Dose-dependent inhibition of cell proliferation induced by lipid peroxidation products in rat hepatoma cells after enrichment with arachidonic acid

Lipids ◽  
1999 ◽  
Vol 34 (7) ◽  
pp. 705-711 ◽  
Author(s):  
Giuliana Muzio ◽  
Raffaella A. Salvo ◽  
Antonella Trombetta ◽  
Riccardo Autelli ◽  
Marina Maggiora ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Proliferation ◽  
Arachidonic Acid ◽  
Hepatoma Cells ◽  
Lipid Peroxidation Products ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Increase in class 2 aldehyde dehydrogenase expression by arachidonic acid in rat hepatoma cells

2001 ◽  
Vol 357 (3) ◽  
pp. 811-818 ◽  
Author(s):  
Rosa A. CANUTO ◽  
Margherita FERRO ◽  
Raffaella A. SALVO ◽  
Anna M. BASSI ◽  
Antonella TROMBETTA ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Arachidonic Acid ◽  
Cell Growth ◽  
Cell Lines ◽  
Aldehyde Dehydrogenase ◽  
Hepatoma Cell ◽  
Hepatoma Cells ◽  
Hepatoma Cell Lines ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Aldehyde dehydrogenase (ALDH) is a family of several isoenzymes important in cell defence against both exogenous and endogenous aldehydes. Compared with normal hepatocytes, in rat hepatoma cells the following changes in the expression of ALDH occur: cytosolic class 3 ALDH expression appears and mitochondrial class 2 ALDH decreases. In parallel with these changes, a decrease in the polyunsaturated fatty acid content in membrane phospholipids occurs. In the present study we demonstrated that restoring the levels of arachidonic acid in 7777 and JM2 rat hepatoma cell lines to those seen in hepatocytes decreases hepatoma cell growth, and increases class 2 ALDH activity. This latter effect appears to be due to an increased gene transcription of class 2 ALDH. To account for this increase, we examined whether peroxisome-proliferator-activated receptors (PPARs) or lipid peroxidation were involved. We demonstrated a stimulation of PPAR expression, which is different in the two hepatoma cell lines: in the 7777 cell line, there was an increase in PPARα expression, whereas PPARγ expression increased in JM2 cells. We also found increased lipid peroxidation, but this increase became evident at a later stage when class 2 ALDH expression had already increased. In conclusion, arachidonic acid added to the culture medium of hepatoma cell lines is able to partially restore the normal phenotype of class 2 ALDH, in addition to a decrease in cell growth.

scholarly journals Bioassay-Guided Isolation of Antiproliferative Compounds from Limbarda crithmoides (L.) Dumort

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1893
Author(s):  
Sabrina Adorisio ◽  
Laura Giamperi ◽  
Anahi Elena Ada Bucchini ◽  
Domenico Vittorio Delfino ◽  
Maria Carla Marcotullio
Keyword(s):  
Cell Proliferation ◽  
Nmr Spectroscopy ◽  
Separation Procedure ◽  
High Cell ◽  
Thymol Derivatives ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
High Cell Proliferation ◽  
Acute Myeloid

Limbarda crithmoides (L.) Dumort (Asteraceae) n-hexane extract displayed high cell proliferation inhibitory activity against acute myeloid leukaemia cells (OCI-AML3) and was therefore subjected to a bioassay-guided multistep separation procedure. Two thymol derivatives, namely 10-acetoxy-8,9-epoxythymol tiglate (1) and 10-acetoxy-9-chloro-8,9-dehydrothymol (2), were isolated and identified by means of NMR spectroscopy. Both of them exhibited a significant dose-dependent inhibition of cell proliferation.

scholarly journals Rifampin Inhibits Prostaglandin E2 Production and Arachidonic Acid Release in Human Alveolar Epithelial Cells

2007 ◽  
Vol 51 (12) ◽  
pp. 4225-4230 ◽  
Author(s):  
Yael Yuhas ◽  
Inbar Azoulay-Alfaguter ◽  
Eva Berent ◽  
Shai Ashkenazi
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Arachidonic Acid Release ◽  
Alveolar Epithelial ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Acid Release ◽  
Dose Dependent ◽  
Human Alveolar Epithelial Cells

ABSTRACT Rifampin, a potent antimicrobial agent, is a major drug in the treatment of tuberculosis. There is evidence that rifampin also serves as an immunomodulator. Based on findings that arachidonic acid and its metabolites are involved in the pathogeneses of Mycobacterium tuberculosis infections, we investigated whether rifampin affects prostaglandin E2 (PGE2) production in human alveolar epithelial cells stimulated with interleukin-1β. Rifampin caused a dose-dependent inhibition of PGE2 production. At doses of 100, 50, and 25 μg/ml, it inhibited PGE2 production by 75%, 59%, and 45%, respectively (P < 0.001). Regarding the mechanism involved, rifampin caused a time- and dose-dependent inhibition of arachidonic acid release from the alveolar cells. At doses of 100, 50, 25, and 10 μg/ml, it significantly inhibited the release of arachidonic acid by 93%, 64%, 58%, and 35%, respectively (P < 0.001). Rifampin did not affect the phosphorylation of cytosolic phospholipase A2 or the expression of cyclooxygenase-2. The inhibition of PGE2, and presumably other arachidonic acid products, probably contributes to the efficacy of rifampin in the treatment of tuberculosis and may explain some of its adverse effects.

Effects of Methylprednisolone and Hydrocortisone on Aggregation of Rabbit Platelets Induced by Arachidonic Acid and Other Aggregating Substances

1981 ◽  
Vol 46 (04) ◽  
pp. 676-679 ◽  
Author(s):  
Frank Glass ◽  
Howard Lippton ◽  
Philip J Kadowitz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Actual Mechanism ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
The Difference ◽  
Induced Aggregation ◽  
Dose Dependent

SummaryThe effects of methylprednisolone and hydrocortisone on platelet aggregation induced by arachidonic acid (AA), collagen, adenosine diphosphate (ADP), prostaglandin (PG) H2, and a stable PGH2 analog, were studied in platelet-rich plasma (PRP) from the rabbit. Incubation of either steroid in PRP inhibited AA-, collagen- and ADP-induced platelet aggregation in a concentration-related manner. The dose of methylprednisolone required to inhibit 0.02 mM AA-induced aggregation was lower than that required to inhibit either 0.08 μg/ml collagen or 0.2 μM ADP-induced aggregation. Methylprednisolone produced a dose dependent inhibition of platelet aggregation induced by PGH2 and the stable PGH2 analog. In washed platelets methylprednisolone was more effective in inhibiting AA-induced aggregation than ADP- or collagen-induced aggregation; however, the difference in effect was less than in PRP. Platelet responses to AA in PRP from rabbits treated with hydrocortisone or methylprednisolone, 100 mg/kg i.v., were inhibited in a transient manner, whereas aggregation induced by ADP under similar conditions was unchanged. Since inhibition of aggregation elicited by AA occurred at concentrations which do not influence PGH2-, PGH2 analog-, collagen- or ADP-induced aggregation, the present data suggest that the steroids may inhibit the incorporation, the release, or the metabolism of arachidonic acid in platelets. The actual mechanism of this relatively specific inhibition of AA-induced aggregation by anti-inflammatory steroids is uncertain but may be related to the membrane “stabilizing” properties of methylprednisolone and hydrocortisone.

Dose-Dependent Inhibition of BrdU Detection in the Cell Proliferation ELISA by Culture Medium Proteins

2009 ◽  
Vol 30 (3) ◽  
pp. 348-357 ◽  
Author(s):  
Lauriane Padet ◽  
Isabelle St-Amour ◽  
Eric Aubin ◽  
Dominic Paquin Proulx ◽  
Renée Bazin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Culture Medium ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

scholarly journals The Effect of Triptolide on Apoptosis of Glioblastoma Multiforme (GBM) Cells

2007 ◽  
Vol 35 (5) ◽  
pp. 637-643 ◽  
Author(s):  
J Lin ◽  
L-Y Chen ◽  
Z-X Lin ◽  
M-L Zhao
Keyword(s):  
Cell Proliferation ◽  
Glioblastoma Multiforme ◽  
Chinese Herb ◽  
P53 Gene ◽  
Growth Curve Analysis ◽  
Apoptotic Protein ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Induction Of Apoptosis ◽  
Dose Dependent

Triptolide, derived from the traditional Chinese herb, Tripterygium wilfordii, sensitizes cancer cells to apoptosis. Glioblastoma multiforme (GBM), which accounts for most cases of central nervous malignancy, has a very poor prognosis and lacks effective therapeutic inventions. We, therefore, investigated the effects of different concentrations of, and different periods of exposure to, triptolide on cell proliferation and apoptosis in the glioma cell lines, U251MG and U87MG, and in normal human fetal astrocytes. Cell proliferation was investigated by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide) assay and growth curve analysis, and apoptosis was assessed from genomic DNA fragmentation. Triptolide showed dose-dependent inhibition of cell proliferation and induction of apoptosis in glioma cells. It also increased the ratio of the pro-apoptotic protein, Bax, to the anti-apoptotic protein, Bcl-2. Since U87MG has the wild-type p53 gene whereas U251MG harbours a mutated p53 gene, our results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway. The dose-dependent inhibition of cell proliferation and induction of apoptosis by triptolide may involve upregulation of Bax and downregulation of Bcl-2.

Study of surface heteroorganic antigens of rat hepatoma cells participating in the cell proliferation process

2008 ◽  
Vol 2 (3) ◽  
pp. 246-252
Author(s):  
N. P. Teryukova ◽  
G. I. Blinova ◽  
Yu. M. Rozanov ◽  
V. A. Ivanov
Keyword(s):  
Cell Proliferation ◽  
Hepatoma Cells ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Mepacrine Blockade of Arachidonate-lnduced Washed Platelet Aggregation: Relationship to Mepacrine Inhibition of Platelet Cyclooxygenase

1983 ◽  
Vol 50 (04) ◽  
pp. 784-786 ◽  
Author(s):  
Amiram Raz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Thromboxane B2 ◽  
Concomitant Increase ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Arachidonate Release ◽  
Dose Dependent

SummaryMepacrine, in addition to its established antilipolytic activity, was also found to inhibit the conversion of 14C-arachidonic acid to 14C-thromboxane B2 in human washed platelets. In the concentration range of 3.33-33 μM, mepacrine exerted a dose dependent inhibition of arachidonate conversion to thromboxane B2 in parallel to inhibition of arachidonate-induced platelet aggregation. Mepacrine inhibition of thromboxane formation was not accompanied by a concomitant increase in other cyclooxygenase products. Furthermore, mepacrine did not affect platelet transformation of added prostaglandin H2 to thromboxane A2 and other products. These results indicate that mepacrine inhibits the cyclooxygenase enzyme and not thromboxane synthase. In washed platelets, mepacrine inhibition of arachidonic acid conversion to thromboxane A2 appears to be a major factor in the overall inhibitory effect of the compound on the combined process of arachidonate release from cellular phospholipids and its conversion to proaggregatory products.

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