, it was aimed to evaluate the anti-cancer activity of newly synthesized Platinum (II) [Pt(II)] complex on DU145, LNCaP and PC-3 prostate cancer cell lines. The cytotoxic activity of Pt(II) complex was tested by SRB and ATP cell viability assays. To detect the mode of cell death; fluorescent staining, flow cytometry and western blot analyses were performed.Results:The Pt(II) complex treatment resulted in a decrease in cell viability and increasing levels of apoptotic markers (pyknotic nuclei, annexin-V, caspase 3/7 activity) and a decrease in mitochondrial membrane potential in a dose dependent manner. Among cell types, tested PC-3 cells were found to be more sensitive to Pt(II) complex, demonstrating elevation of DNA damage in this cell line. In addition, Pt(II) complex induced Endoplasmic Reticulum (ER) stress by triggering ROS generation. More importantly, pre-treatment with NAC alleviated Pt(II) complex-mediated ER stress and cell death in PC-3.Conclusion:These findings suggest an upstream role of ROS production in Pt(II) complex-induced ER stressmediated apoptotic cell death. Considering the ROS-mediated apoptosis inducing the effect of Pt(II) complex, it warrants further evaluation as a novel metal-containing anticancer drug candidate.

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Specific Cytostatic and Cytotoxic Effect of Dihydrochelerythrine in Glioblastoma Cells: Role of NF-κB/β-catenin and STAT3/IL-6 Pathways

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520618666180412122101 ◽

2019 ◽

Vol 18 (10) ◽

pp. 1386-1393 ◽

Cited By ~ 5

Author(s):

Tereza C.C. Silva ◽

Giselle P. de Faria Lopes ◽

Noélio de J. Menezes-Filho ◽

Diêgo M. de Oliveira ◽

Ezequiel Pereira ◽

...

Keyword(s):

Cell Death ◽

Cell Viability ◽

Annexin V ◽

Experimental Models ◽

Blue Dye ◽

Dependent Manner ◽

Glioblastoma Cells ◽

U251 Cell ◽

U251 Cells

Background: A glioblastoma is a primary CNS tumor that is more aggressive and lethal than other brain tumors. Its location, rapid proliferation, invasive growth, angiogenesis and immunosuppression are the main factors that limit its treatment, making it a major challenge to neuro-oncology. Objective: This study investigated the in vitro effects of the alkaloid dihydrochelerythrine (DHC), which is extracted from Zanthoxylum stelligerum, on the viability, proliferation, cell death and β-catenin, NFκB, STAT3/pSTAT3 and interleukins roles. Method: In vitro experimental models of human (U251 and GL-15) and murine (C6) glioblastoma cells were cultured in the presence of DHC at increasing concentrations for MTT assay and exclusion trypan blue dye to determine EC50. Afterward, C6 and U251 cells were treated with 100 µM DHC or DMSO 0.1% for cell cycle, annexin and expression of β-catenin/NFκB/STAT3/pSTAT3 by flow cytometry or immunofluorescence. Interleukin quantification was made by Cytometric Bead Array. Results: A significant decrease was observed in C6 and U251 cell viability in a time and dose-dependent manner. GL-15 cell viability decreased only when treated with 200 µM DHC. This maximum concentration affected neither astrocytes nor microglia viability. A cytostatic effect of DHC was observed in C6 and U251 cells after 48 h of 100 µM DHC treatment. After 72 h of DHC treatment, C6 presented 80% of annexin-V+ cells compared to 10% of annexin-V+ U251 cells. C6 cells demonstrated significant high levels of NFκ B and β-catenin cytoplasmic fraction. Additionally, DHC treatment resulted in higher significant levels of IL-6 than did other interleukins and STAT3 up-regulation in U251 cells. Conclusion: These results demonstrate that DHC acts as a chemosensitizing agent selective for glioma cells not affecting non-tumor cells. Considering tumor heterogeneity, DHC demonstrated an anti-cancer potential to activate different cell death pathways. DHC demonstrated could be used for chemotherapy and immunotherapy applications in glioblastomas in the future.

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The Mitochondrial-Targeted Peptide, SS31, Protects Murine 661W Cells from Oxidative Damage via Induction of Autophagy

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2020.2923 ◽

2020 ◽

Vol 16 (5) ◽

pp. 603-615

Author(s):

Yuan He ◽

Beilei He ◽

Ruixue Zhang ◽

Zhuoya Quan ◽

Yun Xu ◽

...

Keyword(s):

Fluorescence Microscopy ◽

Oxidative Damage ◽

Cell Viability ◽

Annexin V ◽

Illumina Platform ◽

Associated Proteins ◽

Significant Attenuation ◽

Pre Treatment ◽

The Impact ◽

Do So

The goal of this study was to examine the impact of the mitochondrial-targeted antioxidant peptide, SS31, and its role in promoting autophagy in cone photoreceptor 661W cells that were subjected to oxidative damage. To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H2O2 with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3. Autophagy was evaluated by fluorescence microscopy in cells stained with monodansyl cadaverine (MDC). Autophagy was induced with rapamycin (Rap) and inhibited with bafamycin A1 (bafA1) followed by examination of Reactive oxygen species (ROS) levels in target 661W cells by fluorescence microscopy and flow cytometry. Annexin V/PI staining was used to evaluate the rate of apoptosis and mRNA sequencing (mRNA-seq) analysis (Illumina platform) was performed on H2O2-exposed 661W cells treated with SS31. Among our results, we observed a substantial and concentration-dependent decrease in 661W cell viability in response to H2O2-exposure; production of ROS, autophagy and apoptosis were induced at 8 h in response to exposure to 100 μM of H2O2. Pre-treatment with 100 nM SS31 resulted in significant attenuation of H2O2-mediated cytotoxicity, together with reduced ROS production and enhanced autophagy observed in response to oxidative stress. Both Rap and bafA1 were used to modulate SS31-mediated autophagy; the impact of Rap was similar to that of SS31. By contrast, administration of bafA1 counteracted autophagy induced by SS31. Furthermore, mRNAseq analysis revealed that SS31 promoted significant alterations in gene expression in 661W cells and suggested that autophagy was induced via the mTORC1-mediated signaling. In conclusion, our results indicate that exposure to H2O2 resulted in reduced 661W cell viability via mechanisms associated with oxidative damage, apoptosis, and autophagy. Notably, we demonstrated that pre-treatment with SS31 protects 661W cells from H2O2-induced oxidative damage that may result in part from induction of autophagy via mTORC1-mediated signaling pathways.

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Carnosol-Induced ROS Inhibits Cell Viability of Human Osteosarcoma by Apoptosis and Autophagy

The American Journal of Chinese Medicine ◽

10.1142/s0192415x17500951 ◽

2017 ◽

Vol 45 (08) ◽

pp. 1761-1772 ◽

Cited By ~ 6

Author(s):

Yu-Cheng Lo ◽

Yung-Chi Lin ◽

Yi-Fu Huang ◽

Chen-Pu Hsieh ◽

Chia-Chieh Wu ◽

...

Keyword(s):

Cell Viability ◽

Dependent Manner ◽

Human Osteosarcoma ◽

Cycle Arrest ◽

Human Osteosarcoma Cells ◽

Anti Oxidant ◽

Ros Scavenger ◽

Pre Treatment ◽

Induced Apoptosis ◽

Dose Dependent

Carnosol is an anti-oxidant and anti-inflammatory compound from rosemary. In this paper, we investigated antitumor activity of carnosol against human osteosarcoma cells. We found the viability of human osteosarcoma MG-63 cells was significantly decreased in the presence of carnosol (cell viabilities: 17.2% for 20[Formula: see text]μg/ml of CS vs. 100% for control, [Formula: see text]). Carnosol induced apoptosis and cell cycle arrest in a dose-dependent manner in MG-63 cells. Furthermore, carnosol exposure increased the levels of reactive oxygen species (ROS). The pre-treatment of NAC, the ROS scavenger, blocked the inhibition of cell viability in the carnosol treatment, indicating that ROS is important in the antiproliferation effect. Moreover, we demonstrated that carnosol significantly induced autophagy and co-administration of autophagy inhibitor reduced the antiproliferating effect of carnosol. This result exhibited the cytotoxic effect of autophagy induced by carnosol in MG-63 cells. Interestingly, the treatment of NAC decreased carnosol-induced autophagy. Collectively, these data indicate that carnosol suppresses the viability of human osteosarcoma MG-63 cells by upregulation of apoptosis and autophagy, which are both mediated by ROS. Thus, carnosol might serve as a potential therapeutic agent against osteosarcoma.

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