scholarly journals Nepenthes Ethyl Acetate Extract Provides Oxidative Stress-Dependent Anti-Leukemia Effects

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1410
Author(s):  
Wangta Liu ◽  
Li-Ching Lin ◽  
Pei-Ju Wang ◽  
Yan-Ning Chen ◽  
Sheng-Chieh Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Ethyl Acetate ◽  
Cell Lines ◽  
Ethyl Acetate Extract ◽  
Antioxidant Properties ◽  
Leukemia Cells ◽  
Heme Oxygenase 1 ◽  
Mitochondrial Membrane Depolarization ◽  
Stress Dependent

Several kinds of solvents have been applied to Nepenthes extractions exhibiting antioxidant and anticancer effects. However, they were rarely investigated for Nepenthes ethyl acetate extract (EANT), especially leukemia cells. The purpose of the present study was to evaluate the antioxidant properties and explore the antiproliferation impact and mechanism of EANT in leukemia cells. Five standard assays demonstrated that EANT exhibits antioxidant capability. In the cell line model, EANT dose-responsively inhibited cell viabilities of three leukemia cell lines (HL-60, K-562, and MOLT-4) based on 24 h MTS assays, which were reverted by pretreating oxidative stress and apoptosis inhibitors (N-acetylcysteine and Z-VAD-FMK). Due to similar sensitivities among the three cell lines, leukemia HL-60 cells were chosen for exploring antiproliferation mechanisms. EANT caused subG1 and G1 cumulations, triggered annexin V-detected apoptosis, activated apoptotic caspase 3/7 activity, and induced poly ADP-ribose polymerase expression. Moreover, reactive oxygen species, mitochondrial superoxide, and mitochondrial membrane depolarization were generated by EANT, which was reverted by N-acetylcysteine. The antioxidant response to oxidative stress showed that EANT upregulated mRNA expressions for nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), thioredoxin (TXN), heme oxygenase 1 (HMOX1), and NAD(P)H quinone dehydrogenase 1 (NQO1) genes. Moreover, these oxidative stresses led to DNA damage (γH2AX and 8-hydroxy-2-deoxyguanosine) and were alleviated by N-acetylcysteine. Taken together, EANT demonstrated oxidative stress-dependent anti-leukemia ability to HL-60 cells associated with apoptosis and DNA damage.

scholarly journals Nepenthes Extract Induces Selective Killing, Necrosis, and Apoptosis in Oral Cancer Cells

2021 ◽  
Vol 11 (9) ◽  
pp. 871
Author(s):  
Kun-Han Yang ◽  
Jen-Yang Tang ◽  
Yan-Ning Chen ◽  
Ya-Ting Chuang ◽  
I-Hsuan Tsai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Annexin V ◽  
High Sensitivity ◽  
Heme Oxygenase 1 ◽  
Mitochondrial Membrane Depolarization ◽  
Oral Cancer Cells ◽  
Stress Dependent

Ethyl acetate Nepenthes extract (EANT) from Nepenthes thorellii × (ventricosa × maxima) shows antiproliferation and apoptosis but not necrosis in breast cancer cells, but this has not been investigated in oral cancer cells. In the present study, EANT shows no cytotoxicity to normal oral cells but exhibits selective killing to six oral cancer cell lines. They were suppressed by pretreatment of the antioxidant inhibitor N-acetylcysteine (NAC), demonstrating that EANT-induced cell death was mediated by oxidative stress. Concerning high sensitivity to EANT, Ca9-22 and CAL 27 oral cancer cells were chosen for exploring detailed selective killing mechanisms. EANT triggers a mixture of necrosis and apoptosis as determined by annexin V/7-aminoactinmycin D analysis. Still, they show differential switches from necrosis at a low (10 μg/mL) concentration to apoptosis at high (25 μg/mL) concentration of EANT in oral cancer cells. NAC induces necrosis but suppresses annexin V-detected apoptosis in oral cancer cells. Necrostatin 1 (NEC1), a necroptosis inhibitor, moderately suppresses necrosis but induces apoptosis at 10 μg/mL EANT. In contrast, Z-VAD-FMK, a pancaspase inhibitor, slightly causes necrosis but suppresses apoptosis at 10 μg/mL EANT. Furthermore, the flow cytometry-detected pancaspase activity is dose-responsively increased but is suppressed by NAC and ZVAD, although not for NEC1 in oral cancer cells. EANT causes several oxidative stress events such as reactive oxygen species, mitochondrial superoxide, and mitochondrial membrane depolarization. In response to oxidative stresses, the mRNA for antioxidant signaling, such as nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), heme oxygenase 1 (HMOX1), and thioredoxin (TXN), are overexpressed in oral cancer cells. Moreover, EANT also triggers DNA damage, as detected by γH2AX and 8-oxo-2′-deoxyguanosine adducts. The dependence of oxidative stress is validated by the evidence that NAC pretreatment reverts the changes of cellular and mitochondrial stress and DNA damage. Therefore, EANT exhibits antiproliferation involving an oxidative stress-dependent necrosis/apoptosis switch and DNA damage in oral cancer cells.

scholarly journals Ginsenoside Rg1 Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury via Activation of Nrf2/HO-1 Signaling and Inhibition of JNK

2017 ◽  
Vol 44 (1) ◽  
pp. 21-37 ◽  
Author(s):  
Qianhui Li ◽  
Yin Xiang ◽  
Yu Chen ◽  
Yong Tang ◽  
Yachen Zhang
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Ginsenoside Rg1 ◽  
H9c2 Cells ◽  
Stress Injury ◽  
Mitochondrial Membrane Depolarization ◽  
Hypoxia Reoxygenation

Background/Aims: Excessive reactive oxygen species (ROS) disturb the physiology of H9c2 cells, which is regarded as a major cause of H9c2 cardiomyocyte apoptosis. Ginsenoside Rg1 is the main active extract of ginseng, which has important antioxidant properties in various cell models. This project investigated the role of ginsenoside Rg1 in hypoxia/reoxygenation (H/R)-induced oxidative stress injury in cultured H9c2 cells to reveal the underlying signaling pathways. Methods: H9c2 cells were pretreated with ginsenoside Rg1 for 12 h before exposure to H/R. In the absence or presence of Nrf2siRNA, HO-1 inhibitor (ZnPP-IX), and inhibitors of the MAPK pathway (SB203580, PD98059, SP600125), H9c2 cells were subjected to H/R with Rg1 treatment. The effects and mechanisms of H/R-induced cardiomyocyte injury were measured. Results: Ginsenoside Rg1 treatment suppressed H/R-induced apoptosis and caspase-3 activation. Ginsenoside Rg1 treatment decreased ROS production and mitochondrial membrane depolarization by elevating the intracellular antioxidant capacity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and reduced glutathione (GSH). Furthermore, ginsenoside Rg1 stimulation appeared to result in nuclear translocation of NF-E2-related factor 2 (Nrf2), along with enhanced expression of the downstream target gene heme oxygenase-1 (HO-1) in a dose-dependent manner. However, ginsenoside Rg1-mediated cardioprotection was abolished by Nrf2-siRNA and HO-1 inhibitor. H/R treatment increased the levels of phosphorylated c-Jun N-terminal kinases (p-JNK), which was dramatically attenuated by ginsenoside Rg1 and SP600125 (a specific JNK inhibitor). Conclusion: These observations indicate that ginsenoside Rg1 activates the Nrf2/HO-1 axis and inhibits the JNK pathway in H9c2 cells to protect against oxidative stress.

scholarly journals Antioxidant Properties and Cytotoxic Activity of Ethyl Acetate Fraction of Plectranthus amboinicus (Lour.) Spreng. Leaves on HeLa and T47D Cell Lines

2019 ◽  
Vol 10 (1) ◽  
pp. 37
Author(s):  
Poppy Anjelisa Zaitun Hasibuan ◽  
Panal Sitorus ◽  
Denny Satria ◽  
Rizka Damela Sibuea
Keyword(s):  
Ethyl Acetate ◽  
Cytotoxic Activity ◽  
Cell Lines ◽  
Mcf7 Cell ◽  
Ethyl Acetate Extract ◽  
Antioxidant Properties ◽  
T47d Cell ◽  
Flavonoid Content ◽  
Dpph Method ◽  
Plectranthus Amboinicus

Research into plants with anticancer effects is actively encouraged in orderto discover new drugs with lessertoxicity but more potent effects. The aims of study are to evaluate the antioxidant properties and to investigate the cytotoxic activity of Plectranthus amboinicus (Lour.) Spreng. leaves ethyl acetate fractions on HeLa,T47D and MCF7 cell lines. The extract was prepared by graded maceration using n-hexane and ethyl acetate. The ethyl acetate extract was fractionated in vacuum liquid chromatography with n-hexane: ethyl acetate; and ethyl acetate: methanol as mobile phase. Then, the fractions were analyzed with thin layer chromatography (TLC). The free radical scavenging activity was measured by DPPH method, the total flavonoid content was calculated by quercetin equivalent and the absorbance is measured by using UV-Visible spectrophotometry. The cytotoxic activity were determined using MTT assay. The fractions contained 5 sub fractions with same TLC profile. The fractions showed antioxidant activity by DPPH method with different IC50 values, namely: 130 µg/mL(I), 127 µg/mL(II), 137 µg/mL(III), 129 µg/mL(IV), and 124 µg/ mL(V), respectively. The measurement of total flavonoid content showed 118 mg QE/g (I), 50 mg QE/g (II), 207 mg QE/g (III), 56 mg QE/g (IV), and 55 mg QE/g (V). The IC50 of each sub fractions on HeLa cell were 77 µg/mL, 46 µg/mL, 93 µg/mL, 71 µg/mL and 476 µg/mL; for T47D cell were 1621 µg/mL, 111 µg/mL, 128 µg/mL, 150 µg/mL and 209 µg/mL; and for MCF7 were 259 µg/mL, 343 µg/mL, 575 µg/mL, 408 µg/mL and 250 µg/mL. Based on the results, the fractions derived from ethyl acetate extract of Plectranthus amboinicus (Lour.) Spreng. leaves exhibit antioxidant. The Fraction II from ethyl acetate extract of Plectranthus amboinicus (Lour.) Spreng. was the most cytotoxic on HeLa, T47D and MCF7 cell lines. It is potential to undergo further isolation of its cytotoxic compounds.Keywords : antioxidant, cytotoxic, Plectranthus amboinicul (Lour.) Spreng., ethyl acetate fractions

Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

2019 ◽  
Vol 34 (8) ◽  
pp. 891-901 ◽  
Author(s):  
Jen‐Yang Tang ◽  
Sheng‐Yao Peng ◽  
Yuan‐Bin Cheng ◽  
Chun‐Lin Wang ◽  
Ammad Ahmad Farooqi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Ethyl Acetate ◽  
Cancer Cells ◽  
Ethyl Acetate Extract ◽  
Oral Cancer Cells

scholarly journals Withaferin A Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1063
Author(s):  
Tsu-Ming Chien ◽  
Kuang-Han Wu ◽  
Ya-Ting Chuang ◽  
Yun-Chiao Yeh ◽  
Hui-Ru Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Withaferin A ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Dna Damages ◽  
Bladder Cancer Cells ◽  
Stress Dependent

Withaferin A (WFA), the Indian ginseng bioactive compound, exhibits an antiproliferation effect on several kinds of cancer, but it was rarely reported in bladder cancer cells. This study aims to assess the anticancer effect and mechanism of WFA in bladder cancer cells. WFA shows antiproliferation to bladder cancer J82 cells based on the finding of the MTS assay. WFA disturbs cell cycle progression associated with subG1 accumulation in J82 cells. Furthermore, WFA triggers apoptosis as determined by flow cytometry assays using annexin V/7-aminoactinomycin D and pancaspase detection. Western blotting also supports WFA-induced apoptosis by increasing cleavage of caspases 3, 8, and 9 and poly ADP-ribose polymerase. Mechanistically, WFA triggers oxidative stress-association changes, such as the generation of reactive oxygen species and mitochondrial superoxide and diminishment of the mitochondrial membrane potential, in J82 cells. In response to oxidative stresses, mRNA for antioxidant signaling, such as nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), superoxide dismutase 1 (SOD1), thioredoxin (TXN), glutathione-disulfide reductase (GSR), quinone dehydrogenase 1 (NQO1), and heme oxygenase 1 (HMOX1), are overexpressed in J82 cells. In addition, WFA causes DNA strand breaks and oxidative DNA damages. Moreover, the ROS scavenger N-acetylcysteine reverts all tested WFA-modulating effects. In conclusion, WFA possesses anti-bladder cancer effects by inducing antiproliferation, apoptosis, and DNA damage in an oxidative stress-dependent manner.

scholarly journals Assessment of the Antimicrobial, Antioxidant, and Antiproliferative Potential of Sideritis raeseri subps. raeseri Essential Oil

Foods ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 860 ◽  
Author(s):  
Gregoria Mitropoulou ◽  
Marianthi Sidira ◽  
Myria Skitsa ◽  
Ilias Tsochantaridis ◽  
Aglaia Pappa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Essential Oil ◽  
Cell Lines ◽  
Antiproliferative Activity ◽  
Inhibitory Concentration ◽  
Antioxidant Properties ◽  
Diffusion Method ◽  
Hacat Cells ◽  
Cytoprotective Activity

The aim of the present study was to investigate the antimicrobial potential of Sideritis raeseri subps. raeseri essential oil (EO) against common food spoilage and pathogenic microorganisms and evaluate its antioxidant and antiproliferative activity. The EO was isolated by steam distillation and analyzed by GC/MS. The main constituents identified were geranyl-p-cymene (25.08%), geranyl-γ-terpinene (15.17%), and geranyl-linalool (14.04%). Initially, its activity against Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Listeria monocytogenes, Salmonella Enteritidis, Salmonella Typhimurium, Pseudomonas fragi, Saccharomyces cerevisiae, and Aspergillus niger was screened by the disk diffusion method. Subsequently, minimum inhibitory concentration (MIC), non-inhibitory concentration (NIC), and minimum lethal concentration (MLC) values were determined. Growth inhibition of all microorganisms tested was documented, although it was significantly lower compared to gentamycin, ciproxin, and voriconazole, which were used as positive controls. In a next step, its direct antioxidant properties were examined using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays, and the IC50 values were determined. The potential cytoprotective activity of the oil against H2O2–induced oxidative stress and DNA damage was studied in human immortalized keratinocyte (HaCaT) cells using the comet assay. Finally, the antiproliferative activity of the oil was evaluated against a panel of cancer cell lines including A375, Caco2, PC3, and DU145 and the non-cancerous HaCaT cell line using the sulforhodamine B (SRB) assay, and the EC50 values were determined. The oil demonstrated weak radical scavenging activity, noteworthy cytoprotective activity against H2O2–induced oxidative stress and DNA damage in HaCaT cells, and antiproliferative activity against all cell lines tested, being more sensitive against the in vitro model of skin melanoma.

scholarly journals Protective Effect of Simplicillium sp. Ethyl Acetate Extract against High Glucose-Induced Oxidative Stress in HUVECs

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ting-Ting Tian ◽  
Qi-Rui Li ◽  
Shi-Quan Gan ◽  
Chu-Rui Chang ◽  
Xiang-Chun Shen
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Ethyl Acetate ◽  
High Glucose ◽  
Ethyl Acetate Extract ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Rdna Sequences ◽  
Insect Fungi

This study aimed at investigating the cytoprotective effect of an ethyl acetate extract of insect fungi against high glucose- (HG-) induced oxidative damage in human umbilical vein endothelial cells (HUVECs). An insect fungus strain termed CH180672 (CH) was found for protecting HUVECs from HG-induced damage. In this study, CH was identified as Simplicillium sp. based on a phylogenetic analysis of ITS‐rDNA sequences. Ethyl acetate extract (EtOAc) of this strain (CH) was subjected to the following experiments. Cell viability was examined with the MTT method. To evaluate the protection of CH, intracellular reactive oxygen species (ROS), malondialdehyde (MDA) levels, and the activities of antioxidant enzymes were measured and the expression of oxidation-associated proteins was assessed. In the current study, it has been found that CH can increase the survival rate of HUVECs induced by HG. Additionally, we found that HG-induced nuclear factor-erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) signal decreased and increased the intracellular ROS and MDA generation in HUVECs. However, CH treatment strongly promoted the translocation of Nrf2 and its transregulation on HO-1 and ultimately inhibited the high level of ROS and MDA induced by HG. The regulatory ability of CH was similar to Nrf2 agonist bardoxolone, while the effect was abolished by ML385, suggesting that Nrf2 mediated the inhibition of CH on HG-induced oxidative stress in HUVECs. Taken together, CH can improve HG-induced oxidative damage of HUVECs, and its mechanism may be related to the regulation of the Nrf2/HO-1 pathway.

scholarly journals Antiproliferation for Breast Cancer Cells by Ethyl Acetate Extract of Nepenthes thorellii x (ventricosa x maxima)

2019 ◽  
Vol 20 (13) ◽  
pp. 3238 ◽  
Author(s):  
Fu Ou-Yang ◽  
I-Hsuan Tsai ◽  
Jen-Yang Tang ◽  
Ching-Yu Yen ◽  
Yuan-Bin Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Dna Damage ◽  
Ethyl Acetate ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ethyl Acetate Extract ◽  
Mechanistic Study ◽  
Breast Cancer Cell Lines ◽  
Antitumor Effects

Extracts from the Nepenthes plant have anti-microorganism and anti-inflammation effects. However, the anticancer effect of the Nepenthes plant is rarely reported, especially for breast cancer cells. Here, we evaluate the antitumor effects of the ethyl acetate extract of Nepenthes thorellii x (ventricosa x maxima) (EANT) against breast cancer cells. Cell viability and flow cytometric analyses were used to analyze apoptosis, oxidative stress, and DNA damage. EANT exhibits a higher antiproliferation ability to two breast cancer cell lines (MCF7 and SKBR3) as compared to normal breast cells (M10). A mechanistic study demonstrates that EANT induces apoptosis in breast cancer cells with evidence of subG1 accumulation and annexin V increment. EANT also induces glutathione (GSH) depletion, resulting in dramatic accumulations of reactive oxygen species (ROS) and mitochondrial superoxide (MitoSOX), as well as the depletion of mitochondrial membrane potential (MMP). These oxidative stresses attack DNA, respectively leading to DNA double strand breaks and oxidative DNA damage in γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG) assays. Overall these findings clearly revealed that EANT induced changes were suppressed by the ROS inhibitor. In conclusion, our results have shown that the ROS-modulating natural product (EANT) has antiproliferation activity against breast cancer cells through apoptosis, oxidative stress, and DNA damage.

scholarly journals Oxidative Stress-Dependent Synergistic Antiproliferation, Apoptosis, and DNA Damage of Ultraviolet-C and Coral-Derived Sinularin Combined Treatment for Oral Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2450
Author(s):  
Sheng-Yao Peng ◽  
Jen-Yang Tang ◽  
Ruei-Nian Li ◽  
Hurng-Wern Huang ◽  
Chang-Yi Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Combined Treatment ◽  
Ultraviolet C ◽  
Oral Cancer Cells ◽  
Stress Dependent ◽  
Oral Cells

Combined treatment is increasingly used to improve cancer therapy. Non-ionizing radiation ultraviolet-C (UVC) and sinularin, a coral Sinularia flexibilis-derived cembranolide, were separately reported to provide an antiproliferation function to some kinds of cancer cells. However, an antiproliferation function using the combined treatment of UVC/sinularin has not been investigated as yet. This study aimed to examine the combined antiproliferation function and explore the combination of UVC/sinularin in oral cancer cells compared to normal oral cells. Regarding cell viability, UVC/sinularin displays the synergistic and selective killing of two oral cancer cell lines, but remains non-effective for normal oral cell lines compared to treatments in terms of MTS and ATP assays. In tests using the flow cytometry, luminescence, and Western blotting methods, UVC/sinularin-treated oral cancer cells exhibited higher reactive oxygen species production, mitochondrial superoxide generation, mitochondrial membrane potential destruction, annexin V, pan-caspase, caspase 3/7, and cleaved-poly (ADP-ribose) polymerase expressions than that in normal oral cells. Accordingly, oxidative stress and apoptosis are highly induced in a combined UVC/sinularin treatment. Moreover, UVC/sinularin treatment provides higher G2/M arrest and γH2AX/8-hydroxyl-2′deoxyguanosine-detected DNA damages in oral cancer cells than in the separate treatments. A pretreatment can revert all of these changes of UVC/sinularin treatment with the antioxidant N-acetylcysteine. Taken together, UVC/sinularin acting upon oral cancer cells exhibits a synergistic and selective antiproliferation ability involving oxidative stress-dependent apoptosis and cellular DNA damage with low toxic side effects on normal oral cells.

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