[Chemical constituents from Murraya euchrestifolia].[Pubmed: 29090551]

The open silica gel, ODS, and Sephadex LH-20 column chromatography, along with the semi-preparative HPLC was used to isolate and purify the chemical constituents from Murraya euchrestifolia. The structures of the isolates were elucidated by their physiochemical properties, NMR, and MS spectroscopic data, as well as comparison with literature data. Eighteen compounds were isolated from the CH2Cl2 fraction of the 95% aqueous EtOH extract of M. euchrestifolia, and their structures were identified as sakuranetin (1), eriodictyol-7,4'-dimethyl ether (2), isosakuranetin (3), 5-hydroxy-7,4'-dimethoxyflavanone (4), eriodictyol-7-methyl ether (5), lichexanthon (6), 5,6,7-trimethoxycoumarin (7), 5-hydroxy-6,8-dimethoxycoumarin (8), 8-hydroxy-6-methoxy-3-n-pentylisocoumarin (9), ethyl caffeate (10), 4-hydroxy-3,5- dimethoxycinnamic acid ethyl ester (11), methyl 3-(5'-hydroxyprenyl)-coumarate (12), (E)-coniferol (13), β-hydroxypropiovanillone (14), 3-hydroxy-7,8-didehydro-β-ionone (15), 3β-hydroxy-5α, 6α-epoxy-7-megastigmen-9-one (16), grasshopper ketone (17), and 4-hydroxy-3,5-dimethoxybenzaldehyde (18). Compounds 1-15 and 18 were first obtained from the plants of Murraya genus, and compounds 16 and 17 were isolated from M. euchrestifolia for the first time.

Apoptosis of HL-60 leukemia cells induced by carbazole alkaloids isolated from Murraya euchrestifolia.[Pubmed: 21879331]

We carried out primary screening of 13 carbazole alkaloids isolated from the plant species Murraya euchrestifolia (Rutaceae) on cell growth inhibition of the human leukemia cell line HL-60. Among them, murrayafoline-A (1) and murrayazolinine (7) exhibited significant growth suppression due to apoptosis mediated by the activation of the caspase-9/caspase-3 pathway.

Antitumor agents. 203. Carbazole alkaloid murrayaquinone A and related synthetic carbazolequinones as cytotoxic agents.[Pubmed: 10924160]

Murrayaquinone A (1) and murrayafoline A (3), isolated from the root bark of Murraya euchrestifolia, were identified as cytotoxic compounds. Murrayaquinone A (1) demonstrated significant cytotoxicity against SK-MEL-5 and Colo-205 cells, with ED(50) values of 2.58 and 3.85 microg/mL, respectively. In contrast, murrayafoline A (3) exhibited marginal or weak cytotoxicity against SK-MEL-5, Colo-205, HCT-8, KB, and A-549 tumor cell lines, with ED(50) values ranging from 5.31 to 7.52 microg/mL. In total, 20 carbazole alkaloids (1-20), isolated previously by Furukawa et al. from various plant sources were also evaluated for their cytotoxic profiles in the NCI's human disease-oriented, 60-cell line, in vitro antitumor screening protocol. Compounds 3 and 15 showed potent cell-line selective cytotoxicity against MOLT-4 cells, with log GI(50) values of -8.60 and -8.49 M, respectively, while 12 demonstrated better selectivity against the colon cancer subpanel. Moreover, synthetic 2-methyl- or 3-methyl-carbazolequinone derivatives with various substituents in the A-ring were evaluated against KB, SK-MEL-5, Colo-205, and HCT-8 tumor cells. 6-Methoxy- (21), 6-methyl- (22), and 6-chloro- (24) 3-methyl-carbazolequinones demonstrated significant cytotoxicity against SK-MEL-5 cells, with ED(50) values of 0.55, 0.66, and 0.83 microg/mL, respectively. Compounds 21 and 22 were also significantly cytotoxic toward KB cells, with ED(50) values of 0.76 and 0.92 microg/mL, respectively, and 21 displayed a similar level of toxicity against Colo-205 cells (ED(50) 0.87 microg/mL).

Inhibition of cyclooxygenase activity and increase in platelet cyclic AMP by girinimbine, isolated from Murraya euchrestifolia.[Pubmed: 8053931]

Girinimbine is an antiplatelet agent isolated from Murraya euchrestifolia. In washed rabbit platelets, it inhibited arachidonic acid (AA)-, collagen-, U46619- and platelet-activating factor (PAF)-induced aggregation and ATP release in a concentration-dependent manner with IC50 values of 9.1 +/- 1.5, 16.7 +/- 1.7, 60.0 +/- 5.1 and 71.9 +/- 5.6 microM, respectively. However, it did not apparently affect thrombin-induced aggregation and ATP release even when a concentration of 80 microM was used. In citrated human platelet-rich plasma (PRP), girinimbine selectively inhibited secondary aggregation and ATP release without appearing to affect the primary aggregation induced by epinephrine and ADP. The formation of both platelet thromboxane B2 (TxB2) and prostaglandin D2 (PGD2) caused by AA was inhibited by girinimbine concentration dependently, with a maximal effect at 20 microM. Girinimbine also inhibited cyclooxygenase activity as reflected by the attenuation of prostaglandin E2 (PGE2) formation after incubation of sheep vesicular gland microsomes with arachidonic acid. In myo-[3H]inositol-labeled and fura-2-loaded platelets, [3H]inositol monophosphate generation and the increase in intracellular Ca2+ ([Ca2+]i) stimulated by AA and collagen, but not that stimulated by U46619, PAF and thrombin, were inhibited by girinimbine (20 microM). Platelet cyclic AMP levels were elevated by high concentrations of girinimbine (20 and 80 microM). These data indicate that the antiplatelet effect of girinimbine is due to the inhibition of cyclooxygenase activity and elevation of the cyclic AMP level.