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  • Kim et al reported for bioactive compounds


    Kim et al. reported for bioactive compounds originating from the endemic species in Korea, the hexane and EtOAc fractions of the MeOH extracts from the roots of Dystaenia takeshimana (Nakai) Kitagawa (Umbelliferae) showed cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) dual inhibitory activity by assessing their effects on the prodn. of prostaglandin D2 (PGD2) and leukotriene C4 (LTC4) in mouse bone marrow-derived mast cells. By activity-guided fractionation, 5 coumarins, viz. psoralen 31, xanthotoxin 16, scopoletin 13, umbelliferone 32, and (+)-marmesin 25, together with β-sitosterol were isolated from the hexane fraction, and 2 phenethyl alcohol. Derivatives were isolated from the EtOAc fraction using silica gel column chromatog. Two of the coumarins, scopoletin and (+)-marmesin were isolated for the first time from this plant source. Amongst the compounds, the five coumarins showed good COX-2/5-LOX dual inhibitory activity [56]. Kohno et al. reported the chemopreventive ability of a prenyloxycoumarin auraptene 33 and collinin 34 in chemically induced carcinogenesis in digestive tract, liver and urinary SKF38393 HCl receptor of rodents .Their tumor inhibitory effects were assessed at week 20 by counting the incidence and multiplicity of colonic neoplasms and the immunohistochemistry expression of proliferating cell nuclear antigen (PCNA)-labeling index, apoptotic index, cyclooxygenase (COX-2), inducible nitric oxide (iNOS) and nitrotyrosine in colonic epithelial malignancy. In addition, feeding with auraptene or collinin significantly lowered the rates of PCNA, COX-2, iNOS and nitrotyrosine in adenocarcinomas, while the treatment increased the apoptotic index in colonic malignancies [57]. Sciullo et al. further reported antagonistic actions auraptene 33 against the action of TCDD and DDT in up-regulating the mRNA expressions of COX-2 [58]. Okuyama et al. reported anti-inflammatory activity of auraptene 33 (AUR) as suppressed cyclooxygenase (COX)-2 expression in astrocytes, and COX-2 mRNA expression in the hippocampus, it also suppressed the lipopolysaccharide-induced expression of COX-2 mRNA and the mRNA of pro-inflammatory cytokines in cultured astrocytes supporting the suggestion that AUR directly exerts anti-inflammatory effects on the brain [59]. Yoo et al. reported isolation of coumarins bergapten 15, xanthotoxin 16 and isopimpinellin 13, along with flavonoids glycosides and steroids from Euodia daniellii. Among the isolates, bergapten 15 showed cyclooxygenase-2 inhibitory activity with an IC50 value of 6.2μg/mL. Flavonoids isolated from this plant exhibited no cytotoxic activity against the human tumor cell lines, A549, SKOV-3, SKMEL-2, XF498, and HCT15 [60]. Liu et al. reported analysis of Radix Angelicae pubescentis (Duhuo) and substitutes from the genera Angelica, Heracleum (Umbelliferae), and Aralia (Araliaceae) were analyzed for their constituents and inhibitory effect on cyclooxygenase (COX-1) and 5-lipoxygenase (5-LO).HPLC analysis showed that osthole [61] 35, columbianetin 27, columbianetin acetate, and angelol-type coumarins are the principal constituents of the n-hexane and dichloromethane extracts of the roots of Angelica pubescens f. biserrata. The constituents of the substitutes from Angelica and Heracleum species were mainly furanocoumarins and falcarindiol. All the species showed inhibitory effects on COX-1 and 5-LO [62]. Roos et al. reported sixteen coumarins from Angelica archangelica (syn. Archangelica officinalis) were analyzed by means of HPLC-MS and subsequent spectroscopical identification by two-dimensional NMR. Furthermore, the isolated coumarins were tested for anti-inflammatory activity in terms of in vitro cyclooxygenase-1 (COX-1) and 5-lipoxygenase (5-LO) inhibition. They were found to be not active in the COX- 1 assay. However when tested for 5-LO inhibition, osthole 35 and oxypeucedanin hydrate isovalerate turned out to be active [63]. Further Yang et al. decrease in NF-κB activation and COX- 2 expression as well as PGE2 production podocyte injury, and apoptosis supporting that fact that targeting the Nrf2 antioxidant pathway may justify osthole 35 being established as a candidate renoprotective compound for FSGS [64].