AIM To observe the effects of improved prescription of Didang-tang (IPDT) on exprimental atherosclerosis(AS) in rabbits and study the possible mechanism. METHODS Lipid plaque area of aortic endothelium was measured by image analysis method. lipid metabolism was measured by enzyme dynamics method, one-step method and immunization photoextinction. Plasma SOD and MDA was measured by microcontent fast detecting method and modified Ba MuGuoFu method. Ceramide was measured by thinlayer scannig; apoptosis of foam cell of aorta lipid plaque was measured by TUNEL method.RESULTS IPDT reduced lipid plaque area of aortic endothelium,regulated lipid metabolism, improved antioxidation of organism, ced ceramide content of aorta lipid plaque and apoptosis of foam cell.CONCLUSION IPDT has good effects of anti-exprimental AS,the possible mechanism maybe related to regulation of lipid metabolism and antioxidation and depression of apoptosis of foam cell.

Objective:To probe into the mechanism of Shenshuai Capsule in delaying advance of chronic renal failure(CRF)and against interstitial renal fibrosis.Methods:74 cases of CRF at decompensation phase were randomly divided into a treatment group and a control group.Changes of their serum urea nitrogen(BUN),creatinie(SCr),endogenous creatinine clearance rate(Ccr),collegen Ⅳ (Col Ⅳ),procollagen Ⅲ(PC Ⅲ),laminin(LN),and improvement of urinary protein(uPro),urinary ?_2-microglobulin(?_2-MG)and clinical symptoms and signs were observed.Results:After treatment of Shenshuai Capsule,BUN,SCr,Col Ⅳ,PC Ⅲ,LN,urinary protein and ?_2-MG decreased and Ccr increased in the treatment group,with a significant differences between the two group in the above mentioned indexes except LN(P

AIM: To observe the effect of Tangmaiantai on the plasma lipid and renal function of rat with diabetic nephropathy. METHODS: The rat model of diabetic nephropathy was established by using STZ. The effect of Tangmaiantai on rat blood glucose before meal, serum TC, TG, Ccr, BUN and urinary protein were observed. RESULTS: Tangmainantai could decrease the level of serum TC, TG, Ccr, BUN and urinary protein, comparing to that of the model group (P

BACKGROUND: It is reported that ceramide signal pathway may play an important role in the apoptosis of vascular endothelial cell and then lead to the progress of atherosclerosis, such as the formation of foam cells and the proliferation of smooth muscular cells.OBJECTIVE: To study the changes of the sphingomylinase activity and ceramide content in aorta of rabbits with experimental atherosclerosis and investigate the regulative effects and mechanism of emodin on them as compared with positive fenofibrate.DESIGN: Completely randomized controlled design.SETTING: Laboratory of Pharmacology & Toxicology, School of Pharmaceutical Science of Sun Yat-sen University.MATERIALS: The experiment was completed at the Laboratory of Pharmacology & Toxicology, School of Pharmaceutical Science of Sun Yat-sen University from July to December 2003. Totally 48 New Zealand male rabbits were selected. Forty animal models of atherosclerosis were made with high cholesterol feed, and the other 8 rabbits were selected as the normal controls. Model animals were divided randomly into model group, 5 mg/kg emodin group, 10 mg/kg emodin group, 20 mg/kg emodin group and 25mg/kg fenofibrate group with 8 in each group.METHODS: At the seventh weeks of model duplication, 5 mg/kg, 10 mg/kg and 20 mg/kg emodin were perfused in rabbits of emodin groups respectively, and 25 mg/kg fenofibrate was perfused in rabbits of fenofibrate group. Emodin and fenofibrate were diluted or suspensed with 2 mL saline once per day respectively. Rabbits in normal control group and model group were administrated with the same volume of saline for 4 weeks. The rabbits were raised separately and were fed with 135-150 g food per day.MAIN OUTCOME MEASURES: [1] The area of the lipid plaque in aortal intima; [2] the content of serum TC and TG; [3] SOD activity and MDA content; [4] SMase activity and CER content in aorta.RESULTS: Totally 48 rabbits entered the final analysis. [1] Area of the lipid plaque: Area of the lipid plaque was (48.87±15.5) % in the model group, which was larger than that in each emodin group (P ＜ 0.05 or 0.01),especially larger than that in the 10 mg/kg emodin group (22.19±12.9)%while that in the fenofibrate group was similar to that in the model group (P ＞ 0.05). [2] Content of serum TC and TG: The anrtal intima of control was smooth. Content of serum TC and TG in each emodin group were similar to those in the model group (P ＞ 0.05), but those in the 25 mg/kg fenofibrate group were lower than those in the model group (P ＜ 0.05). [3]Content of SOD and MDA in plasma: SOD activity of rabbits in each emodin group was higher than that in the model group (P ＜ 0.05, P ＜ 0.01),but the MDA activity in the 10 mg/kg and 20 mg/kg emodin group was lower than that in the model group (P ＜ 0.05). The MDA activity in the25 mg/kg fenofibrate group was similar to that in the model group (P ＞ 0.05).[4] Content of SMase and CER: Those in the model group were higher than those in the normal control group, but those in the 5, 10 and 20 mg/kg emodin groups were lower than those in the model group; those in the 25 mg/kgfenofibrate group were similar to those in the model group (P ＞ 0.05). [5]Analysis of correlation: Content of SMase was in positive relation with blood cholesterol (r=0.542, P ＜ 0.01), in positive relation with blood MDA (r=0.789, P ＞ 0.01), and in negative relation with blood SOD(r=-0.936, P ＞ 0.01); content of CER was in positive relation with blood cholesterol (r=0.433, P ＞ 0.05), in positive relation with blood MDA (r=0.673, P ＞ 0.01), and in negative relation with blood SOD (r=-0.876, P ＞ 0.01).CONCLUSION: The study finds that emodin, despite its insignificant effects on decreasing TG or TC, can protect vascular endothelial cells and reduce the area of lipid-laden plague of aortal intima by antioxidation, inhibition of the sphingomyelinase activity and reduction of the content of ceramide. It is suggested that moderate dosage of emodin employed in the study may be most appropriate to atherosclerosis treatment.

AIM: To study the effects of prearuptorin C (Pra-C) on myocardial sarcolemma Na~+, K~+-ATPase activity, myocardial mitochondria Na~+, K~+-ATPase, Ca~ 2+ -ATPase, Mg~ 2+ -ATPase activities and apperent Km and Vmax in spontaneously hypertensive (SHR) and renovascular hypertensive rats (RHR). METHODS: ATPase activity was measured with colourmetric method. Apparent Km and Vmax of both Na~+, K~+-ATPase in myocardial sarcolemma and Ca~ 2+ -ATPase in myocardial mitochondria were calculated according to Lineweaven-Burk double-reciprocal plot method with liner regression. RESULTS: The Vmax of both Na~+, K~+-ATPase in myocardial sarcolemma and Ca~ 2+ -ATPase in myocardial mitochondria were lower in SHR untreated group than that in SD control rats, while Km was higher than that in SD control rats. In RHRs untreated group, only Vmax was decreased, while the Km had no statistically change. Pra-C prevented the reduction of ATPase in amount, but not affected their intrinsic characteristics. CONCLUSIONS: The results suggest that both amounts and affinities to ATP of Na~+, K~+-ATPase and Ca~ 2+ -ATPase were decreased in SHRs, but in RHRs, only amounts of ATPase was decreased, while their affinities to ATP were unchanged. Treatment with Pra-C prevents the decrease in amount of ATPase.

AIM: To study the changes of the sphingomylinase activity and ceramide content in rabbit aorta of experimental atherosclerosis and investigate the effects of emodin on them. METHODS: The qualified rabbits were fed with food containing 1% cholesterol and 5% lard for 10 weeks to establish the animal models. The concentration of cholesterol (TC) was assayed by a enzyme method. Trace-fast-test method was used to test the activity of superoxide dismutase (SOD) and motified-BAMuGuoFu methods was employed to assay the content of myocardial malondialdehyde (MDA). Radiolabeled-enzyme-tracing was used to detect the activity of the sphingomyelinase,and thin-layered scanning was conducted to analyze the content of the ceramide in aorta. RESULTS: The ceramide content in aorta and the sphingomyelinase activity were markedly increased in the rabbits with experimental atherosclerosis. The increase was positively correlated with the content of TC and MDA and negatively correlated with the activity of SOD in blood. Compared to the model animals, emodin at concentration of 5 mg?kg -1 , 10 mg?kg -1 and 20 mg?kg -1 respectively reduced the area of plague on endothelium in rabbit's aortic artery and elevated the activity of SOD (P

AIM:To investigate the change of short-chain acyl-CoA dehydrogenase (SCAD) expression during cardiomyocyte apoptosis and to explore the relationship between SCAD and cardiomyocyte apoptosis .METHODS: The neonatal rat cardiomyocytes treated by tert-butyl hydroperoxide (tBHP) were used as the model of cardiomyocyte apoptosis . The cell viability , the expression of SCAD at mRNA and protein levels , the activity of SCAD and the content of free fatty acids were determined .RESULTS:The mRNA and protein expression of SCAD decreased in the cardiomyocyte apoptosis model.Compared with negative control group , SCAD expression and activity were both significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the cardiomyocytes .Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP .CONCLUSION: Down-regulation of SCAD may play an important role in primary cardiomyocyte apoptosis .Increase in the expression of SCAD may become an impor-tant part in intervening cardiomyocyte apoptosis .

[ABSTRACT]AIM:ToinvestigatethedifferenteffectsofERK1/2/PPARα/SCAD(short-chainacyl-CoAdehy-drogenase) signal pathways on the cardiac hypertrophy induced by insulin-like growth factors 1 ( IGF-1) or phenylephrine ( PE) .METHODS:The neonatal rat cardiomyocytes induced by IGF-1 were used as the model of physiological cardiac hypertrophy , and those induced by PE were used as the model of pathological cardiac hypertrophy .The surface area of the cardiomyocytes, the expression of p-ERK1/2, PPARαand SCAD, the activity of SCAD and the content of free fatty acid in the cardiomyocytes were measured .RESULTS:Compared with the control cells , the surface area of the cardiomyocytes in-duced by IGF-1 and PE were both increased .Compared with the controls , the expression of SCAD and PPARα, and the activity of SCAD in the cardiomyocytes induced by IGF-1 were increased , while the expression of p-ERK1/2 was de-creased.However, the cardiomyocytes treated with PE showed decreased expression of SCAD and PPARα, decreased activ-ity of SCAD and increased expression of p-ERK1/2.Meanwhile, the decrease in free fatty acid in IGF-1-induced cardio-myocytes and the increase in PE-induced cardiomyocytes indicated that the fatty acid utilization was increased in the cardio -myocytes induced by IGF-1, but decreased in the cardiomyocytes induced by PE .CONCLUSION: The changes of p-ERK1/2, PPARαand SCAD in the cardiac hypertrophy induced by IGF-1 or PE indicate that the effects of ERK 1/2/PPARα/SCAD signal pathways are different between physiological cardiac hypertrophy and pathological cardiac hypertro -phy , and that SCAD may be a molecular marker of these 2 different cardiac hypertrophies and a potential therapeutic target for pathological cardiac hypertrophy .

AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .

Objective To study the effect of comprehensive Chinese medicine therapy,including Chinese herbal medicine fumigation,massage,and quadriceps exercise,on adipokines of visfatin and chemerin content in joint fluid of patients with knee osteoarthritis (KOA),and to explore its possible therapeutic mechanism for KOA.Methods A total of 60 cases of KOA patients were randomly divided into treatment group and control group,30 cases in each group.The treatment group was treated with comprehensive Chinese medicine therapy,and the control group was treated with Chinese medicine fumigation alone.After treatment for 2 weeks,the clinical efficacy of both groups was evaluated,and the changes in the scores of the Western Ontario and McMaster Universities Arthritis Index (WOMAC)were observed.Moreover,the contents of visfatin and chemerin in jointfluid were examined.Results (1) The total effective rate of the treatment group was 96.7％ and that of the control group was 83.3％,the difference being significant (P ＜ 0.01).(2) After treatment,WOMAC scores of both groups were obviously decreased(P ＜ 0.01 compared with those before treatment),and the decrease in the treatment group was superior to that in the control group (P ＜ 0.01).(3) The contents of visfatin and chemerint in joint synovial fluid of both groups were decreased (P ＜ 0.01 compared with those before treatment),and the decrease in the treatment group was superior to that in the control group(P ＜ 0.05).Conclusion The comprehensive Chinese medicine therapy of Chinese herbal medicine fumigation,massage and quadriceps exercise is effective for the treatment of KOA,and can decrease the contents of visfatin and chemerin in joint fluid of KOA patients,which may be one of its therapeutic mechanisms.