Effects of Some Non-Steroidal Anti-Inflammatory Drugs and Other Agents on Cyclooxygenase and Lipoxygenase Activities in Some Enzyme Preparations

Miyazawa, Kazuhiro; Iimori, Yayoi; Makino, Masao; Mikami, Takashi; Miyasaka, Katsuhiko

doi:10.1254/jjp.38.199

Cited by 34 publications

(11 citation statements)

References 22 publications

(6 reference statements)

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“…TNFR2-and PMA-mediated activation of CMV promoterenhancer and NFκB is resistant to NDGA and sodium salicylate, while the TNFR1-response is inhibited The antioxidant nordihydroguaiaretic acid (NDGA) (Niki, 1987) inhibits a variety of reactions dependent on oxidative processes, like lipoxygenase mediated generation of arachidonic acid metabolites (Miyazawa et al, 1985) and cytochrome P-450 catalysed electron transfer (Montag et al, 1993). NDGA inhibited TNFR1-and TNF-induced activation of the CMV promoter-enhancer (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Distinct Differences between TNF Receptor 1- and TNF Receptor 2- mediated Activation of NFκB

Thommesen¹,

Lægreid²

2005

BMB Reports

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Tumor necrosis factor (TNF) signaling is mediated via two distinct receptors, TNFR2 and TNFR1, which shows partially overlapping signaling mechanisms and biological roles. In the present study, TNFR2 and TNFR1 signal transduction mechanisms involved in activation of NFκB and CMV promoter-enhancer were compared with respect to their susceptibility towards inhibitors of intracellular signaling. For this, we used SW480 cells, where we have shown that TNF-signaling can occur independently through each of the two receptors. The TNFR1 response was inhibited by D609, bromophenacyl bromide (BPB), nordihydroguararetic acid (NDGA), and by sodium salicylate, while TNFR2-mediated activation of NFκB and CMV promoter-enhancer was resistant to these compounds. The signaling mechanisms known to be affected by these inhibitors include phospholipases as well as redox-and pH-sensitive intracellular components. Our results imply that TNFR2 signaling involved in NFκB activation proceeds independently of these inhibitor-sensitive signaling components, indicating distinct signaling pathways not shared with TNFR1.

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Section: Resultsmentioning

confidence: 99%

“…Alternatively, NDGA and salicylate, both being weak organic acids, may act through pH-sensitive intracellular components in the TNFR1 signaling pathway, as cytoplasmic acidification is proposed to be an important factor for the inhibitory effect of salicylate (Miyazawa et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Distinct Differences between TNF Receptor 1- and TNF Receptor 2- mediated Activation of NFκB

Thommesen¹,

Lægreid²

2005

BMB Reports

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“…More marked inhibition of ovulation by NDGA might be ascribed to two additional effects of this inhibitor. One is an antioxidant property (Carlson et al 1995, Takami et al 1999 since oxidative stress contributes to the ovulation process (Riley & Behrman 1991), and another is some cross-reactivity with COX that becomes expressed at the high dose (Van Wauwe & Goossens 1983, Miyazawa et al 1985. Preovulatory follicles that looked healthy and were with the largest diameter over 500 mm were examined for indicated numbers of ovaries in each group.…”

Section: Discussionmentioning

confidence: 99%

“…In all of the studies with a significant impact of LOX inhibition, the action mechanism of the inhibitor on ovulatory process has been virtually obscure. The specificity of the widely used inhibitor nordihydroguaiaretic acid (NDGA) against LOX is somewhat doubted (Van Wauwe & Goossens 1983, Miyazawa et al 1985. The effect of timing of drug administration relative to that of LH/human chorionic gonadotropin (hCG) stimulus has not been taken into consideration.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of ovulation by a lipoxygenase inhibitor involves reduced cyclooxygenase-2 expression and prostaglandin E2 production in gonadotropin-primed immature rats

Kurusu¹,

Jinno²,

Ehara³

et al. 2009

Reproduction

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Potential roles of cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism are established in a murine model of induced ovulation. Pharmacological inhibition of an alternative lipoxygenase (LOX) pathway has been shown to cause defective ovulation, but the mechanism is still undefined. This study investigated the effects of two LOX inhibitors and their time dependency on ovulation and COX activity in gonadotropins (eCG and human chorionic gonadotropin (hCG))-primed immature rats. Intra-ovarian bursal treatment with a general LOX inhibitor nordihydroguaiaretic acid (NDGA) at 0 h post-hCG (hCG0h) dose dependently inhibited ovulation rate. The drug was still but less effective when treated at hCG6h. A more specific inhibitor, 3,4-dihydroxyphenyl ethanol (DPE) was also inhibitory when treated at hCG0h but not at hCG6h. Interestingly, treatment with DPE at hCG0h resulted in attenuated expression of immunoreactive PTGS2 in granulosa layers and concomitant decrease in ovarian prostaglandin E 2 (PGE 2 ) content at hCG8h. NDGA treatment reduced immunoreactive PTGS2. Ovulatory impairment by both inhibitors was prevented by systemic administration of PGE 2 at hCG6h. Immunohistochemistry revealed the expression of ALOX5 and ALOX12 in both thecal and granulosa layers of preovulatory follicles and, notably, the augmented immunoreactivities during 8 h after hCG treatment. Our results indicate the probable presence of multiple LOX isoforms and that specific inhibition of LOX at an early stage of hCG-signaling led to reduced PTGS2 activity and thus defective ovulation. They reveal a probable relationship between two pathways of AA metabolism and account at least partly for the mechanism by which the LOX inhibitor causes impaired ovulation.

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“…After 4 h, IL-1␤ production was unaffected by the presence of indomethacin, an inhibitor of cyclooxygenase, or phenidion, an inhibitor of lipoxygenase (10). However, IL-1␤ release was abrogated by AACOCF 3 , an inhibitor of both cPLA 2 and iPLA 2 (11) (Fig.…”

Section: Il-1␤ Maturation Is Suppressed By Bel An Inhibitor Of Iplamentioning

confidence: 93%

Potassium Regulates IL-1β Processing Via Calcium-Independent Phospholipase A2

Walev

Klein

Husmann

et al. 2000

The Journal of Immunology

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We report that potassium leakage from cells leads to activation of the Ca2+-independent phospholipase A2 (iPLA2), and the latter plays a pivotal role in regulating the cleavage of pro-IL-1β by the IL-converting enzyme caspase-1 in human monocytes. K+ efflux led to increases of cellular levels of glycerophosphocholine, an unambiguous indicator of phospholipase A2 activation. Both maturation of IL-1β and formation of glycerophosphocholine were blocked by bromoenol lactone, the specific iPLA2 inhibitor. Bromoenol lactone-dependent inhibition of IL-1β processing was not due to perturbation of the export machinery for pro-IL-1β and IL-1β or to caspase-1 suppression. Conspicuously, activation of Ca2+-dependent phospholipase A2 did not support but rather suppressed IL-1β processing. Thus, our findings reveal a specific role for iPLA2 activation in the sequence of events underlying IL-1β maturation.

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Effects of Some Non-Steroidal Anti-Inflammatory Drugs and Other Agents on Cyclooxygenase and Lipoxygenase Activities in Some Enzyme Preparations

Cited by 34 publications

References 22 publications

Distinct Differences between TNF Receptor 1- and TNF Receptor 2- mediated Activation of NFκB

Distinct Differences between TNF Receptor 1- and TNF Receptor 2- mediated Activation of NFκB

Inhibition of ovulation by a lipoxygenase inhibitor involves reduced cyclooxygenase-2 expression and prostaglandin E2 production in gonadotropin-primed immature rats

Potassium Regulates IL-1β Processing Via Calcium-Independent Phospholipase A2

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