A ROS-mediated mitochondrial pathway and Nrf2 pathway activation are involved in BDE-47 induced apoptosis in Neuro-2a cells

Chen, Hongmei; Tang, Xuexi; Zhou, Bin; Zhou, Zhongyuan; Xu, Ningning; Wang, You

doi:10.1016/j.chemosphere.2017.06.006

Cited by 66 publications

(31 citation statements)

References 28 publications

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“…Intracellular ROS overproduction results in oxidative stress, thereby tiggering DNA damage to induce cell apoptosis through regulating Akt/MAPK signaling pathways (Chen et al, ; Li, Lin, Zhao, Xu, Wang, Hua, et al, ; Li, Lin, Zhao, Xu, Wang, Xia, et al, ). To address whether DNA damage induced by inclusion complex is related to the accumulation of ROS and to further support the results of proteomics, ROS generation was detected by DHE fluorescence assay.…”

Section: Resultsmentioning

confidence: 99%

Proteomic analysis of the molecular mechanism of curcumin/β‐cyclodextrin polymer inclusion complex inhibiting HepG2 cells growth

et al. 2019

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This research aimed to explore whether curcumin/β-cyclodextrin polymer (CUR/ CDP) inclusion complex caused inhibitory effect on HepG2 cells proliferation and its possible molecular mechanisms. We found that CUR/CDP inclusion complex exhibited inhibitory effects on HepG2 cells growth. To understand the underlying mechanism of how CUR/CDP inclusion complex inhibited HepG2 cells growth, we examined the proteome of HepG2 cells treated at 640 μg/ml CUR/CDP inclusion complex using proteomic approach. We found that 15 protein spots identified by MALDI-TOF/TOF MS were changed. Biological progress analysis demonstrated that protein related to cell cycle and apoptosis accounted for 33% of the detected proteins. Among these proteins, nucleophosmin (NPM1) and peroxiredoxin-6 (PRDX6) were involved in the ROS-P53 pathway. PRDX6 and NPM1 were down-regulated, thereby improving the expression level of phosphorylated p53 and ROS content, which regulated cell apoptosis. This findings provide a better understanding of CUR/CDP regulatory antitumor mechanisms. Practical applicationsCyclodextrins polymer was used to prepare the curcumin/cyclodextrins polymer inclusion complex to improve curcumin solubility and stability in our group. And we found that it showed novel anticancer activity. However, the molecular mechanisms is unclear. This research elucidates the underlying molecular mechanisms of the curcumin/cyclodextrins polymer inclusion complex-inhibited HepG2 cells growth. The inclusion complex has the potential to be a novel complex of curcumin to treat human cancers K E Y W O R D S apoptosis, curcumin/β-cyclodextrin polymer inclusion complex, HepG2 cells, proteomic analysis

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Section: Resultsmentioning

confidence: 99%

Proteomic analysis of the molecular mechanism of curcumin/β‐cyclodextrin polymer inclusion complex inhibiting HepG2 cells growth

et al. 2019

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“…A number of published data suggest that NQO1 provides protection of the cells from oxidative stress and apoptosis, for example, KMS04014, a compound that induces NQO1 gene expression and protects dopaminergic neuronal cells from oxidative stress generated by tetrahydrobiopterin, 1‐methyl‐4‐phenylpyridinium, and H 2 O 2 . NQO1 plays a critical role in protection in Neuro‐2 cells against energy depletion caused by acetaminophen by stabilizing their mitochondrial membrane potential …”

Section: Resultsmentioning

confidence: 99%

Identification of NQO1 and ferrochelatase as interaction partners for neuroprotective N‐{[2‐(4‐phenyl‐piperazin‐1‐yl)‐ethyl]‐phenyl}‐arylamides

et al. 2018

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Affinity chromatography was used to identify potential cellular targets that are responsible for neuroprotective activity of N-{[2-(4-phenyl-piperazin-1-yl)-ethyl]-phenyl}-arylamides. Active and inactive representatives of N-{[2-(4-phenyl-piperazin-1-yl)-ethyl]-phenyl}-arylamides bearing an extended linker were synthesized and immobilized on an agarose-based matrix. This was followed by the identification of specifically bound proteins isolated out of the whole rat brain extract. Inducible flavoprotein NAD(P)H:quinone oxidoreductase (NQO1) was identified as candidates for cellular targets.

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“…These three signaling pathways communicate and interact with one another in physiological conditions, and are important in regulating cell dissolution (34). Accumulating evidence suggests that mitochondria are not only the major source of intracellular ROS, but they are also the major targets of their detrimental effects in mammalian cells (15,35). Luteolin exerts its function as an antioxidant and ROS-generating agent (36), and various contrasting reports have been published regarding the effects of luteolin in the generation of ROS.…”

Section: Discussionmentioning

confidence: 99%

“…There is accumulating evidence that luteolin exerts its anticancer actions by affecting numerous biochemical pathways, which are critical for the regulation of cell proliferation, cell cycle arrest, apoptosis, angiogenesis, matrix metalloproteinase and metastasis (10)(11)(12)(13). Additionally, luteolin has been demonstrated to inhibit the proliferation of leukemia cells and other cells through a mitochondrial-dependent pathway mediated by reactive oxygen species (ROS) (9,(14)(15)(16)(17). currently, the effect of luteolin on patients with MdS has not been addressed.…”

Section: Introductionmentioning

confidence: 99%

“…It is recognized that the induction of apoptosis of cancer cells is one of the most important and direct approaches to attenuate the development of cancer and eliminate tumors (18). Increasing evidence from multiple studies has shown that cell apoptosis is closely associated with the loss of mitochondrial inner membrane structure and integrity (9,15). Mitochondria are central to the intrinsic apoptotic pathway, which involves a cascade of molecular events that occur entirely within the cell, and the increased ROS generation that occurs during apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Luteolin induces myelodysplastic syndrome‑derived cell apoptosis via the p53‑dependent mitochondrial signaling pathway mediated by reactive oxygen species

et al. 2018

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Luteolin, a common dietary flavonoid, induces the apoptosis of cells in several types of cancer. However, its role in myelodysplastic syndrome (MDS) and the potential underlying mechanisms remain to be elucidated. To evaluate the potential benefit and underlying mechanisms of luteolin in MDS cells, the viability of SKM‑1 cells and primary bone marrow (PBM) mononuclear cells from patients with intermediate‑ or high‑risk MDS were assessed using a Cell Counting Kit‑8 assay. The apoptotic features of cell morphology were assessed using Wright‑Giemsa staining, DNA fragmentation was analyzed by agarose gel electrophoresis, and the extent of apoptosis was quantified by flow cytometry (FCM). Reactive oxygen species (ROS) were measured by FCM with 2,7‑dichlorodihydrofluorescein diacetate staining and mitochondrial membrane potential (ΔΨm) was determined using 5,5',6,6'‑tetrachloro‑1,1',3,3'‑tetraethylbenzimidazolylcarbocyanine iodide staining. Caspase activity was detected using a fluorometric protease assay. Furthermore, the effects of luteolin on the expression of apoptosis‑related proteins were analyzed using western blot analysis. The resulting data revealed that luteolin significantly inhibited the proliferation of SKM‑1 cells in vitro, and its half maximal inhibitory concentration was 139.41 µM at 24 h and 23.95 µM at 72 h. Luteolin also markedly inhibited the proliferation of mononuclear cells from patients with intermediate‑ or high‑risk MDS. Luteolin suppressed cell proliferation, mainly as a result of the induction of apoptosis, as demonstrated by typical apoptotic morphological features, the ladder pattern of genomic DNA fragmentation, and the results of FCM using Annexin V‑FITC/PI double staining. It was also found that short‑term exposure of SKM‑1 cells to luteolin led to a marked increase in the accumulation of ROS. The increased intracellular level of ROS appeared to induce the activation of p53 and elevate the B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio, which modulates ΔΨm and triggers the release of cytochrome c, and may increase the activities of apoptotic protease activating factor 1, caspase‑3, ‑8 and ‑9 to further trigger the destruction of structural and specific proteins and thereby cell apoptosis. Notably, the inhibition of ROS generation by the antioxidant N‑acetyl‑L‑cysteine significantly attenuated the luteolin‑induced loss of ΔΨm and activities of caspase‑3, ‑8 and ‑9. These data suggested that luteolin exerts its pro‑apoptotic action partly through the p53‑dependent mitochondrial signaling pathway mediated by intracellular ROS, which provides a promising therapeutic candidate for patients with MDS.

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A ROS-mediated mitochondrial pathway and Nrf2 pathway activation are involved in BDE-47 induced apoptosis in Neuro-2a cells

Cited by 66 publications

References 28 publications

Proteomic analysis of the molecular mechanism of curcumin/β‐cyclodextrin polymer inclusion complex inhibiting HepG2 cells growth

Proteomic analysis of the molecular mechanism of curcumin/β‐cyclodextrin polymer inclusion complex inhibiting HepG2 cells growth

Identification of NQO1 and ferrochelatase as interaction partners for neuroprotective N‐{[2‐(4‐phenyl‐piperazin‐1‐yl)‐ethyl]‐phenyl}‐arylamides

Luteolin induces myelodysplastic syndrome‑derived cell apoptosis via the p53‑dependent mitochondrial signaling pathway mediated by reactive oxygen species

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