OBJECTIVE: To determine the content of 5-Fu in human serum.METHODS: Serum protein was precipitated with trichloroacetic acid .HPLC was used for determination of 5-Fu .The column was Shimpack CLC C18(150 × 6mm, 5μm)with YWG for protection.The mobile phase was 0.25% KH2PO4-acetonitrile(98: 2, pH7.0) .The flow rate was 1ml/min.The detection wavelength was 265nm.Two standard curves were made in the concentrations of 0.195～6.250μg/ ml and 6.25～200.00μg/ml, respectively.RESULTS: The calibration curves revealed linearity in the range of 0.195～200μg/ml.The with-in-day recoveries and RSDs of 5-Fu at 0.8, 4, 20 and 100μg/ ml concentration points were 104. 88%, 1.95%; 104.58%,1.38%; 101.40%, 0.39%and 99.14%, 0.37%, and the between-day recoveries and RSDs of 5-Fu were 105.12%, 2.02%;106.30 %, 0.78 %; 100.60 %, 0.65 % and 99.38 %, 0.92 % respectively. CONCLUSION: This method is rapid, accurate and suitable for pharmacokinetical study and conventional monitoring of 5-Fu.

OBJECTIVE:To establish HPLC method for the simultaneous content determination of metronidazole,tetra-caine hydrochloride and dexamethasone acetate in metronidazole compound.METHODS:The content determination was per-formed on column C 18 ;the mobile phase consisted methanol-water-triethylamine(65∶35∶0.36),the detection wavelength of both metronidazole and tetracaine hydrochloride was310nm,and240nm for dexamethasone acetate,the flow rate was1ml/min and the column temperature was25℃.RESULTS:The linear ranges of metronidazole,tetracaine hydrochloride and dexameth_ asone acetate were0.412?g～2.06?g(r=0.9999),0.191?g～0.956?g(r=0.9999)and0.121?g～0.604?g(r=0.9998),respectively,and their average recoveries were100.69%(RSD=1.28%),101.37%(RSD=0.23%)and102.40%(RSD=0.89%),respectively.CONCLUSION:The method was simple,accurate,reproducible,and suitable for the quality control of metronidazole compound.

Aim To evaluate the effects of ferulic acid ( FA ) on lipopolysaccharide ( LPS )-induced neuroin-flammation in microglia cells and its potential mecha-nisms. Methods Microglial activation was induced by stimulation with LPS, and the effects of FA pretreat-ment on microglial activation and production of proin-flammatory mediators, nitric oxide/iNOS were investi-gated. The role of the mitogen-activated protein kinases in the antiinflammatory actions of FA in LPS-stimulated microglia was further elucidated. Results Cell viabil-ity experiments revealed that FA did not produce cyto-toxicity in microglia. FA significantly inhibited LPS-in-duced production of tumour necrosis factor-alpha ( TNF-α) , interleukin-6 ( IL-6 ) , interleukin-1 beta ( IL-1β) , and nitric oxide ( NO ) . Protein and mRNA levels of COX-2 and inducible nitric oxide synthase ( iNOS) were also attenuated by FA. Further experi-ments on intracellular signalling mechanisms showed that inhibition of extracellular regulated kinase ( ERK) contributed to the anti-neuroinflammatory actions of FA. Conclusion The results suggest that FA inhibits LPS-induced microglial inflammation by partial targe-ting of ERK signalling and attenuation of ERK.