J Asian Nat Prod Res. 2009; 11(5): 397-400Lu X, Xu N, Dai HF, Mei WL, Yang ZX, Pei YHThree new compounds, 4-hydroxyphenethyl-2'-hydroxypropanoate (1), 6-(1',2'-dimethyloxiran-1'-yl)-4-methoxy-3-methyl-2H-pyran-2-one (2), 6-(1-hydroxyethyl)-4-methoxy-3-methyl-2H-pyran-2-one (3), along with the two known compounds, nectriapyrone (4) and wermopyrone (5), have been isolated from the endophytic fungus of Cephalotaxus hainanensis. Their structures were determined on the basis of chemical and spectroscopic methods.

J Asian Nat Prod Res. 2009; 11(5): 426-32Li ZL, Li DY, Hua HM, Chen XH, Kim CSThree new flavone C-glycosides with the substitution of the unusual acyl, 2''-O-veratroylisoswertisin (1), 3''-O-2-methylbutyrylisoswertiajaponin (2), and 3''-O-2-methylbutyrylvitexin (3), together with the known compounds of 2''-O-2-methylbutyrylisoswertisin (4), 3''-O-2-methylbutyrylisoswertisin (5), and trollisin I (6) were isolated from the antibacterial fraction of the aqueous extract of the flowers of Trollius chinensis. The structural elucidations of these compounds were carried out by a detailed analysis of the NMR and MS spectra.

J Asian Nat Prod Res. 2009; 11(5): 433-8Gao HM, Liu JX, Wang ZM, Wang WHPhytolacacinoside A (1), a novel triterpenoid saponin, together with the seven known compounds, was isolated from 75% ethanol extract of the root of Phytolacca acinosa Roxb (Phytolaccaceae). Their structures were elucidated on the basis of analysis of spectroscopic data and physicochemical properties as 3-O-beta-[(beta-d-glucopyranosyl-(1 --> 4)-O-beta-D-xylopyranosyl)]-11beta-methoxy-jaligonic acid 30-methyl ester 28-O-beta-D-glucopyranoside (1), 3-O-beta-[(beta-D-glucopyranosyl-(1 --> 4)-O-beta-D-xylopyranosyl)]-jaligonic acid 30-methyl ester 28-O-beta-D-glucopyranoside (2, esculentoside G), 3-O-beta-[(beta-D-glucopyranosyl-(1 --> 4)-O-beta-D-xylopyranosyl)]-jaligonic acid 30-methyl ester (3, phytolaccoside E), 3-O-beta-D-xylopyranosyl-jaligonic acid 30-methyl ester (4, phytolaccoside B), hypaphorine (5), palmitic acid monoglyceride (6), beta-sitosterol (7), and daucosterol (8).

J Nat Prod. 2009 Jun 5; Shao Y, Zhang HK, Ding H, Quan HT, Lou LG, Hu LHA series of 3-demethoxycarbonyl-3-amide methyl anhydrovinblastine derivatives (5b-24b) was designed, synthesized, and evaluated for their proliferation inhibition activities against two tumor cell lines (A549 and HeLa). Most of the amide anhydrovinblastine derivatives exhibited potent cytotoxicity, with the size of the introduced substituents being the foremost factor in determining the resultant cytotoxic activity. Test results in vivo against sarcoma 180 of three potent compounds (6b, 12b, and 24b) indicated that the introduction of an amide group at the 22-position of anhydrovinblastine (1e) improved both potency and toxicity.

PLoS ONE. 2009; 4(6): e5811Chen XQ, Zhang J, Neumeyer JL, Jin GZ, Hu GY, Zhang A, Zhen X(+/-) SKF83959, like many other arylbenzazepines, elicits powerful neuroprotection in vitro and in vivo. The neuroprotective action of the compound was found to partially depend on its D(1)-like dopamine receptor agonistic activity. The precise mechanism for the (+/-) SKF83959-mediated neuroprotection remains elusive. We report here that (+/-) SKF83959 is a potent blocker for delayed rectifier K(+) channel. (+/-) SKF83959 inhibited the delayed rectifier K(+) current (I(K)) dose-dependently in rat hippocampal neurons. The IC(50) value for inhibition of I(K) was 41.9+/-2.3 microM (Hill coefficient = 1.81+/-0.13, n = 6), whereas that for inhibition of I(A) was 307.9+/-38.5 microM (Hill coefficient = 1.37+/-0.08, n = 6). Thus, (+/-) SKF83959 is 7.3-fold more potent in suppressing I(K) than I(A). Moreover, the inhibition of I(K) by (+/-) SKF83959 was voltage-dependent and not related to dopamine receptors. The rapidly onset of inhibition and recovery suggests that the inhibition resulted from a direct interaction of (+/-) SKF83959 with the K(+) channel. The intracellular application of (+/-) SKF83959 had no effects of on I(K), indicating that the compound most likely acts at the outer mouth of the pore of K(+) channel. We also tested the enantiomers of (+/-) SKF83959, R-(+) SKF83959 (MCL-201), and S-(-) SKF83959 (MCL-202), as well as SKF38393; all these compounds inhibited I(K). However, (+/-) SKF83959, at either 0.1 or 1 mM, exhibited the strongest inhibition on the currents among all tested drug. The present findings not only revealed a new potent blocker of I(K) , but also provided a novel mechanism for the neuroprotective action of arylbenzazepines such as (+/-) SKF83959.