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AIM: To investigated the effects of Chlamydia pneumoniae (C.pneumoniae) infection on the expression of intercellular adhesion molecule-1 (ICAM-1) in cultured human umbilical vein endothelial cells (HUVECs). METHODS: After propagated in HEP-2 cells, C. pneumoniae organisms were infected to HUVECs. The infection was assessed by ectromicroscope and PCR. The expression of ICAM-1 on HUVECs was detected by flow cytometry before infection and 12 h, 24 h, 48 h, 72 h after infection. RT-PCR was used to detect the ICAM-1 mRNA expression. RESULTS: C.pneumoniae was able to infect cultured HUVECs. After infection, the expression of ICAM-1 on the surface of cultured HUVECs was increased,, the peak was at the time of about 24-48 h; The light quantative RT-PCR analysis demonstrated that the infection also enhanced the ICAM-1 mRNA expression. CONCLUSION: The ability of C.pneumoniae to grow in HUVECs and to stimulate the expression of ICAM-1 protein and mRNA suggests that C.pneumoniae may play a role in atheriosclerosis.
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AIM: To investigate the effects of long-term TCV116 on left ventricular remodeling and heart function after myocardial infarction. METHODS: Myocardial infarction (MI) was caused by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance, the surviving rats were randomly assigned to the following treatment protocols: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control; (4) Sham-operated rats, treated with TCV116 2 mg/kg per day. At 22 weeks, cardiac hemodynamic parameters such as MAP, LVSP, dp/dt_(max) and LVEDP, and histomorphometric parameters such as (LVW/BW) and LVCA/BW were measured, mRNA of cardiac genes such as ?MHC, BNP, TGF-?_1, collagen I and III were quantified, and survival rates were calculated. RESULTS: Compared with sham-operated rats, MI rats without therapy showed significant increases in histomorphometric parameters as well as in mRAN expressions of cardiac genes (P
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AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of G?q/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP 3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats ( P 0.05). At 10 days, the level of IP 3 significantly increased in left ventricle of CA rats compared with the control animals ( P
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AIM: To study the effect of cocaine on caspase-3 in myocardiac cells of male rats in different age. METHODS: Three-week-old( n= 16), six-week-old( n= 16) and twelve-week-old( n= 16)male Sprague Dawley rats were all divided into control groups and experiment groups randomly, each group had eight animals, experiment groups were given cocaine hydrochloride (15 mg?kg -1 body weight) subcutaneously daily for four weeks.The ratio of heart weight to body weight (HW/BW,mg/g) were measured. DNA fragmentation of myocardia cells was determined by gel electrophoresis, and caspase-3 activity in myocardia cells was tested by flow cytometry (FCM). RESULTS: In three experiment groups, the DNA isolated from myocardial cells displayed clear ladder pattern. The HW/BW and the caspase-3 activity were increased significantly than those of control groups ( P
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AIM: To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS: Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H, n=29 ) and the control group (group C, n=26 ). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS: ①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na + channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION: Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na + channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.
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In order to investigate the action of calcium antagonists on metabolism of intracellular macromolecules, The authors observed the effects of verapamil on the incor-poration of 〔 3H 〕 TdR, 〔 3H 〕 UR and 〔 3H 〕 Leu into human fibroblasts. The inhibitory effects on DNA and RNA synthesis were concentration dependent, ID50 was l2.3mg/L and 22mg/L, respectively. The inhibitory effect on the synthesis of protein was weak.
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AIM: Cross talk between oxidized low-density lipoprotein (ox-LDL) and angiotensin II(Ang-Ⅱ) may play an important role in the pathogenesis of atherosclerosis. In this study, we tested the hypothesis that AngⅡ can induce expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), a new receptor for ox-LDL, in cultured THP-1 cells. METHODS: Cultured THP-1 cells were treated with 0.1 ?mol/L PMA for 48 hours at first .Then the cells were incubated with 10 -9 -10 -5 mol/L Ang II for 24 hours, or with 10 -6 mol/L Ang II for various time up to 48 hours. LOX-1 protein expression was examined by cell enzyme linked immunosorbent assay (ELISA), and LOX-1 mRNA was detected by quantitative competitive reverse transcription-polymerase chain reaction (RT-PCR) . RESULTS: PMA-untreated THP-1 cells didn't express LOX-1 mRNA. After 48 h of PMA treatment, THP-1 cells differentiated and LOX-1 mRNA was detected. Incubation of AngII with THP-1 cells for 24 h significantly increased LOX-1 mRNA and protein expression in a concentration-dependent manner (10 -9 -10 -5 mol/L, P