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Hypertension with high serum Homocysteine (Hcy) significantly increases the incidence of cardiovascular and cerebrovascular events, which is defined as H-Type Hypertension by Chinese scholars. Plenty of researches have confirmed that high prevalence of H-Type Hypertension in Chinese population is now the big public problem in China. Traditional Chinese Medicine(TCM)treatment shows the advantages in integral regulation, less side effect, and anti-Hcy effect in hypertension. This paper discussed the prevalence, TCM syndrome and TCM treatment progress in H-Type Hypertension to provide some ideas and references for the intervention of H-Type Hypertension by TCM.
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Objective To observe the effect of carvedilol and motoprolol on the weight of cardiac muscle in patients with hypertensive heart disease.Methods One hundred patients with hypertensive heart disease were divided into two groups by random number and treated with carvedilol(n =54) and motoprolol(n =46) respectively for 12 months.Data were recorded (left ventricular end-diastolic dimension (LVEDD),left ventricular end-systolic dimension (LVESD),left ventricular ejection fraction (LVEF),interventricular septal thickness (IVST),and left ventricular posterior wall thickness (LVPWT)) before and after the treatment.Left ventricular muscle mass(LVW),left ventricular mass index(LVWI) were calculated.Results After treatment,both groups improved with declined LVEDD (motoprolol group:(43.60 ± 4.43) mm vs.(46.70 ± 3.21) mm,t =18.143,P ＜ 0.01 ; carvedilol group:(42.50 ± 2.56) mm vs.(46.5 ± 3.18) mm,t =18.232,P ＜ 0.01),thinner IVST (motoprolol group:(9.68 ± 1.65) mm vs.(12.01 ± 1.56) mm,t =12.785,P ＜ 0.01 ; carvedilol group:(9.05 ± 1.04) mm vs.(11.59 ± 1.54) mm,t =7.865,P ＜ 0.01),and increased LVEF (motoprolol group:(52.89 ± 8.78)％ vs.(50.23 ± 7.88)％; carvedilol group:(54.65 ± 8.87％)％ vs.(50.22 ±7.89)％).In the carvedilol treatment group,LVMI significantly (t =4.987,P ＜ 0.01) declined from (133.75 ±25.89) g/m2 to (109.25 ± 22.53) g/m2.In the motoprolol treatment group,LVMI declined from (134.76 ± 25.87) g/m2 to (119.78 ± 23.65.53) g/m2 (t =5.689,P ＜ 0.01).After the treatment,each index of carvedilol group improved significantly compared with metoprolol group (P ＜ 0.05).Conclusion Both medications are able to reduce the weight of cardiac muscle of patients with hypertensive heart disease,and carvedilol is better than motoprolol.
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ObjectiveTo investigate the influence of cobalt chloride ( CoCl2 )-mimetic hypoxia on theproliferation,apoptosis and migration of human pancreatic cancer cell fine PANC1.MethodsPANC1 cells were treated with 0(control),100,200,400,800 μmol/L CoCl2 respectively for 24 h.Real-time RT-PCR and Western blot were used to determine hypoxia induced factor ( HIF)-1o mRNA and protein expression respectively,and cell counting kit-8(CCK-8) assays,flow cytometry and cell scratch test were used to examine the proliferation,apoptosis and migration of PANC1 cells,respectively.ResultsIn the control group and 100,200,400 and 800 μmol/L CoCl-2 groups,the expressions of HIF-1t mRNA were 1,1.08 ±0.12,1.12 ± 0.09,1.04±0.11,0.66 ±0.07,and the expressions of VEGF mRNA were 1,2.69±0.35,4.81 ±0.54,2.19 ± 0.21,0.79 ± 0.08,while the expressions of HIF-1 α protein were 0.23 ± 0.03,0.36 ± 0.04,1.15 ± 0.11,1.08 ± 0.09,0.44 ± 0.04; and the expressions of VEGF protein were 0.14 ± 0.02,0.12 ± 0.01,0.95 ±0.09,0.87 ±0.09,0.55 ±0.06; and cell viability rates were 100％,(98.43 ±2.88)％,(76.15 ± 0.70)％,(53.87 ±0.77)％,(35.23 ±0.67)％ ; while cell apoptotic rates were (5.2 ±1.12)％,(5.74 ± 1.07)％,(6.82 ± 1.85)％,(12.09 ±3.53)％,(31.88 ±6.95)％ ; the cell migration distance of PANC1 cells were (43.24 ±3.67)％,(59.46 ±5.39)％,(80.56 ±8.05)％,(63.89 ±5.96)％,(9.09 ± 1.59 ) ％.Compared with those of control group,the expressions of VEGF mRNA,VEGF and HIF-1 α protein,cell migration distance showed a two-way variation ( ascending first and descending later) (P ＜0.05 ),and the expression of HIF-1α mRNA and cell proliferation rate was decreased in a dose-dependent manner,while the cell apoptosis was increased in a dose-dependent manner.Conclusions CoCl2 significantly inhibits the proliferation and promotes apoptosis of PANC1 cells at certain level.CoCl2 has a two-way effect on the migration of PANC1 cells,and it may be related to the direct injury of high concentration of CoCl2 on cells.
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Objective To investigate the expressions of RGC-32 and E-cadherin in pancreatic cancer and analyze their clinicopathological significance and the correlation with each other.Methods SP immunohistochemistry was used to detect the expressions of RGC-32 and E-cadherin in 42 cases of pancreatic cancer tissues,12 cases of chronic pancreatitis tissues and 8 cases of normal pancreatic tissues.Results The positive staining for RGC-32 was predominantly observed in the cytoplasm of pancreatic acinar cells.The positive staining for E-cadherin was mainly observed in the cytomembrane of normal pancreatic and chronic pancreatitis acinar cells,but aberrant expression ( cytoplasm expression and ( or ) weaker expression) could be found in pancreatic cancer cells.The positive expression rate of RGC-32 and aberrant expression rate of E-cadherin were 78.6％ (33/42) and 54.8％ (23/42),respectively,in pancreatic cancer tissues,which were significantly higher than those in normal pancreatic tissues [37.5％ (3/8) and 0] and chronic pancreatitis [41.7％ (5/12)and 8.3％ (1/12) with statisticai significance,P ＜0.05].The expression of RG C-32 in pancreatic cancer was associated with lymph node metastasis and TNM staging (P =0.016,0.025,respectively),but not with age,gender and differentiation degree ( P =0.831,1.000,0.629,respectively).The aberrant expression of E-cadherin was associated with differentiation degree,lymph node metastasis and TNM staging ( P =0.024,0.004,0.004,respectively),but not with age and gender ( P =0.970,1.000,respectively).A significantly positive correlation was found between positive expression rate of RGC-32 and aberrant expression rate of E-cadherin (r =0.458,P ＜0.01 ).Conclusions Both positive expression rate of RGC-32 and aberrant expression rate of E-cadherin are up-regulated significantly in pancreatic cancer tissues and RGC-32 may be involved in the invasion and metastasis of pancreatic cancer by regulating epithelial mesenchymal transition.