Invasion and metastasis are the distinct biological characterstics of cancer. They are the key factors influencing tumour patients' theraputic effect and prognosis. Recent study shows that metalloproteinases can facilitate tumour cell invasion and metastasis. In this review we evaluate the novel aspects of the function of matrix metalloproteinases in tumor invasion and metastasis. The regulation of the expression and activity of MMPs are summarized. The potential clinical application of metalloproteinase and their tissue inhibitors were also presented.

AIM To investigate the effect of puerarin on the formation of advanced glycation end products (AGEs) and RAGE(receptor for advanced glycation end products)mRNA expression in the arota of diabetic rats induced by streptozotocin (STZ). METHODS Rats were injected streptozotocin into intraperitonel with a dose of 60 mg?kg -1 . Four days later, blood glucose was measured using glucose oxygen kit. The rats with over 16 7 mmol?L -1 blood glucose were considered as diabetic ones, and then divided randomly into five groups: diabetic mellitus(DM), aminoguanidine(AG 0 1 g?kg -1 , ig), pue1(0 5 g?kg -1 , ig), pue2(0 25 g?kg -1 , ig) and pue3(0 125 g?kg -1 , ig). In order to set up a chronic model, we observed 12 weeks according to our past experiments. The fasting blood glucose(FBG) was and the contents of serum fructosamine (FMN) were measured using the test kit. The quantity of AGEs accumulation, the expression of RAGE in the arota was detected using fluorescence method and reverse transcription polymerase chain reaction(RT PCR). RESULTS The contents of FBG and FMN, the accumulation of AGEs in the aorta of rats treated with puerarin were lower than that of diabetic model rats( P

s:Cardiomyocyte apoptosis and regeneration are present in overload cardiac hypertrophy. Cardiac myocyte apoptosis might be a critical factor during the transition from compensatory hypertrophy to heart failure. The mechanisms of apoptosis include extrinsic factors and some cellular signal pathways. On the other hand, cardiomyocyte hyperplasia, as well as hypertrophy, contributes to cardiac hypertrophy. Caridomyocyte regeneration is related to cyclin, cyclin dependent kinase (Cdk), Cdk inhibitors (CdkI), bcl-2, p53 and telomere. Cardiaomyocyte regeneration and apoptosis are linked through several factors.

AIM: To investigate the effect of puerarin on the alteration of ET and ANF in plasma, NO and NOS in serum of diabetic rats induced by streptozotocin(STZ). METHODS: Rat modeling was set up by means of intraperitoneal injection of ST2 with a dose of 60mg?kg -1. Four days later, blood glucose was measured by glucose oxygen kit. On the basis of present documents, the rats that blood glucose was over 16.7mM were accepted as diabetic ones, and then were divided randomly into five groups: diabetic mellitus (DM), aminoguanidine (AG 0.1g?kg -1,ig.), puel (0.5g?kg -1,ig.),pue2(0.25g?kg -1,ig.), pue3(0.125g?kg -1,ig.) and a normal group additionally. In order to set up a chronic model, we observed 12 weeks according to our past experiments. The FBS was measured at the twelfth week using the test kit. NO and NOS in serum were determined by checking their OD values, ET and ANF in plasma were determined by radio-immunization, respectively. RESULTS: In diabetic rats, Plasma ET and ANF levels increased obviously, NO and NOS levels decreased greatly (P

Objective: Qualitative and quantitative determination of the contents of inorganic elements in Corium Bufo bufo gargarizans Cantor. Methods: Qualitative determination by atomic emission spectrometry and quantitative determination by ICP AES.Conclusion: The content of calcium is the highest in Corium Bufo bufo gargarizans Cantor.

[Objective]The study focus on the analgesic effect of polysaccharopeptide(PSP)and discuss the mechanism of this analgesia. [Methods]A total of 80 rats were divided randomly into high dose of psp,medium dose of psp,low doses of psp,positive control group,negative control group.After intragastric(ig) administration of different(high,medium and low)doses of PSP for 6 days,The tail stimulation-vocalization test was used to observe the analgesic effect of PSP.The IL-2 and IL-2R expression in mediobasal hypothalamus(MBH) was studied immunohistochemically.[Results]After intragastric(ig) administration of PSP for 6 days,the pain threshold was increased significantly and a dose-effect relationship was observed.After PSP administration the IL-2 expression in MBH was increased,while the IL-2R expression in MBH was decreased.[Conclusion]PSP has a definite analgesic effect and its analgesic site is in the MBH.The analgesia might be produced by the binding with the IL-2R in MBH by IL-2 secreted by T cells after PSP was injected into the brain.

AIM To study the action of danshengsuan (Dan) on expression of CD11b, P selectin, ICAM 1, VCAM 1 and E slectin in vitro. METHODS Adheshion molecule expression on the cell surface was measured by flow cytometry. RESULTS Treatment of neutrophils with N fomyl met leu phe(fMLP), resulted in a marked increase of CD11b expression. Dan inhibited the effects of fMLP in a concentration dependent manner. Dan did not inhibit the increase of P selectin expression of thrombin actived human blood platelets. Treatment of cultured human umbilical vein endothelial cells (HUVEC) with TNF ? resulted in an increase of ICAM 1, VCAM 1 and E slectin. Dan inhibited the increase of VCAM 1 and E slectin expression, not ICAM 1. CONCLUSION Dan inhibited expression of adhesion molecules CD11b, ICAM 1, VCAM 1 in human neutrophils and HUVEC.

Huntington's disease is a fetal neurological disorder manifested as movement disorder accompanied by cognitive and psychological impairments. The disease is inherited as autosomal dominant. Huntington's disease is caused by an expansion of a polyglutamine tract in a protein named huntingtin. The length of polyglutamine tract in huntingtin in normal individual is less than 35 glutamines. In Huntington's disease patients the length of polyglutamine tract increases to more than 37 glutamines. The pathogenic mechanisms by which mutant huntingtin causes Huntington's disease have not been fully understood. This paper reviews main progresses in studying the pathogenic mechanisms of mutant huntingtin.