Archives of Pharmacal Research

Second derivative (D2) spectrometry using ion-pair extraction technique was developed for the determination of total glycyrrhetic acid (GA) in Glycyrrhizae Radix. Glycyrrhizin (G) obtained from Glycyrrhizae Radix was hydrolyzed into GA in 2 N-HCl and methanol (1∶1) and extracted from aqueous phase in the form of an ion-pair complex with tetrapentylammonium bromide (TPA) as a counter ion. Maximum D2 amplitude (Z value) was obrained when 1000-fold or greater molar ratio of TPA was used at pH 11. Reaction time, temerature and ionic strength did not affect ion-pair formation. Dichloromethane was an effective extraction solvent of the ion-pair complex. The linearity of standard curve of ion-pair GA was obtained in the range of 4–120 μg/ml as GA. Assayed contents of GA in dry powder by D2 UV spectrometry and HPLC method were 5.31±0.04% and 5.20±0.008%, respectively.

Ginsenosides, major active ingredients ofPanax ginseng, are known to regulate excitatory ligand-gated ion channel activity such as nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides affect inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human recombinant GABAA receptor (α1β1γ2S) channel activity expressed inXenopus oocytes using a two-electrode voltage-clamp technique. Among the eight individual ginsenosides examined, namely, Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg2, we found that Rc most potently enhanced the GABA-induced inward peak current (l GABA). Ginsenoside Rc alone induced an inward membrane current in certain batches of oocytes expressing the GABAA receptor. The effect of ginsenoside Rc onI GABA was both dose-dependent and reversible. The half-stimulatory concentration (EC50) of ginsenoside Rc was 53.2 ± 12.3 μM. Both bicuculline, a GABAA receptor antagonist, and picrotoxin, a GABAA channel blocker, blocked the stimulatory effect of ginsenoside Rc onI GABA. Niflumic acid (NFA) and 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), both Cl− channel blockers, attenuated the effect of ginsenoside Rc onI GABA. This study suggests that ginsenosides regulated GABAA receptor expressed inXenopus oocytes and implies that this regulation might be one of the pharmacological actions ofPanax ginseng.

Nystatin is commonly employed to treat fungal infections in the mouth. It is not absorbed via the stomach and it will therefore not treat fungal infections in any part of the body other than the mouth. Nystatin buccoadhesive tablets release the drug very slowly due to the poor solubility of nystatin in water and also the presence of polymers with mucoadhesive properties. Therefore, the aim of the present study was to improve drug release from buccoadhesive tablets, while retaining adequate mucoadhesive properties. To this end, a solid dispersion of nystatin: lactose (1:3) was prepared and mixed with xanthan. The effects of hydrophilic surfactants such as cremophor RH40 and Tween 80 on drug release and mucoadhesive properties of nystatin tablets were also investigated as were swelling and erosion indices and strength of bioadhesion in vitro to a biological membrane. The interaction between nystatin and lactose in solid dispersion formulation was investigated by XRPD, FT-IR and DSC. The results showed that a solid dispersion formulation and mucoadhesive tablets containing surfactants led to faster drug release than their simple physical mixtures. Drug release was also faster from a solid dispersion compared to tablets containing surfactants. Swelling and erosion results showed that tablets made of a solid dispersion swelled and eroded faster than a physical mixture formulation. The presence of surfactant slightly increased the degree of swelling and erosion of buccoadhesive tablets.

(±)-Myodesmone was synthesized, starting from 2-cyclopentenone. The key reaction involved α-dimethoxymethylation of 2-cyclopentenone and organocopper conjugate addition reaction.

Different bacteria were separated from saliva and teeth of cariogenic patients and identified by a variety of morphological and biochemical tests. Extracts of green tea strongly inhibitedEscherichia coli, Streptococcus salivarius andStreptococcus mutans. The antibacterial effect of green and black tea extracts were compared with those of amoxicillin, cephradine and eugenol.

A facile convenient syntheses of the titled compounds, via reacting the precursor 2-amino-2-(pentane-2,4-dion-3-ylthio)-6-phenylpyrimidine-5-carbonitrile (1) with nitrogen nucleophiles and with the carbanions of some active methylene compounds, is reported. Chemical and spectroscopic evidence of the newly synthesised compounds are described.

The synthesis of 5-heterocyclicmethyl-2′-deoxyuridines (4a-f) has been accomplished by displacement reaction of 5-(bromomethyl)-3′,5′-di-O-acetyl-2′-deoxyuridine with heterocyclic compounds, followed by removal of acetyl protecting group with methanolic ammonia. The compounds synthesized were evaluated the inhibitory effects on L1210 cell proliferation and antiviral activities against Herpes simplex virus type 1 (HSV-1). None of the compounds exhibited sufficient biological activities.

The levels of extracellular glutamate, intracellular Ca2+ ([Ca2+]i) and cGMP were determined for 1 h with the excitatory amino acids, N-methyl-D-aspartate (NMDA) or kainate in cultured cerebellar granule cells. Both NMDA and kainate produced a time-dependent release of glutamate, and kainate was more potent than NMDA in glutamate elevation. The elevation of extracellular glutamate was not purely governed by intracellular Ca2+ concentration. However, in opposite to the time-dependent elevation of glutamate, the elevation of cGMP by NMDA and kainate were at maximum level in short-time (1 min) incubation then remarkably decreased with longer incubation times. Post-applications (30 min after agonist) of EAA antagonst did not block EAAs-induced glutamate elevation. However, NMDA antagonist, phencyclidine (PCP), blocked NMDA-induced cGMP elevation at pre- or post-application, but kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), paradoxically augmented kainate-induced cGMP elevation for 1 h incubation. These results show that NMDA or kainate induces time-dependent elevations of extracellular glutamate, while the elevations of cGMP by these EAAs are remarkably decreased with longer incubation times. However, NMDA- and kainate-induced glutamate release was blocked by pre-application of each receptor antagonist but not by post-application while EAA-induced [Ca2+]i was blocked by post-application of antagonist. These observations suggest that EAA-induced elevation of [Ca2+]i is not parallel with elevation of glutamate release or cGMP.