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.

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.

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

Aim To compare the effects of the non-peptide angiotensin Ⅱ receptor type Ⅰ antagonist,Losartan,and the active vascular peptide,calcitonin gene-related peptide(CGRP),on the proliferation of vascular smooth muscle cells induced by angiotensin Ⅱ,and to explore the mechanism of depressor effect of Losartan and CGRP in vivo.Methods MTT,Thymidine incorporation and flow cytometry,were used to determine the ability of proliferation of VSMC induced by angiotensin Ⅱ in the presence or absence of Losartan or CGRP,Western blotting was used to determine the activity of ERK1/2.Results Losartan or CGRP inhibited the viability,DNA synthesis,cell proliferation index,and the activity of ERK1/2 in a dose-dependent manner.Conclusion Losartan or CGRP significantly inhibits the proliferation of VSMC induced by angiotensin Ⅱ;the inhibitory effect of CGRP is stronger than that of Losartan.The signaling path way is involved in ERK1/2.

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 investigate pharmacdogical mechanism of Negundo Chastetree extract liquor (NCEL), the effect of (NCEL) on blood-fat, liver-fat and blood-sugar in the rat and the mouse were studied in this paper. METHODS: The experimental models were established by giving rats and mice NCEL orally at dosages 5.0, 7.5, 10.0 mL/kg.b.w respectively. Then the level of blood-fat, liver-fat, and blood-sugar were observed. RESULTS: The level of serum triglyceride and total cholesterol decreased considerably in mice, at the same time, the increase of triglyceride induced by high lipid diet in liver of mice were inhibited significantly. In addition, the level of fatty liver of hepatic homogenization triglyceride in rats with induced by DL-ethionine was lowered obviously by oral administration of NCEL. CONCLUSION: These results suggest that NCEL may have effects of reducing blood-fat and pretecting liver.

Objective To investigate the effect of angiotensin Ⅱ-1 receptor antagonist losartan on expression of tumor necrosis factor-alpha (TNF-?) in the ventricular myocardium in the renovascular hypertension rats. Methods Renovascular hypertension model was obtained by clip left renal artery in Sprague-Dawley(SD) rats. After operation the rats were divided into 3 groups: sham group, two-kidney one clip (2K1C) group, and losartan treatment group(2K1C and losartan 20 mg/kg?d by drinking). Tail blood pressure was determined every week. Animals were euthanized after treatment with losartan for four weeks. Cardiac index(CI)was calculated by HW/BW, and TNF-? protein of ventricle myocardium was determined by ELISA and immunohistochemistry. Results Losartan significantly decreased blood pressure(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.