Induction of Apoptosis in Human Promyelocytic Leukemia Cell Line HL-60 by C-Benzylated Dihydrochalcones, Uvaretin, Isouvaretin and Diuvaretin

Nakatani, Noriyoshi; Ichimaru, Momoyo; Moriyasu, Masataka; Kato, Atsushi

doi:10.1248/bpb.28.83

Cited by 28 publications

(17 citation statements)

References 13 publications

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“…21) After SH-SY5Y cells were directly treated with the vehicle (control group) or 6.25-500 nM rotenone for 48 h, a concentration-dependent decrease of cell viability was found by MTT reduction assay (Fig. 1).…”

Section: Thp-1 Enhanced Rotenone Neurotoxicity Through Stimulated Celmentioning

confidence: 94%

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Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

Zhao

Zhu

2006

Biological & Pharmaceutical Bulletin

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Rotenone, a naturally occurring, lipophilic compound from the roots of certain plants (Derris species) is used as the main component of many insecticides. Increasing evidence has suggested an important role for rotenone in the pathogenesis of Parkinson's disease (PD). Mechanistically, rotenoneinduced dopaminergic neurodegeneration has been associated with both its inhibition of neuronal mitochondrial complex I and the enhancement of activated microglia. [1][2][3][4][5] The activation of glia, particularly microglia is the hallmark of brain inflammation. Recently, increasing evidences from human and animal studies have suggested that neuroinflammation is an important contributor to the neuronal loss in PD. 3,[6][7][8][9] In addition, inhibition of the inflammatory reaction could attenuate degeneration of nigrostriatal dopaminecontaining neurons in several models of PD.10) Previous studies have demonstrated that microglia-enhanced rotenone neurotoxicity can be attributed to the release of NADPH oxidase-derived superoxide from activated microglia and in turn the oxidation of dopamine (DA) to the o-quinone dopaminochrome (DACHR) extracellularly. 4,11) In these cultures, superoxide was considered a dominant degenerative factor for the dopaminergic neurons. However, given that SOD and catalase afforded only a partial neuroprotection and microglia also have the ability to release pro-inflammatory and neurotoxic factors, 3,12,13) exact mechanisms underlying the role of inflammatory response involved in rotenone-induced PD remain to be identified. Though several approaches have been used to examine direct neuron-glia interactions under controlled in vitro conditions, 3,14) in these primary coculture systems it is nearly impossible to study the intracellular events in pure microglia and dopaminergic neuron and the sequence of microglia-activation and DA neurotoxicity can not be clarified specifically. As a result, the potential implications of these two cells can not be validated precisely.Recent evidence indicates that cellular redox state promi- In the present study, we adopted two consequential linking cell systems to study the mechanisms underlying the microglia-enhanced rotenone neurotoxicity. The supernatant from rotenone-stimulated human monocytic THP-1 line was then used as the culture medium for SH-SY5Y neuroblastoma which was used as target neuronal cells. Human postmortem microglia behaved similarly to THP-1 cells. 18,19) We further investigated whether rotenone can regulate the intracellular signaling of monocytic THP-1 cells. MATERIALS AND METHODS MaterialsDulbecco's modified Eagle's medium (DMEM-F12) was purchased from GibcoBRL (Gaithersburg, MD, U.S.A.). Fetal calf serum was obtained from Hyclone (Logan, UT, U.S.A). Rotenone, propidium iodide (PI), 3-(4,5-dimethylthiazal-z-yl)-2,5-diphenylterazolium (MTT), chromatin dye bisbenzimide (Hoechst 33258), RNase were purchased from Sigma (St. Louis, MO, U.S.A). Antibodies for phospho-ERK (Thr202/Tyr204), phospho-JNK (Thr183/ Tyr185), phospho-p38 (Thr180/Tyr182) we...

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Section: Thp-1 Enhanced Rotenone Neurotoxicity Through Stimulated Celmentioning

confidence: 94%

“…21) Cultures were fixed for 10 min with 4% formaldehyde in PBS at 37°C, and then permeabilized by treatment with a 19 : 1 mixture of ethanol/ acetic acid for 15 min at 25°C. After being washed with PBS, the cells were stained with 1 mg/ml Hoechst 33258 in PBS for 20 min at room temperature and then washed again.…”

Section: Methodsmentioning

confidence: 99%

Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

Zhao

Zhu

2006

Biological & Pharmaceutical Bulletin

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“…The Hoechst reagent was taken up by the nuclei of the cells, and apoptotic cells showed a bright blue fluorescence. Analysis was done by fluorescence microscopy using uv-excitation at 350 nm and emission at 460 nm, apoptotic cells being characterized by pyknotic and fragmented nuclei emitting intense fluorescence [37]. Stained cells from each treatment group were examined and counted under an Olympus fluorescence microscope (Olympus, Melville, NY, USA).…”

Section: Methodsmentioning

confidence: 99%

Fisetin, a Dietary Flavonoid, Induces Cell Cycle Arrest and Apoptosis through Activation of p53 and Inhibition of NF‐Kappa B Pathways in Bladder Cancer Cells

Cheng

et al. 2010

Basic Clin Pharma Tox

104

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There is an obvious urgent need to find effective and safe therapies to prevent both recurrence and progression of bladder cancer. In the present study, we report that fisetin-induced apoptosis in human bladder cancer is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro-and anti-apoptotic proteins. The results showed that fisetin inhibited the proliferation of T24 and EJ cells by inducing apoptosis and blocking cell cycle progression in the G0 ⁄ G1 phase. Western blot assay showed that fisetin significantly increases the expression of p53 and p21 proteins, and decreases the levels of cyclin D1, cyclin A, CDK4 and CDK2, thereby contributing to cell cycle arrest. In addition, fisetin increased the expression of Bax and Bak but decreased the levels of Bcl-2 and Bcl-xL and subsequently triggered mitochondrial apoptotic pathway. Our study suggests that the activation of p53 and inhibition of the NF-kappa B system may play important roles in the fisetin-induced apoptosis in bladder cancer cells.

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“…A large spectrum of chalcone derivatives with proapoptotic properties have been found in various edible or medicinal plants. Induction of apoptosis in gastric cancer cells has been reported for 2 0 ,4 0 -dihydroxychalcone (29) isolated from Herba oxytropis [110] and for uvaretin (35), isouvaretin (36), and diuvaretin (37) from Uvaria acuminata in leukemia cells [125]. Similarly, 2 0 ,4…”

Section: Chalcones As Inducers Of Cell Death Mechanismsmentioning

confidence: 79%

Dietary chalcones with chemopreventive and chemotherapeutic potential

et al. 2011

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Chalcones are absorbed in the daily diet and appear to be promising cancer chemopreventive agents. Chalcones represent an important group of the polyphenolic family, which includes a large number of naturally occurring molecules. This family possesses an interesting spectrum of biological activities, including antioxidative, antibacterial, anti-inflammatory, anticancer, cytotoxic, and immunosuppressive potential. Compounds of this family have been shown to interfere with each step of carcinogenesis, including initiation, promotion and progression. Moreover, numerous compounds from the family of dietary chalcones appear to show activity against cancer cells, suggesting that these molecules or their derivatives may be considered as potential anticancer drugs. This review will focus primarily on prominent members of the chalcone family with an 1,3-diphenyl-2-propenon core structure. Specifically, the inhibitory effects of these compounds on the different steps of carcinogenesis that reveal interesting chemopreventive and chemotherapeutic potential will be discussed.

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Induction of Apoptosis in Human Promyelocytic Leukemia Cell Line HL-60 by C-Benzylated Dihydrochalcones, Uvaretin, Isouvaretin and Diuvaretin

Cited by 28 publications

References 13 publications

Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

Fisetin, a Dietary Flavonoid, Induces Cell Cycle Arrest and Apoptosis through Activation of p53 and Inhibition of NF‐Kappa B Pathways in Bladder Cancer Cells

Dietary chalcones with chemopreventive and chemotherapeutic potential

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