Fluorescence enhancement reaction of flavoxate hydrochloride (FX) in strong alkali solution was studied, the mechanism of the reaction was investigated, and a novel fluorimetric method for analysis of FX in drug sample was established. FX has no intrinsic fluorescence, but it can slowly produce fluorescence in strong alkali solution. Heating can promote the fluorescence enhancement reaction. In 3D fluorescence spectra of the decomposition product of FX, two fluorescence peaks, located respectively at excitation wavelengths λex/ emission wavelength λem =223/410 nm, and 302/410 nm, were observed. Using quinine sulfate as a reference, fluorescence quantum yield of the decomposition product was measured to be 0.50. The structural characteriza- tion and spectral analysis of the decomposition product reveal that ester bond hydrolysis reaction of FX is firstly occurred during heating process, forming 3-methylflavone-8-carboxylic acid (MFA), then a cleavage reaction of the γ-pyrone ring of MFA occurred, producing α, β-unsaturated ketone. This product includes adjacent hydroxyl benzoic acid group in its molecule, which can form intramolecular hydrogen bond under alkaline condition, so that increase the conjugate degree and enhance the rigidity of the molecule, and thereby cause fluorescence enhancement. Based on this fluorescence enhancement reaction, a fluorimetric method was proposed for the determination of FX. A linear calibration curve covered the concentration range 0.020 3-0.487 µg · mL. The regression equation was I(F) = 23.9 + 5357.3 c, with correlation coefficient r = 0.999 7 (n = 8), detection limit D = 1.1 ng · mL(-1). The method was applied to the analysis of FX tablets, with a spiked recovery rate of 100.2%. The reliability of the method was verified by a UV-spectrophotometric method.

Objective To investigate the effects of chemokine CCL18 on the proliferation and invasion of a human melanoma cell line A375. Methods Human peripheral blood monocytes were isolated from healthy volunteers, cultured in vitro and divided into two groups to be induced by IL-4 for 48 hours or remain untreated. A375 cells were classified into 3 groups to be cultured with IL-4-induced monocytes, untreated monocytes or CCL18 of 200 g/L for various durations. A375 cells receiving no treatment served as the control.MTT assay was performed to detect the proliferation of A375 cells, chemotaxis test and Matrigel-transwell assay to evaluate the chemotaxis and invasion ability of A375 cells, and chicken chorioalllantoic memebrane (CAM)was used to detect the effect of CCL18 on tumor angiogenesis. Results The proliferation of A375 cells was statistically accelerated by IL-4-induced monocytes and untreated monocytes, but unaffected by CCL18.Matrigel-transwell assay revealed that IL-4-induced monocytes and CCL18 promoted the chemotaxis and invasion ability of A375 cells (all P＜0.05). Tumor angiogenesis was also increased by IL-4-induced monocytes and CCL18 (both P ＜ 0.05). Conclusion The chemokine CCL18 can promote the invasion ability of A375 cells and tumor angiogenesis.

Objective To investigate the expression of insulin-like growth factor-Ⅱ(IGF-Ⅱ) mRNAbinding protein-3 (IMP3) in tissue of benign nevi and malignant melanoma,and to evaluate the role of IMP3 in the development and diagnosis of malignant melanoma.Methods Immunohistochemistry was performed to measure the expression of IMP3 in tissue samples from 28 cases of malignant melanoma,8 Spitz nevi,6 dysplastic nevi and 25 benign nevi.Results Immunohistochemically,IMP3 was observed in 23 of 28 melanoma samples,4 of 8 Spitz nevus samples and 2 of 6 dysplastic nevus samples,but not in benign nevus samples.The expression level of IMP3 wag significantly higher in tissue of melanoma than in that of Spitz nevi and dysplastic nevi (both P<0.05),also higher in tissue of aggressive melanoma than that of melanoma in situ(P<0.01).Conclusions IMP3 seems to be a biomarker for the progression of benign nevi to malignant melanoma,and may be utilized to distinguish melanoma from benign nevi.