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A simple and sensitive method for the determination of triptolide, wilforlide A and triptonide in human plasma was developed and validated, using high-performance liquid chromatography-electrospray ionization mass spectrometry (LC-ESI-MS). Plasma samples were purified using solid-phase extraction (SPE) columns. The HPLC separation of the analytes was performed on a MACHEREY-NAGEL C 18 column (2.0 mm؋125 mm, 3 m mm), using 2.7 mM formic acid containing 10 mM ammonium acetate-acetonitrile (55 : 45, v/v) as mobile phase, with a flow-rate of 0.25 ml/min. The compounds were ionized in the electrospray ionization (ESI) ion source of the mass spectrometer and were detected in the selected ion recording (SIR) mode. The calibration curves were linear in the 0.80-300 ng/ml range for all the three analytes, and the limits of detection were 0.25, 0.40, and 0.35 ng/ml for triptolide, wilforlide A, and triptonide, respectively. The average absolute recoveries for all the three analytes were above 81%. The methodology recoveries were greater than 91% and the relative standard deviations (RSD) of intra-day and inter-day were less than 15%. The developed method was successfully applied to the determination of triptolide, wilforlide A and triptonide concentration in patients' plasma after taking the medicament containing Tripterygium wilfordii HOOK. F.

We have investigated the antiproliferative effects of TBIDOM (N-(4-(2,2,2-trifluoroethyl) benzylidene) (7-isopropyl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octahydrophenanthren-1-yl) meth-anamine) and have explored its possible mechanisms on human hepatocellular carcinoma SMMC-7721 cells. The proliferative status of cells treated with TBIDOM was measured by the colorimetric MTT assay. Cellular apoptosis was analysed using Hoechst 33342 staining and flow cytometry. Reduction of mitochondrial membrane potential (Delta psi(m)) was also detected by flow cytometry. Western blotting assay was used to evaluate the release of cytochrome c and expression of p53, Bcl-2 and Bax proteins. It was shown that TBIDOM displayed a significant inhibitory effect on growth of SMMC-7721 cells in a dose- and time-dependent manner. Hoechst 33342 staining and flow cytometry analysis showed an increase of apoptosis rate and decrease of mitochondrial membrane potential after SMMC-7721 cells were exposed to TBIDOM for 24 h. Pretreatment of SMMC-7721 cells with TBIDOM significantly induced a decrease of Bcl-2 protein expression and an increase of caspase-3 activity and Bax protein expression. The results indicated that TBIDOM could effectively inhibit proliferation by induction of apoptosis and could be a promising candidate in the development of a novel class of antitumour agent.

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