Influence of protein phosphatase inhibitors on HL60 cells death induction by dehydrocrotonin

Freire, Ana Claudia Galvão; Assis, Cristiane Fernandes de; Frick, Alexander Otto; Melo, Patrı́cia da Silva; Haun, Marcela; Aoyama, Hiroshi; Durán, Nélson; Sauer, Mariana M.; Kallás, Esper G.; Ferreira, Carmen Verı́ssima

doi:10.1016/s0145-2126(03)00013-4

Cited by 26 publications

(15 citation statements)

References 27 publications

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“…The samples were analyzed by FACS (Becton Dickinson) using Cell Quest Research Software (Becton Dickinson). Annexin V - /PI - cells are viable, annexin V + /PI - cells are in early apoptosis and annexin V + /PI + cells are necrotic or in late apoptosis [32, 33]. …”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Shi

Wang

Teng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ginsenoside Rb1 (Rb1) has been reported to have varieties of neuroprotective effects. This study aimed to evaluate the effects of Rb1 on pentylenetetrazol (PTZ)-induced rat brain injury and Mg²⁺ free-induced neuron injury and analyzed the detailed molecular mechanisms in vivo and in vitro. Methods: Seizure duration and latency were measured in epilepsy kindled rat. The cognitive impairment was assessed by Morris water maze (MWM) test. Oxidative stress parameters, malondialdehyde (MDA) and glutathione (GSH) were measured by the 2-thiobarbituric acid methods and the DTNB-GSSG reductase recycling methods. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Neuronal apoptosis was measured by Annexin V-FITC and propidium iodide (PI) staining. Immunohistochemistry and immunofluorescence staining were performed to evaluate Nrf2 and HO-1 expressions. Expression of Nrf2, HO-1, Bcl-2, iNOS and LC3 were evaluated by western blot. Results: The PTZ-injured rats presented longer seizure duration and shorter seizure latency. Rb1 ameliorated these effects, as well as the cognitive deficits caused by PTZ exposure. Besides, Rb1 dose-dependently increased GSH levels, decreased MDA levels and alleviated neuronal damage in PTZ-treated rats. In vitro, Rb1 increased cell viability and decreased neuronal apoptosis in a dose-dependent manner under Mg²⁺ free condition. Moreover, in vivo and in vitro, Rb1 enhanced both the Nrf2 and HO-1 expressions. Furthermore, upregulation of the expression of Bcl-2 and downregulation of the expression of iNOS and LC3 were observed. However, knockdown of Nrf2 adversely affected the protective effects of Rb1 in epileptic hippocampal neurons. Conclusion: Rb1 conferred neuroprotective effects against PTZ-induced brain damage and Mg²⁺ free-induced neuron injury by activating Nrf2/ARE signaling.

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Section: Methodsmentioning

confidence: 99%

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Shi

Wang

Teng

et al. 2018

Cell Physiol Biochem

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“…11 Among the pharmacological activities of t-DCTN, the antitumor activity merits particular attention. Currently, its cytotoxicity effect has been evaluated in several tumor cell lines, such as Ehrlich ascites cells, 2 3 promyelocytic leukemic cells (HL60), [12][13][14] Chinese hamster fibroblasts (V79) [15][16][17] and rat hepatocytes. 14 17 The in vivo antitumor activity has also been evaluated against two experimental ascites tumors: Sarcoma 180 (S-180) 2 and Erlich carcinoma.…”

Section: Introductionmentioning

confidence: 99%

Encapsulation of <I>Trans</I>-Dehydrocrotonin in Liposomes: An Enhancement of the Antitumor Activity

Lapenda¹,

Morais²,

Almeida³

et al. 2013

Journal of Biomedical Nanotechnology

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The aim of this study was the encapsulation of trans-dehydrocrotonin (t-DCTN) and its inclusion complexes with hydropropyl-beta-cyclodextrin (HP-beta-CD) in liposomes to improve t-DCTN antitumor activity. The in vitro kinetic profiles of t-DCTN-loaded liposomes (LD) and t-DCTN:HP-beta-CD-loaded liposomes (LC) were evaluated using the dialysis technique. The antitumor activity of LD and LC were investigated against Sarcoma 180 in Swiss mice. Histopathological and hematological analyses were carried out. The amounts of t-DCTN and t-DCTN:HP-beta-CD inclusion complex encapsulated in liposomes were equivalent to 1 mg of t-DCTN. The encapsulation efficiencies of LD and LC were 95.0 +/- 3.8% and 91.1 +/- 5.6%, respectively. In relation to kinetics, the drug release profiles of t-DCTN are in substantial agreement with the Fickian model. The treatment of animals with LD and LC produced tumor inhibitions of 79.4 +/- 9.6% and 63.5 +/- 5.5%, respectively. The liposomal encapsulation of t-DCTN by entrapment in the phospholipid bilayer increased at twice the antitumor activity. Moreover, the liposomal formulations reduced the hepatotoxicity effect of the drug and no significant hematological toxicity was observed in the treated animals. However, the counting of platelets was slightly decreased. Thus, the results show that the development of liposomal formulations containing t-DCTN or t-DCTN:HP-beta-CD is an important advance for enabling this drug to be use in therapy.

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“…For ROS analysis, the cells were re-suspended in 500 ll 10 lM of 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA); for DWm analysis, the cells were re-suspended in 500 ll 1 lM of 3,3 0 -dihexyloxcarbocyanine (DiOC6), and for Ca 2+ detection, the cells were re-suspended in 3 lg/ml Indo 1/AM, respectively and analyzed by flow cytometry as previously described . The superoxide anion measurement, the cells were incubated with 500.0 lg/ml of GPE for 2, 4, 6, 12, 24 and 48 h, based on the NBT assays, was carried out according to the method of Freire et al (2003).…”

Section: 8mentioning

confidence: 99%

Anti-invasion and apoptosis induction of chlorella (Chlorella sorokiniana) in Hep G2 human hepatocellular carcinoma cells

Chung¹,

Peng

Chu

et al. 2012

Journal of Functional Foods

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Apoptosis Invasion Human hepatocellular carcinoma cells Hep G2 cells A B S T R A C T The effects of 80% ethanolic extract derived from commercial granule chlorella (GPE) on cell viability, invasion capacity and apoptosis in human hepatoma cell line (Hep G2 cells) were investigated. The results demonstrated that GPE decreased cell viability, induced apoptosis and showed invasion inhibitory effects in the Hep G2 cells. GPE-triggered apoptosis was confirmed by 4 0 -6-diamidino-2-phenyindole (DAPI) staining and comet assay. GPE promoted an increase of reactive oxygen species (ROS) and Ca 2+ , and loss of mitochondrial membrane potential (DWm) accompanied by cytochrome c release that was due to the decrease of Bcl-2 in the Hep G2 cells. GPE also induced the protein levels of apoptosisinducing factor (AIF), increased the levels of caspase-3, -8 and -9, and stimulated the levels of fatty acid synthase (Fas) and Fas ligand (FasL) in the Hep G2 cells. Additionally GPE inhibited invasion of Hep G2 cells by down-regulation of the expression of matrix metalloproteinase (MMP)-2 and -9. Furthermore, cellular glutathione content and superoxide dismutases (SOD) activities were significantly reduced and thiobarbituric acid-reactive substances (TBARS) levels were significantly increased after GPE treatment. These results suggest that GPE can induce cytotoxicity on Hep G2 cells and inhibit the invasive capacity of malignant cells.

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Influence of protein phosphatase inhibitors on HL60 cells death induction by dehydrocrotonin

Cited by 26 publications

References 27 publications

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Encapsulation of <I>Trans</I>-Dehydrocrotonin in Liposomes: An Enhancement of the Antitumor Activity

Anti-invasion and apoptosis induction of chlorella (Chlorella sorokiniana) in Hep G2 human hepatocellular carcinoma cells

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