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1 usly used to characterize cyclooxygenase and lipoxygenase inhibitors.
2 droxyl radicals, and most of them are potent lipoxygenase inhibitors.
3 dependent gene expression was inhibited by 5-lipoxygenase inhibitors.
4 rious agents were given in the presence of 5-lipoxygenase inhibitors.
5 ndpoints for future clinical trials of 12/15-lipoxygenase inhibitors.
6 rategies for future development of selective lipoxygenase inhibitors.
9 ONO-RS-082, quinacrine and AACOCF3) and the lipoxygenase inhibitor AA861 delayed the initial outgrow
10 tor, nordihydroguaiaretic acid (NDGA), the 5-lipoxygenase inhibitor, AA861, the epoxygenase inhibitor
14 ygenase inhibitors, the lack of benefit from lipoxygenase inhibitors, and possible future methodologi
16 hes such as NO-COX-2 inhibitors and dual COX-lipoxygenase inhibitors are already warranting interest.
18 enzymes was examined in the presence of the lipoxygenase inhibitor baicalein and/or exogenous 12(S)H
19 4-aminopyridine (4-AP; 100 microM) and a 12-lipoxygenase inhibitor, baicalein (5 microM), suggesting
21 bited by both nonspecific cyclooxygenase and lipoxygenase inhibitors but not by inhibitors specific f
24 ects these cells from apoptosis induced by 5-lipoxygenase inhibitors, confirming a critical role of 5
30 e cyclooxygenase inhibitor aspirin and the 5-lipoxygenase inhibitor MK-886 both partially inhibited D
31 ether inhibition of LT biosynthesis with a 5-lipoxygenase inhibitor (MK-591) induces remission in pat
36 In this study, we examined the effects of 5-lipoxygenase inhibitors (nordihydroguaiaretic acid and A
37 addition, MA-10 cells were treated with the lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA)
38 s of superoxide-generating enzymes, only the lipoxygenase inhibitor, nordihydroguaiaretic acid reduce
39 rompted the development of a large number of lipoxygenase inhibitors of possible therapeutic and prob
40 mes; and nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor on human lung cancer cell lines.
41 ombination with EGF, countered the effect of lipoxygenase inhibitors on PKC activation, and 12(S)HETE
43 asthma received either 600 mg zileuton, a 5-lipoxygenase inhibitor, or a placebo four times daily fo
49 viorally in rats in vivo, NRM infusion of 12-lipoxygenase inhibitors significantly reduced DOR-induce
50 The addition of nordihydroguaiaretic acid, a lipoxygenase inhibitor, significantly increased NaBT-ind
52 scovery of second generation N-hydroxyurea 5-lipoxygenase inhibitors was accomplished through the dev
53 in-treated cells, whereas cyclooxygenase and lipoxygenase inhibitors were ineffective, indicating tha
58 kast, zafirlukast, and pranlukast, and the 5-lipoxygenase inhibitor, zileuton, are unique in their ab
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