scholarly journals RETRACTED ARTICLE: Suppressor capacity of copper nanoparticles biosynthesized using Crocus sativus L. leaf aqueous extract on methadone-induced cell death in adrenal phaeochromocytoma (PC12) cell line

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Peng Zhang ◽  
Jian Cui ◽  
Shirin Mansooridara ◽  
Atoosa Shahriyari Kalantari ◽  
Akram Zangeneh ◽  
...  
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Membrane Potential ◽  
Inflammatory Cytokines ◽  
Aqueous Extract ◽  
Copper Nanoparticles ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Crocus Sativus ◽  
Leaf Aqueous Extract

AbstractIn this research, we prepared and formulated a neuroprotective supplement (copper nanoparticles in aqueous medium utilizing Crocus sativus L. Leaf aqueous extract) for determining its potential against methadone-induced cell death in PC12. The results of chemical characterization tests i.e., FE-SEM, FT-IR, XRD, EDX, TEM, and UV–Vis spectroscopy revealed that the study showed that copper nanoparticles were synthesized in the perfect way possible. In the TEM and FE-SEM images, the copper nanoparticles were in the mean size of 27.5 nm with the spherical shape. In the biological part of the present research, the Rat inflammatory cytokine assay kit was used to measure the concentrations of inflammatory cytokines. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) test was used to show DNA fragmentation and apoptosis. Caspase-3 activity was assessed by the caspase activity colorimetric assay kit and mitochondrial membrane potential was studied by Rhodamine123 fluorescence dye. Also, the cell viability of PC12 was measured by trypan blue assay. Copper nanoparticles-treated cell cutlers significantly (p ≤ 0.01) decreased the inflammatory cytokines concentrations, caspase-3 activity, and DNA fragmentation and they raised the cell viability and mitochondrial membrane potential in the high concentration of methadone-treated PC12 cells. The best result of neuroprotective properties was seen in the high dose of copper nanoparticles i.e., 4 µg. According to the above results, copper nanoparticles containing C. sativus leaf aqueous extract can be used in peripheral nervous system treatment as a neuroprotective promoter and central nervous system after approving in the clinical trial studies in humans.

scholarly journals Retraction Note: Suppressor capacity of copper nanoparticles biosynthesized using Crocus sativus L. leaf aqueous extract on methadone-induced cell death in adrenal phaeochromocytoma (PC12) cell line

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Peng Zhang ◽  
Jian Cui ◽  
Shirin Mansooridara ◽  
Atoosa Shahriyari Kalantari ◽  
Akram Zangeneh ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Aqueous Extract ◽  
Copper Nanoparticles ◽  
Pc12 Cell ◽  
Crocus Sativus ◽  
Pc12 Cell Line ◽  
Leaf Aqueous Extract ◽  
Retraction Notice ◽  
Crocus Sativus L

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1038/s41598-020-77741-4.

scholarly journals Application of a novel lung protective drug formulated by silver nanoparticles containing Curcuma longa L leaf aqueous extract on α-Guttiferin-induced DNA fragmentation and apoptosis in lung HEL 299, MRC-5, IMR-90, CCD-19Lu, WI-38, and BEAS-2B cell lines

2020 ◽  
Author(s):  
Yi Han ◽  
Yuan Gao ◽  
Xiaoqing Cao ◽  
Akram Zangeneh ◽  
Mohammad Mahdi Zangeneh ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Dna Fragmentation ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Aqueous Extract ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Curcuma Longa ◽  
Antioxidant Properties ◽  
Leaf Aqueous Extract

Abstract Recently, scientists have understood that metallic nanoparticles green-synthesized by medicinal plants have significant anti-cancer effects in the in vitro, in vivo, and clinical trial conditions. Also, the anti-lung cancer properties of metallic nanoparticles containing natural compounds have been indicated in many studies. In the recent research, we tried to investigate the application of a novel lung protective drug formulated by silver nanoparticles containing Curcuma longa L leaf aqueous extract on α-Guttiferin-induced DNA fragmentation and apoptosis in HEL 299, MRC-5, IMR-90, CCD-19Lu, WI-38, and BEAS-2B cell lines. Also, we assessed the concentrations of inflammatory cytokines, activity of caspase-3, and potential of mitochondrial membrane in the in vitro condition. Silver nanoparticles were characterized and analyzed by common physicochemical techniques including Transmission Electron Microscopy, Ultraviolet–Visible Spectroscopy, Fourier-Transform Infrared Spectroscopy, and Field Emission-Scanning Electron Microscopy. In the biological part of the present research, the cell viability of HEL 299, MRC-5, IMR-90, CCD-19Lu, WI-38, and BEAS-2B cell lines was measured by trypan blue assay. Caspase-3 activity was assessed by the caspase activity colorimetric assay kit and mitochondrial membrane potential was studied by Rhodamine123 fluorescence dye. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) test was used to show DNA fragmentation and apoptosis. Also, the Rat inflammatory cytokine assay kit was used to measure the concentrations of inflammatory cytokines. Silver nanoparticles-treated cell cutlers significantly (p ≤ 0.01) reduced the DNA fragmentation, caspase-3 activity, and inflammatory cytokines concentrations, and raised the mitochondrial membrane potential and cell viability in the high concentration of α-Guttiferin-treated HEL 299, MRC-5, IMR-90, CCD-19Lu, WI-38, and BEAS-2B cells. The best result of lung protective and antioxidant properties of silver nanoparticles containing Curcuma longa L leaf aqueous extract was seen in the high dose of silver nanoparticles i.e., 4 µg. Assessment of the antioxidant properties of silver nanoparticles was done with the common free radical scavenging test i.e., DPPH in the presence of butylated hydroxytoluene as the positive control. The nanoparticles inhibited half of the DPPH molecules in the concentration of 149 µg/mL. According to the above results, silver nanoparticles containing Curcuma longa L leaf aqueous extract can be administrated as a lung protective drug for the treatment of lung diseases after approving in the clinical trial studies in humans.

scholarly journals Co-involvement of the mitochondria and endoplasmic reticulum in cell death induced by the novel ertargeted protein HAP

2006 ◽  
Vol 11 (2) ◽  
Author(s):  
Hua Xu ◽  
Qing Zhou ◽  
Xin Liu ◽  
Yi-Peng Qi
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Membrane Potential ◽  
Hela Cells ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Protein A ◽  
The Novel ◽  
Induce Cell Apoptosis

AbstractHAP (a homologue of the ASY/Nogo-B protein), a novel human apoptosis-inducing protein, was found to be identical to RTN3. In an earlier study, we demonstrated that HAP localized exclusively to the endoplasmic reticulum (ER) and that its overexpression could induce cell apoptosis via a depletion of endoplasmic reticulum (ER) Ca2+ stores. In this study, we show that overexpression of HAP causes the activation of caspase-12 and caspase-3. We still detected the collapse of mitochondrial membrane potential (Δωm) and the release of cytochrome c in HAP-overexpressing HeLa cells. All the results indicate that both the mitochondria and the ER are involved in apoptosis caused by HAP overexpression, and suggest that HAP overexpression may initiate an ER overload response (EOR) and bring about the downstream apoptotic events.

scholarly journals The combined effect of dichloroacetate and 3-bromopyruvate on glucose metabolism in colorectal cancer cell line, HT-29; the mitochondrial pathway apoptosis

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hojatolla Nikravesh ◽  
Mohammad Javad Khodayar ◽  
Babak Behmanesh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Lines ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Ht29 Cell ◽  
Ros Production ◽  
Apoptosis And Necrosis

Abstract Background 5-Fluorouracil (5-FU) is regarded as the first line treatment for colorectal cancer; however, its effectiveness is limited by drug resistance. The ultimate goal of cancer therapy is induction of cancer cell death to achieve an effective outcome with minimal side effects. The present work aimed to assess the anti-cancer activities of mitocans which can be considered as an effective anticancer drug due to high specificity in targeting cancer cells. Methods MTT (3–4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide) assay was performed to determine the effects of our mitocans on cell viability and cell death. Apoptosis and necrosis, caspase 3 activity, mitochondrial membrane potential and ROS production in HT29 cell lines were analyzed by ApopNexin™ FITC/PI Kit, Caspase- 3 Assay Kit, MitoTracker Green and DCFH-DA, respectively. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression level of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) genes in HT29 cell lines. Results Treatment with mitocans (3Br-P + DCA) inhibited the growth of HT29. Moreover, 3Br-P + DCA significantly induced apoptosis and necrosis, activation of caspase 3 activity, depolarize the mitochondrial membrane potential, and ROS production. At a molecular level, 3Br-P + DCA treatment remarkably down-regulated the expression of Bcl-2, while up-regulated the expression of Bax. Conclusion Mitocans, in particular the combined drug, 3Br-P + DCA, could be regarded and more evaluated as a safe and effective compound for CRC treatment. Targeting hexokinase and pyruvate dehydrogenase kinase enzymes may be an option to overcome 5-FU -mediated chemo-resistant in colorectal cancer.

Abstract 4362: Antibodies against KChIP2 Induce Ionic Imbalance and Cell Death in Isolated Rat Cardiomyocytes

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Sangita Choudhury ◽  
Michael Schnell ◽  
Jan Lüdemann ◽  
Alexander Staudt ◽  
Heyo K Kroemer ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Dilated Cardiomyopathy ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Nuclear Translocation ◽  
Rat Cardiomyocytes ◽  
Ionic Imbalance ◽  
Isolated Rat

Disturbances of humoral immunity have been described in patients with dilated cardiomyopathy (DCM). Antibodies against Kv channel-interacting proteins (KChIPs) may be associated with heart failure. Isolated rat cardiomyocytes were treated with antibodies against rat KChIP2 (80 pmol/ml) up to 24 hours. RNA and proteins were isolated after two hours by standard procedures and mRNA (TaqMan®) and protein (Western blot) expression was quantified. Translocations of NF-κB subunits p50, p65, c-Rel, and Rel-B were measured in nuclear protein extracts by ELISA after 60 minutes. Mitochondrial membrane potential ΔΨm and caspase-3 and -9 activities were determined by flow cytometry. Necrotic and apoptotic cells were distinguished by staining with Hoechst 33258 and propidium iodide. Total Ca 2+ and K + concentrations were quantified by a colorimetric assay and atomic absorption spectrometry, respectively, and normalized to the protein content of the cells. Antibodies against KChIP2 induced nuclear translocation of all NF-κB subunits analyzed. Pre-incubation with a blocking peptide or an NF-κB inhibitor, CAPE, prevented nuclear translocation. Anti-KChIP2-treatment for two hours significantly reduced KChIP2 mRNA (55±10%; n=4) and protein (73 ±5%, n =4) expression compared to cells treated with experimental buffer (100%). Treatment for 24 hours did not induce changes in mitochondrial membrane potential, ΔΨm. Caspase-3 and -9 activities were not altered as well. The anti-KChIP2-treated cell population consisted of 75±3% necrotic, 2±1% apoptotic, and 13±2% viable cells. In contrast, cells treated with experimental buffer were viable to 86±1%. After five minutes, anti-KChIP2 induced significant increases in total intracellular Ca 2+ (plus 11±2%) and K + (plus 18±2%) concentrations. These antibody-mediated effects were prevented in the presence of a blocking peptide. Antibodies against KChIP2 induce ionic imbalance, activate the transcription factor NF-κB, down-regulate KChIP2 expression and enhance cell death rate probably due to necrosis. Antibodies against KChIP2 may contribute to the development and progression of dilated cardiomyopathy.

scholarly journals The Combined Effect of Dichloroacetate and 3-Bromopyruvate in Colorectal Cancer Cell Line, HT-29; The Mitochondrial Pathway Apoptosis

2021 ◽  
Author(s):  
Hojatolla Nikravesh ◽  
Mohammad Javad Khodayar ◽  
Babak Behmanesh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Lines ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Ht29 Cell ◽  
Ros Production ◽  
Apoptosis And Necrosis

Abstract Background 5-Fluorouracil (5-FU) is regarded as the first line treatment for colorectal cancer; however, its effectiveness is limited by drug resistance. The ultimate goal of cancer therapy is induction of cancer cell death to achieve an effective outcome with minimal side effects. The present work aimed to assess the anti-cancer activities of mitocans which can be considered as an effective anticancer drug due to high specificity in targeting cancer cells. Methods MTT (3–4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide) assay was performed to determine the effects of our mitocans on cell viability and cell death. Apoptosis and necrosis, caspase 3 activity, mitochondrial membrane potential and ROS production in HT29 cell lines were analyzed by ApopNexin™ FITC/PI Kit, Caspase- 3 Assay Kit, MitoTracker Green and DCFH-DA, respectively. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression level of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) genes in HT29 cell lines. Results treatment with mitocans (3Br-P + DCA) inhibited the growth of HT29. Moreover, 3Br-P + DCA significantly induced apoptosis and necrosis, activation of caspase 3 activity, depolarize the mitochondrial membrane potential, and ROS production. At a molecular level, 3Br-P + DCA treatment remarkably down-regulated the expression of Bcl-2, while up-regulated the expression of Bax. Conclusion mitocans, in particular the combined drug, 3Br-P + DCA, could be regarded and more evaluated as a safe and effective compound for CRC treatment. Targeting hexokinase and pyruvate dehydrogenase kinase enzymes may be an option to overcome 5-FU -mediated chemo-resistant in colorectal cancer.

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

Abstract 371: Mitochondrial Antiviral Signaling (MAVS) Protects Cardiomyocytes Under Oxidative Stress by Interfering with Bax-Mediated Cell Death

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Toshitaka Yajima ◽  
Stanley Park ◽  
Hanbing Zhou ◽  
Michinari Nakamura ◽  
Mitsuyo Machida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Membrane Potential ◽  
Cytochrome C ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cytochrome C Release ◽  
Antiviral Signaling ◽  
Cell Death Pathway ◽  
The Impact

MAVS is a mitochondrial outer membrane protein that activates innate antiviral signaling by recognizing cytosolic viral RNAs and DNAs. While the discovery of MAVS is the first molecular evidence that links mitochondria to innate immune mechanisms, it is still unclear whether MAVS affects mitochondrial cell death as a member of caspase activation and recruitment domain (CARD)-containing proteins. We found that MAVS interacts with Bax through CARD by Yeast two-hybrid and a series of immunoprecipitation (IP) assay, which led us to hypothesize that MAVS functions not only in the innate antiviral mechanisms but also in the mitochondrial cell death pathway. Methods: 1) We examined molecular interaction between MAVS and Bax under oxidative stress by IP using isolated myocytes with H2O2 stimulation and the heart post ischemia-reperfusion (I/R). 2) We evaluated the effect of MAVS on mitochondrial membrane potential and apoptosis under H2O2 stimulation using isolated myocytes with adenoviral MAVS knockdown. 3) We investigated the impact of MAVS on %myocardial infarction (%MI) post I/R using cardiac-specific MAVS knockout (cKO) and transgenic (cTg) mice which we have originally generated. 4) We examined the effect of MAVS on recombinant Bax (rBax)-mediated cytochrome c release using isolated mitochondria from wild type (WT) and MAVS KO mice. Results: 1) The amount of Bax pulled down with MAVS was significantly increased in isolated myocytes with 0.2 mM H2O2 compared to those without stimulation (mean±SD; 1.808±0.14, n=5, p<0.001) and in the heart post I/R compared to sham (2.2±1.19, n=3, p=0.0081). 2) Myocytes with MAVS knockdown showed clear abnormalities in mitochondrial membrane potential and caspace-3 cleavage with 0.2 mM H2O2 compared to control cardiomyocytes. 3) MAVS cKO had significantly larger %MI than WT (81.9 ± 5.8% vs. 42.6 ± 13.6%, n=8, p=0.0008). In contrast, MAVS cTg had significantly smaller %MI that WT (30.0 ± 4.8% vs. 49.2 ± 4.8%, n=10, p=0.0113). 4) Mitochondria from MAVS KO exhibited cytochrome c release after incubation with 2.5 μ g of rBax while those from WT required 10 μ g of rBax. Conclusion: These results demonstrate that MAVS protects cardiomyocyte under oxidative stress by interfering with Bax-mediated cytochrome c release from mitochondria.

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