Anandamide-Induced Cell Death: Dual Effects in Primary Rat Decidual Cell Cultures

Placenta ◽  
2009 ◽  
Vol 30 (8) ◽  
pp. 686-692 ◽  
Author(s):  
B.M. Fonseca ◽  
G. Correia-da-Silva ◽  
N.A. Teixeira
2014 ◽  
Vol 74 (1) ◽  
pp. 33-45
Author(s):  
Jing Zhang ◽  
Yicheng Yu ◽  
Zongyun Li ◽  
Cunhua Sun ◽  
Jian Zhang ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.


1993 ◽  
Vol 122 (3) ◽  
pp. 523-532 ◽  
Author(s):  
A Batistatou ◽  
LA Greene

Serum-free PC12 cell cultures have been used to study the mechanisms of neuronal death after neurotrophic factor deprivation. We previously reported that PC12 cells undergo "apoptotic" internucleosomal DNA cleavage after withdrawal of trophic support. Here, we have used a sensitive method to detect PC12 cell DNA fragmentation within three hrs of serum removal and have exploited this assay to examine several aspects regarding the mechanisms of neuronal survival/death. Major advantages of this assay are that it permits acute experiments to be performed well before other manifest signs of cell death and under conditions that cannot be applied chronically. We find that this apopotic DNA fragmentation is distinct from the random DNA degradation that occurs during necrotic death. Major observations include the following: (a) There is a good correlation between the ability of trophic substances to promote PC12 cell survival and to inhibit early DNA fragmentation. (b) Phorbol ester, an activator of PKC, acutely suppresses DNA fragmentation, but does not promote long-term survival or inhibition of endonuclease activity when applied chronically due to its downregulation of PKC. (c) Cells undergoing apoptosis within 3 h of serum withdrawal have a "commitment point" of only 1.0-1.5 h beyond which they can no longer be rescued by NGF. (d) Aurin, a non-carboxylic analog of the endonuclease inhibitor ATA, also inhibits DNA fragmentation and promotes short-term survival of PC12 cells. (e) Macromolecular synthesis is not required for DNA fragmentation or for NGF to prevent this event. (f) Extracellular Ca2+ is not required for internucleosomal DNA cleavage caused by serum withdrawal or for suppression of this by NGF. (g) DNA fragmentation can also be detected in cultures of rat sympathetic neurons as early as 10 h after removal of NGF. As in PC12 cell cultures, this precedes morphological signs of cell death.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 446-448 ◽  
Author(s):  
J. Koehl ◽  
E.F. Elstner ◽  
W. Oßwald ◽  
I. Heiser

Mode of action of β-quercinin, a novel elicitin on tobacco cell suspension cultures (cvs. Bel B and Bel W3) was investigated by measuring the oxidative burst and cell death in these cell cultures. β-quercinin induced an oxidative burst comparable to that excited by zoospores from P. quercina. Adding superoxidedismutase, catalase and diphenyleneiodonium to elicited cell cultures, it could be demonstrated, that the induction of cell death in tobacco cell cultures is not correlated to the oxidative burst.


Weed Science ◽  
1994 ◽  
Vol 42 (2) ◽  
pp. 310-315 ◽  
Author(s):  
Thouraya Souissi ◽  
Robert J. Kremer

Bioassays using cell cultures and callus tissues of leafy spurge were devised to evaluate the potential of rhizobacteria as biocontrol agents. Rhizobacteria isolated from roots of leafy spurge seedlings were screened in suspension-cultured leafy spurge cells. Cell viability was assessed using the Evan's blue bioassay 48 h after bacterial inoculation. Among the 30 isolates tested, LS102 and LS105 consistently caused intensive cell death determined by measuring the A630of the inoculated cell cultures. Cell death was 2.5 to 3 times higher in cultures inoculated with LS105 and LS102, respectively, than in the control. Population levels of the two isolates within cell cultures and callus tissues of leafy spurge increased during the first 48 h. Leafy spurge callus tissues were inoculated with rhizobacteria either directly or by using the Host Pathogen Interaction System (HPIS). The latter exposes calli to bacteria without any physical contact. LS102 caused cellular leakage and eventually death of the callus tissue. Callus growth was reduced by about 30 to 70% when exposed to LS102 and LS105, respectively. Results suggest that these two isolates may affect leafy spurge at the cellular level by different mechanisms. A screening method based on cell cultures and callus tissues offers a good and rapid technique for detecting deleterious rhizobacteria with potential as biocontrol agents for leafy spurge.


2009 ◽  
Vol 13 (04n05) ◽  
pp. 544-551 ◽  
Author(s):  
Magdalena Cañete ◽  
Juan C. Stockert ◽  
Angeles Villanueva

Photodynamic therapy (PDT) is a subject of increasing biomedical research and represents a very promising therapeutic modality for palliative or even curative treatment of some superficial or endoscopically accessible tumors. In addition to the first photosensitizers (PSs) applied (hematoporphyrin-based drugs), second generation PSs with improved photophysical and photobiological properties are now studied using cell cultures, experimental tumors and clinical trials. On the other hand, there is a growing interest in the analysis of cell death mechanisms by apoptosis, which is especially relevant in oncology, because many anticancer drugs work, at least in part, by triggering apoptosis in neoplastic cells both in vitro and in vivo. The evaluation of cell death mechanisms is an important parameter to determine the efficacy and the potential toxicity of a treatment, allowing better adjustment of protocol. Using cell cultures, our research team has studied the mechanisms of cell damage and death implicated in the photodynamic processes, as well as the relationship between the cellular localization of the PS and the organelle damage during photosensitization. The results obtained in our laboratory provide a deeper understanding on the action mechanisms that lead to cell inactivation by PDT, and also allow selection of PSs with higher potential for clinical application than those currently in use.


Nephron ◽  
2001 ◽  
Vol 87 (3) ◽  
pp. 269-273 ◽  
Author(s):  
Michele Buemi ◽  
Demetrio Marino ◽  
Giuseppe Di Pasquale ◽  
Fulvio Floccari ◽  
Massimino Senatore ◽  
...  

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