Protein Kinase C-zeta (PKC-?) is a new member of protein kinase C family and has some specific characteristics as comparing with the classical PKC. It lacks the C 2 domain making its kinase activity Ca 2+ -independent, and it possesses only one zinc-finger region in its regulatory domain. Therefore, PKC-? does not bind Ca 2+ and can not be activated by diacylglycerol or phorbol esters. In addition, many researches showed that PKC-? could induce differentiation, mediate insulin-stimulation protein synthesis, activate immunity of human neutrophils, inhibit proliferation of cancer cells and regulate the function of actin cytoskeleton. What is more, PKC-? plays an important role in signal transduction of cells, such as mediating MAPK and NF-?B activation.

Daxx is found in the nucleus where it localizes to PML oncogenic domains (PODs). Its multiple domains can interact proteins involved in transcriptional regulation and apoptotic signal transduction. In addition, Daxx is associated with viral infection、tumorigenesis and embryonic development.

AIM: To investigate the relationship between the prevention of probucol on restenosis and vascular remodeling after percutaneous transluminal angioplasty(PTA) in rabbits. METHODS: New Zealand rabbit thoracic aorta atherosclerosis was induced by 3.5F ballon catheter injury following a 4-weeks feeding of high cholesterol diet, and PTA was performed by using 3.5F balloon catheter. Probucol(1g/d) or vitamin E (400 mg/d) was administrated one week before PTA. Two weeks after PTA, the bore and outside diameter (OD) of arteries, the area circumscribing by intimal elastic lamina (IEL), the area circumscribing by extral elastic lamina (EEL), medial area (MA), neointima area/medial area (NEA/MA) were analyzed by computerized digitizer system. Lipids of serum were measured by means of biochemical assay.RESULTS: After two weeks of PTA, the intima proliferation and lumen restenosis were observed obviously. However, with probucol treatment for 3 weeks, the restenosis of aorta was inhibited significantly by increasing bore, outside diameter, and lumen area of rabbits aortas and decreasing NEA, NEA/MA. Furthermore, probucol regulated vascular remodeling by increasing the area circumscribing by IEL [(3.50?0.20)mm 2 vs (1.59?0.23) mm 2, P

This paper studied the protective effect of gypenosides (GPS) on oxidative damage of myocardium of guinea pig, Using xan-thine-xanthine oxidase (X-XOD) producing free radicals. In the isolated guinea pig papillary muscles, X- XOD produced the quick positive inotropism at first and then the continuous negative one, shortened the functional refractory period (FRP) and elevated the excitability and increased the automaticity induced by adrenaline, inhibited the activity of superoxide dismutase (SOD) and increased the content of malondi-aldehyde (MDA). GPS inhibited the negative inotropism of papillary muscles produced by X-XOD,resisted the changes of FRP, automaticity and excitability induced by X- XOD. Meanwhile, GPS antagonized the effect of X-XOD which decreased activity of SOD and increased the content of MDA. These studies indicate that GPS can protect the myocardium from oxidative damage.

Object To investigate the effects of tetramethylpyrazine (TMP) and Danshen (DS) on the growth and metastasis of Lewis lung carcinoma and tumor angiogenesis. Methods C 57BL mice with Lewis lung carcinoma were used in this study, which were injected respectively with TMP injection 50, 100, and 200 mg/(kg?d) and DS injection 5, 10, and 20 g/(kg?d), ip, for 21 days. Then the volume, weight, and numbers of the metastatic foci on lungs, tumor microvessel density (MVD) were determined, the expression of vascular endothelial growth factor (VEGF) of Lewis lung carcinoma was observed. Results TMP could remarkably reduce the volume, weight, and numbers of the metastatic foci, MVD, and the expression of VEGF of Lewis lung carcinoma. But DS did not show remarkably effect on Lewis lung carcinoma. Conclusion TMP can remarkably inhibit the growth and metastasis of Lewis lung carcinoma on mice, and its mechanism might be relative to inhibiting the expression of VEGF and angiogenesis. DS injection has no remarkably effect on Lewis lung carcinoma.

AIM To investigate the protective action of onychin aganist the growth inhibition of endothelial cell injured by menadione and its mechanism. METHODS The injured model was established by endothelial cell treated with menadione.Protective effect of onychin aganist growth inhibition of injured endothelial cell was determined by MTT assay and cell counting method; NO concentration in the medium was determined by nitrate reductase assay; eNOS and phosph ERK1/2 protein levels were determined by Western blot. RESULT Onychin significantly decreased the growth inhibitory rate of injured endothelial cells,increased NO concentration in the medium and eNOS activity and up regulated phosph ERK1/2 expressing. CONCLUSION Onychin has protective action and against the growth inhibition of endothelial cell injured by menadione may be via NO and ERK1/2 signal pathway.

AIM To investigate the relationship between the prevention of probucol against restenosis and functional vascular remodeling after percutaneous transluminal angioplasty(PTA) in rabbits. METHODS New Zealand rabbit thoracic aorta atherosclerosis was induced by 3 5 F balloon catheter injury following a 4 week feeding of high cholesterol diet, and percutaneous transluminal angioplasty(PTA) was performed by using 3 5 F ballon catheter. Probucol(1 g?d -1 ) or vitamin E(400 mg?d -1 ) was administrated one week before PTA. Two weeks after PTA, lumen area,neointima area(NEA),medial area(MA) and NEA/MA were analyzed by computerimage system.The relaxation response of restenotic arteries to acetylcholine and the contractive response to norepinephrine, potassium chloride and serotonin of thoracic aorta rings were measured by bioassay. Nitric oxide of serum was measured by means of biochemical assay.RESULTS After two weeks of PTA, probucol increased lumen area and decreased neointima area significantly. The relaxation response of restenotic arteries to acetylcholine was significantly lower than that of normal arteries〔relaxation percent to acetylcholine (1 ?mol?L -1 ):(18 4?4 0)% vs (63 5?6 4)%, P

Aim To study the effects of probucol on THP-1 macrophage apoptosis and CD36、Caveolin-1 expression induced by ox-LDL.Methods Apoptosis of THP-1 macrophages was determined by flow cytometry analysis.RT-PCR and immunofluorescence were used to detect CD36,Caveolin-1 mRNA level and protein expression respectively.Results Probucol had no effect on mRNA level of CD36,Caveolin-1 in THP-1 macrophages,but it attenuated Caveolin-1 protein expression.Conclusions Probucol can inhibit apoptosis induced by ox-LDL in THP-1 macrophages by down-regulating Caveolin-1 protein expression.

In order to study the effects and the possible mechanisms of Daxx overexpressed in HepG2 to hydrogen peroxide treatment, and to search new targets for cancer chemotherapy, HepG2cells were transfected using lipofectamine 2000, and selected by treatment with G418. Stable cell lines were confirmed by reverse transeriptase polymerase chain reaction (RT-PCR) targeting vector gene. Experiments include the following groups: (1) control group (non-transfected cells); (2) transfected with empty vector (HepG2/GFP cells); and (3) transfected with pEGFP-C1-Daxx (HepG2/GFP-Daxx cells). After incubation with hydrogen peroxide (H2O2) for 24 h, cellular viability was analyzed by MTT, and cellular apoptosis was measured by flow cytometric analysis. Gene expression at protein level was detected by Western blot. The RT-PCR results showed that Daxx RNA in cells transfected with pEGFP-C1-Daxx was increased significantly compared with that in the HepG2/GFP cells. Fluorescence microscopy revealed that Daxx protein was localized in the nuclei. Hydrogen peroxide was used to induce apoptosis of HepG2 cells and observed that the hydrogen peroxide decreased the viability of HepG2 cells in concentration-dependent pattern. The IC50 values in three groups (Normal cells, HepG2/GFP cells and HepG2/GFP-Daxx cells) were 0.72, 0.76, and 0.49 mmol/L respectively. The apoptotic ratio was significantly higher in HepG2/GFP-Daxx cells as compared to the other two groups. HepG2/GFP-Daxx cell incubated with hydrogen peroxide, showed a significant increase in the activation of caspase-3 and JNK as compare with the other groups. Over-expression of Daxx facilitated HepG2 cells apoptosis induced by hydrogen peroxide. Furthermore, there may be a synergetic relation with apoptosis and increase of JNK activity.

AIM: To elucidate the effects of losartan on the expression ofmatrix metalloproteinases-2, JNK1/2 and proliferation in cardiac fibroblast. METHODS: Neonatal rat cardiac fibroblasts were cultured. The cells proliferation was determined by MTT. To determine effects of AngⅡ on JNK1/2 activity, cells were incubated (for 0, 2, 5, 10, 30, 60, 120 min) in serum-freemedia with AngⅡ, and the other group fibroblasts were exposed to serum-free media with or without AngⅡ and losartan (AngⅡ 100 nmol/L, AngⅡ 100 nmol/L+losartan 100 nmol/L, losartan100 nmol/L, losartan for 45 min before). Cells protein was collected with MBST buffer. The relative abundance of MMP-2, JNK1/2 and p-JNK1/2 in cells was determined by immunoblotting. The secretion of MMP-2 in media of cell culture was determined by ELISA. RESULTS: AngⅡ increased the proliferation of CFB in a dose-dependent manner, whereas losartan decreased the proliferation of CFB stimulated by AngⅡ in a dose-dependant manner, too (P＜0.05). The relative abundance of JNK1/2 was highest in AngⅡ of the 2-min-stimulated group. AngⅡincreased expression of JNK1/2 and MMP-2 protein (P＜0.05), on the contrary, losartan inhibited JNK1/2 and MMP-2 protein expression.CONCLUSION: AngⅡ induce the increase of proliferation of CFB, expression of JNK1/2 and MMP-2 in CFB, and losartan inhibits these effects of AngⅡ.