AIM: To explore the effect of the combination of captopril and losartan on the sICAM-1, sVCAM-1, TNF-?, and TGF-? in the patients with coronary heart disease. METHODS: sICAM-1, sVCAM-1 and TGF-? were measured with ELISA, and TNF-? was measured with RIA in the patients with or without the treatment of captopril and losartan. RESULTS: sICAM-1 and TNF-? decreased, and TGF-? increased distinctly in the patients given a combination of captopril and losartan compared with patients without the drugs. sVCAM-1 had the tendency of decrease in combined therapy, but no significant difference showed compared with the control patients. CONCLUSION: The combination of captopril and losartan has the effects on the cell adhesion molecules and cytokins in patients with coronary heart disease.

Objective To study the effect of angiotensin II in its different concentrations and different action time on VEC apoptosis and the expression of Fas, Bcl-2 in vascular endothelial cells (VEC) and to study the influences of enoxaparin on the above roles. Methods Flow cytometer was used to measure the apoptosis ratio and the expression of Fas, Bcl-2 which were induced by angiotensin II in its different concentrations and different action time, and influenced by enoxaparin. Results Apoptosis ratio(1.86?0.18,30.62?4.20;1.67?0.15,30.08?4.41)and the expression of Fas(1.13?0.16,14.85?1.47;1.13?0.16,15.67?1.97), Bcl-2 (2.38?0.43,9.62?1.81;2.38?0.43,12.33?1.73)were induced and increased by angiotensin II with the increase of concentrations and action time. Enoxaparin had an effect on apoptosis ratio and the expression of Fas, Bcl-2, which were induced by angiotensin II(30.62?4.20,18.31?2.64;14.85?1.47,7.28?1.36;9.62?1.81,16.05?1.79). Conclusions Apoptosis ratio and the expression of Fas, Bcl-2 may be induced and increased by angiotensin II with the increase of the concentrations and the action time. Enoxaparin may have the reduce effect on apoptosis ratio and the expression of Fas and Bcl-2 in vascular endothelial cells.

AIM : To investigate the effects of angiotensin II (AngII) in different concentrations and different action times on the rate of apoptosis and expression of apoptosis genes in vascular smooth muscle cells and the influences of fosinopril on it. METHODS : Flow cytometer was used to measure the apoptosis rate and the expression of apoptosis genes (Fas and Bcl 2) induced by AngII in different concentrations and different action times and the influence caused by fosinopril. RESULTS BZ : The rate of apoptosis and the expression of apoptosis genes were induced and increased by AngII with the increase of concentrations and action times compared with that in the control group. The expression of Fas was increased and Bcl 2 was decreased with the increase of the concentrations and action times of AngII in fosinopril group compared with that in the AngII group. CONCLUSION : The apoptosis rate and the expression of apoptosis genes are induced and increased by angiotensin II with the increase of the concentrations and the action times. Fosinopril has the regulation effect on the apoptosis rate and the expression of apoptosis genes in vascular smooth muscle cells.

AIM:To explore the effect of the combination of ACEI and ARB on left ventricle in pressure-overloaded hypertrophy rats, and also the relationship between left ventricular hypertrophy (LVH) and cytokines, matrix metalloproteinases, apoptosis, and apoptosis genes. METHODS: IL-6, IL-10, MMP-2 and MMP-9 were evaluated by ELISA method. TNF-alpha was measured with radioimmunoassays. Flow cytometer was used to measure the apoptosis ratio and the expression of Fas, Bcl-2 and Bax. RESULTS: 6 weeks after abdominal aortic coarctation operation, the weight of the left ventricle ( 0.983 ? 0.316 g ) and heart weight/body weight ( 0.382 ? 0.154 ) were significantly increased in control group compared with the sham operated group. And also IL-6 ( 208.71 ? 84.51 pg?ml -1 ), TNF-? ( 1.983 ? 0.842 ng?ml -1 ), MMP-2 ( 74.63 ? 37.62 ), MMP-9 ( 57.74 ? 25.61 ), apoptosis ratio ( 8.47 ? 4.18 ) and apoptosis genes (fas, bax, bcl-2, bcl-2/bax) expression were increased, but IL-10 ( 86.23 ? 40.13 pg?ml -1 ) was decreased compared with sham operated group. The 3 groups with drugs (CP, LT, CP+LT) decreased the increasing weight of LV and ventricular weight/body weight and inhibited the changes of influencing factors (IL-6, IL-10, TNF-?, MMP-2, MMP-9, apoptosis ratio and apoptosis genes expression), especially in the group of combination of 2 drugs. CONCLUSION: LVH might be related with many influencing factors. ACEI and ARB may have the positive importance in the treatment and prevention of LVH.

Objective To explore the possible immunological mechanism of laminarin sulfate in the prevention of experimental atherosclerosis. Methods Serum soluble interleukin 2 receptor (sIL-2R) , circulating immuno-complex, sub units of T lymphocyte, inter leukin-6(IL-6) , in-terleukin-8(IL-8), tumor necrosis factor-a (TNF-a) and lipid metabolism were determined by ELISA, RIA in rats and quails. Results The lipid metabolism and immunologic function were prominent disturbance in animals after feeding with high-lipid food. However, Laminarin sulfate has obvious regulating effects on above-mentioned index. Conclusions The mechanism of laminarin sulfate in the prevention of atherosclerosis might be closely related to the regulation of the disturbance of lipid metabolism and to the regulation of the immunologic function of the body.

Objective To investigate the effect of angiotensin converting enzyme inhibitor (ACEI) captopril and angiotensin Ⅱ receptor antagonist losartan on the mRNA expression of matrix metalloproteinase (MMP)-1 and MMP-9 in vascular smooth muscle cells induced by angiotensin Ⅱ (Ang Ⅱ ).Methods Male Wistar rats' thoracic aortic vascular smooth muscle cells were cultured in vitro.The cultured cells were divided in to control group,Ang Ⅱ group,captopril group,losartan group,and captopril plus losartan group.Cells in all groups were collected at the culture end-point.MMP-1 and MMP-9 mRNA expressions were detected by RT-PCR method in the collected specimens,and the effects of Ang Ⅱ on MMP-1 and MMP-9 mRNA expression and the intervention effects of captopril and losartan were observed in different Ang Ⅱ concentrations and different action times to vascular smooth muscle cells.Results ( 1 ) MMP-1 mRNA expression gradually increased along with the increments of Ang Ⅱ concentration and the action time (P＜0.05),and the most significant concentration was 10-6 mol/L (P＜0.01).(2)Captopril (5 × 10-6 mol/L) and losartan (5 × 10-6mol/L) inhibited the action of AngⅡ (P＜0.05,P＜0.01).MMP-9 mRNA expression was 0.47±0.03 ,0.86 ± 0.04,0.94±0.14 and 1.12±0.19 vs.0.10±0.04 (P＜0.05,P＜0.01) respectively when Ang Ⅱ concentration was 10-7 ,10-6 ,10-5 and 10-4 mol/L respectively.Captopril (5 × 10-6mol/L) and losartan (5 × 10-6 mol/I) significantly inhibited the MMP-9 mRNA expression which was stimulated by Ang Ⅱ (P＜0.05,P＜0.01),especially in captopril plus losartan group.The MMP-9 mRNA expression increased with the prolonging of stimulating time of Ang Ⅱ,MMP-9 mRNA expression was earlier than that of MMP-1.Conclusions AngⅡ increases the expression of MMP-1 and MMP-9 of vascular smooth muscle cells in a dose-and time-dependence manner.Captopril and losartan inhibit the MMP-1 and MMP-9 mRNA expression of vascular smooth muscle cells induced by Ang Ⅱ ,and the inhibition is the strongest when losartan was combined with captopril.The inhibitive effects is positively correlated to action time.

Objective To investigate whether there is amyloid fibers in the mature neutrophils and to reveal the molecular mechanism of the formation of AD amyloidosis. Method Thirty cases of AD patients and 30 healthy control were enrolled. The white blood cell, the red blood cell,hemoglobin and neutrophil absolute value were determined by Sysmex X5-500i hematology analyzer. The neutrophils and amyloid variable specific probe affinity were measured, The starch like variable fluorescence intensity in plasma was dtected by the sulfur T (Thioflavin T, ThT) method. Results The affinity test results showed that the amyloidosis fluorescent probe (ThT) can be combined with tissue amyloid fibers specifically. The neutrophil amyloid fibers staining also showed a positive reaction. Compared with the AD group, no significant differences were found in white blood cell, red blood cell, hemoglobin and neutrophil absolute value level in the healthy control group The serum amyloid variable fluorescence intensity in the AD group was significantly higher than that in the control group (P < 0.05). Conclusion The amyloid fibers was found in the mature neutrophils, and the level of plasma amyloid fibers was significantly increased in the AD patients.

Objective To investigate the pathogenesis in patients with uterine leiomyoma complicated by amyloidosis. Methods A total of 36 uterine leiomyoma patients were recruited in this study, and divided into two group by Congo red staining:amyloidosis group (n=6) and non-amyloidosis group (n=30). (1) Amyloidosis deposition was observed in amyloidosis group. (2) HE staining was used to compare changes of inflammatory cells in two groups. (3)PAS staining was used to observe polysaccharide difference in two groups. (4)Values of serum hemoglobin (HGB), white blood cell count (WBC), lymphocyte absolute value (LYM), neutrophil absolute value (NEU), total protein (TP), albumin (Alb) and prealbumin (PA) were com?pared between two groups. Results (1)Leiomyoma entity cells were negatively Congo red stained, while 5 out of 6 pseudo-capsule fiber deposition and 2 out of 6 blood vessel were positively Congo red stained. (2)Infiltrations of inflammatory cells were observed in two groups. (3) The PAS positive staining was found in amyloidosis deposition and non-amyloidosis deposi?tion groups. (4)There were no significant differences in HGB, WBC, NEU, LYM, TP, Alb and PA levels between two groups (P>0.05). Conclusion Metabolism changes resulted from cell function alterations in local micro-environment by uterine leiomyoma may be related to the formation of the amyloidosis.