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Aim To explore new ways for developing anticancer drugs by the separation of pigment from Fu-sarium species JN158 ( Fusarium sp JN158 ) , the iden-tification of its structure, the screening of anticancer components and the study of its partial mechanism. Methods Pigment separation was done by HPLC, structural analysis by UV, IR, NMR, the screening of anticancer activity by MTT. Western blot was used to analyze the protein expression of CyclinD1, NF-κB, VEGF in tumor cells. Results The results showed that the pigment from Fusarium produced a total of six different peaks, of which peak Ⅵ was the anthocya-nins. Its molecular weight is about 382, molecular for-mula is C17 H18 O10 . According to investigation, this pig-ment was probably a new compound, which could in-hibit the proliferation of MCF-7 cells markedly ( IC50:0.011mmol·L-1 ,P<0.05;the control medicine ube-nimex IC50:10 mmol · L-1 ) in a concentration-de-pendent manner, and had no effect on human umbilical cord intravenous endotheliocyte ( HUVEC ) . The influ-ence on the gene expression of CyclinD1, NF-κB, VEGF in MCF-7 cells varied with the concentration of this compound. The Western blot results showed that VI pigment compound inhibited CyclinD1, NF-κB, VEGF gene expression (P<0.05 or 0. 01),compared with the control group. Conclusion The Ⅵ pigment compound from Fusarium sp JN158 could inhibit MCF-7 proliferation by inhibiting CyclinD1, NF-κB, VEGF gene expression. The compound may be a promising compound against breast cancer.
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Objective:To investigate the mechanism of Buguozhi Decoction in improving learning-memory of vascular dementia model rats.Methods:The rat models with VaD were established by bilateral occlusion of both common carotid arteries(2 一V0).The gene expressions of ER-?,NR2B were evaluated by RT-PCR and immunohistochemistry.Results:Buguozhi Decoction can significantly improve mRNA and protien pruducts of ER-?,NR2B gene in hippocampus of the vascular dementia model rats,compared with the model group(P
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Aim To elucidate the biochemical mechanism of gossypol in inducing the decline of sperm quality.Methods Gossypol was administered orally at the dose of 50 mg?kg-1/2 d for two weeks.Then,the sperm was collected from the left caudal epididymis and was analysed by CASA.The morphological changeand the concentration of nitric oxide(NO)in testes as well as the level of hormone〔follicle-stimulating hormone(FSH)〕,luteotrophic hormone(LH),testosterone(T)in serum were assayed.Results Gossypol could induce the decrease of sperm number and sperm quality.The concentration of NO in testes increased significantly.Among the three kind of hormone,only the concentration of T showed decrease after the oral administration of gossypol.NA1108 could antagonize the decline of sperm quality damaged by gossypol and decrease the content of NO in testes.Conclusions The concentration of NO in testes beyond normal value was one of the toxic mechanism of gossypol that contributed to the inhibition of spermatogenesis.Some drugs with the ability to reduce NO content in testes could also increase sperm quality.
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AIM To elucidate the mechanism of taurine-regulated amino acid release from synaptosomes. METHODS Endogenous aspartate, glutamate and GABA release from cortical synaptosomes were measured by high performance liquid chromatography using stepwise elution system, Glutamate release was monitored by continuous fluorometry. RESULTS 4-Aminopyridine (3.0×10-2 mol*L-1) counteracted the taurine-induced inhibition of glutamate overflow (P<0.05), while aspartate and GABA release was not affected. Nimodipine (10-5 mol*L-1) combined with 4-aminopyridine was shown to decrease glutamate release (P<0.05). CONCLUSION Taurine may regulate glutamate release through presynaptic L-type calcium channel and aslo act on Asp-and GABA-nereve terminal to regulate Asp and GABA release in rat cortex.
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AIM Taurine can regulate Asp、 Glu、 GABA from rat cortical synaptosomes. But its mechanism is unclear. The release regulated effects were investigated through analysis of GABA receptors.METHODS Bicuculline、Phaclofen、Baclofen were added in a Krebs Ringer buffer with resuspended synapotomes.Endogenous Asp、 Glu and GABA release during the 5 min superfusion were measured by high perfusion liquid chromatography using percolumn durivatization with Dans Cl. RESULT Phaclofen,but not bicucullion baclofen, counteracted the inhibition of GABA overflow,although the inhibition of Asp and Glu overflow was not attenuated. CONCLUSION Taurine inhibits the depolarization evoked release of GABA through the activation of presynaptic autoreceptors and taurine also acts on presynaptic sits of Asp Glu nerve terminals to inhibit their evoked release in rat cerebral cotex.