Effect of Lipoxygenase Inhibition on Mucous Glycoprotein Secretion from Chinchilla Middle Ear Fpithelial Cells in Vitro

1996 ◽  
Vol 105 (11) ◽  
pp. 916-921 ◽  
Author(s):  
Jizhen Lin ◽  
Youngki Kim ◽  
Frank Ondrey ◽  
Chris Lees ◽  
Steven K. Juhn
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Middle Ear ◽  
Platelet Activating Factor ◽  
Lipoxygenase Inhibitor ◽  
Lipoxygenase Inhibition ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Glycoprotein Secretion

Lipoxygenase is an enzyme that metabolizes arachidonic acid down to leukotrienes. Recent studies have shown that the enzyme is implicated in mucous glycoprotein (MGP) secretion stimulated by inflammatory mediators in the airways, suggesting its possible role in secretion of MGP from middle ear epithelial cells. To investigate a correlation between MGP secretion and the arachidonic acid metabolites, we examined the effects of nordihydroguaretic acid (NDGA, both a cyclooxygenase and lipoxygenase inhibitor), low-dose indomethacin (an inhibitor of cyclooxygenase), and A63162 (an inhibitor of lipoxygenase) on MGP secretion in cultured chinchilla middle ear epithelial cells. It was found that lipoxygenase inhibition led to reduction of MGP secretion from cultured chinchilla middle ear epithelial cells, while cyclooxygenase inhibition did not. Both cyclooxygenase and lipoxygenase inhibition resulted in profound blockage of MGP secretion in baseline and platelet activating factor-stimulated MGP secretion. It was concluded, therefore, that MGP secretion was linked to arachidonic acid metabolites, especially lipoxygenase products.

Arachidonic acid metabolites induced β-adrenoceptor densitization in rat lung in vitro

1985 ◽  
Vol 30 (5) ◽  
pp. 799-809 ◽  
Author(s):  
Luisa Daffonchio ◽  
Maria Pia Abbracchio ◽  
Alicia Hernandez ◽  
Emanuela Giani ◽  
Flaminio Cattabeni ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Lung ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation

1996 ◽  
Vol 134 (6) ◽  
pp. 1060-1064 ◽  
Author(s):  
S. IZAKI ◽  
T. YAMAMOTO ◽  
Y. GOTO ◽  
S. ISHIMARU ◽  
F. YUDATE ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Activating Factor ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Interleukin-1β Modulates in Vitro Mucous Glycoprotein Secretion and Proliferation of the Middle Ear Epithelial Cells

1995 ◽  
Vol 113 (2) ◽  
pp. P122-P122
Author(s):  
Jizhen Lin ◽  
Youngki Kim ◽  
Chris Lees ◽  
Steven K. Juhn
Keyword(s):  
Epithelial Cells ◽  
Middle Ear ◽  
Interleukin 1Β ◽  
Glycoprotein Secretion

Studies on the roles of phospholipase A2 and eicosanoids in the regulation of corticotrophin secretion by rat pituitary cells in vitro

1991 ◽  
Vol 130 (1) ◽  
pp. 21-32 ◽  
Author(s):  
A. M. Cowell ◽  
R. J. Flower ◽  
J. C. Buckingham
Keyword(s):  
Arachidonic Acid ◽  
Platelet Activating Factor ◽  
Nordihydroguaiaretic Acid ◽  
Cyclooxygenase Inhibitors ◽  
Pituitary Cells ◽  
Lipoxygenase Inhibitor ◽  
Acth Secretion ◽  
Lipoxygenase Inhibitors ◽  
Prostaglandin F

ABSTRACT Dispersed anterior pituitary cells were used to investigate the possible roles of phospholipid metabolites released by phospholipase A2 (PLA2) in the control of immunoreactive ACTH (ir-ACTH) secretion in vitro. PLA2 (15 600–62 500 U/1), the PLA2 activator melittin (0·5–20 mg/l) and arachidonic acid (1 mmol/l) all produced increases in ir-ACTH release from the cells, whilst platelet-activating factor (PAF), prostaglandin F2α (PGF2α), the prostacyclin analogues iloprost and BW245C, the thromboxane A2 (TXA2) analogue U46619, and the leukotrienes LTB4 and LTC4 were ineffective in this respect. PGF2α (100 nmol/l and 1 μmol/l), iloprost (1 μmol/l) and BW245C (100 nmol/l and 1 μmol/l) depressed corticotrophin-releasing factor-41-induced ir-ACTH secretion, while the PAF antagonist BN52021 (10 and 100 μmol/l) and LTC4 (100 nmol/l and 1 μmol/l) had no discernable effects. The secretory responses of the cells to hypothalamic extracts (0·2 hypothalami/ml) and arachidonic acid (1 mmol/l) were generally unaffected by the cyclooxygenase inhibitors ibuprofen (10 and 100 μmol/l) and indomethacin (10 μmol/l), the TXA2 synthetase inhibitor imidazole (10 μmol/l–1 mmol/l), the lipoxygenase inhibitor nordihydroguaiaretic acid (10 and 100 μmol/l) and the dual cyclo-oxygenase/lipoxygenase inhibitors phenidone (1–100 μmol/l) and BW755C (10 and 100 μmol/l). They were, however, inhibited by the dual cyclo-oxygenase/lipoxygenase inhibitor eicosatetraynoic acid (10 and 100 μmol/l), which also blocks epoxygenase and PLA2 activity and by the cytochrome P450 inhibitor SKF-525A (1 mmol/l). The results suggest that the stimulatory effects of PLA2 and arachidonic acid on ir-ACTH secretion are not effected by products generated by the cyclo-oxygenase or lipoxygenase pathways but may be mediated by metabolites generated by the cytochrome P450 pathway. Journal of Endocrinology (1991) 130, 21–32

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