Objective To study the effect of homocysteine(Hcy) on the expression of c-fos and c-jun mRNA and neointimal hyperplasia in rat common carotid artery, and to explore the possible mechanism of homocysteine exacerbating neointima formation after balloon injury. Methods The mRNA expression of c-fos and c-jun were detected by semi-quantitative RT-PCR in the common carotid artery. The morphology of arterial intima and media was studied by optical microscopy and image analysing system. Results The mRNA expression of c-fos and c-jun was significantly elevated in the low methionine(LM)〔(1.40?0.21),(1.43?0.25)〕 and high methionine(HM) 〔(1.68?0.27),(1.71?0.30)〕 than that in the control group 〔(1.10?0.15),(1.00?0.13), P

This study examined the effect of artesunate (Art) on the proliferation, DNA replication, cell cycles and apoptosis of vascular smooth muscle cells (VSMCs). Primary cultures of VSMCs were established from aortas of mice and artesunate of different concentrations was added into the medium. The number of VSMCs was counted and the curve of cell growth was recorded. The activity of VSMCs was assessed by using MTT method and inhibitory rate was calculated. DNA replication was evaluated by [3H]-TdR method and apoptosis by DNA laddering and HE staining. Flowmetry was used for simultaneous analysis of cell apoptosis and cell cycles. Compared with the control group, VSMCs proliferation in Art interfering groups were inhibited and [3H]-TdR incorprating rate were decreased as well as cell apoptosis was induced. The progress of cell cycle was blocked in G0/G1 by Art in a dose-dependent manner. It is concluded that Art inhibits VSMCs proliferation by disturbing DNA replication, inducing cell apoptosis and blocking cell cycle in G0/G1 phase.
Aorta/cytology ; Apoptosis/*drug effects ; Artemisinins/*pharmacology ; Cell Cycle/drug effects ; Cells, Cultured ; DNA Replication/*drug effects ; Muscle, Smooth, Vascular/*cytology ; Sesquiterpenes/*pharmacology

AIM: To study the mechanism for biological effect of ? 1-adrenoceptors by inves tigating the molecular mechanism involving in the apoptotic processi on in myocardium. METHODS: The expressions of Bcl-2, Bax, cytochrome C, caspase-3 were determined by means of immunohistochemistry and molecular technique. RESULTS: Bcl-2 was increased but apoptosis, Bax, cytochrome C, caspase-3 were decreased when phenylephrine was used before ischemia. CONCLUSION: ? 1 -adrenoceptors may influence the expression of Bcl-2 ,change the permeabil ity of mitochondrion and adjust the expression of apoptotic protein to control apoptosis.

Aim To determine the effects of sodium tashinoneⅡA sulfonate(TSN) on monophasic action potential(MAP) and tachycardia-induced electrical remodeling of rabbit atria in vivo.Methods Twenty-four rabbits were equally divided into two groups randomly: control group and TSN group.Electrical catheters were localized in the right atrium through right internal jugular vein.Right atrial MAP was recorded by multiple channel recording. ERP of right atrial(AERP) was assessed by programmed electrical stimulation before pacing and from 0～8 hours after the onset of the pacing.Results The AERP_(200 ms) of control group was shortened from (105.9?3.8) ms to(114.7?7.2) ms and the rate-dependent of control group's atrium was lost through the pacing process compared with TSN group before pacing(P

AIM:To observe the effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial ultramicro-structure and membrane potential in rats. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham-operated (SO) group, ischemia reperfusion (IR) group, pioglitazone preconditioning group (Pio-P) and 5-HD+pioglitazone (5-HD+Pio) group. Apart from the SO group, IR, Pio-P and 5-HD+Pio groups were subjected to 30 min ischemia and 4 h reperfusion. The heart was quickly removed for observing the structure of mitochondria and measurement of the apoptosis index (AI) by TUNEL. Primary cultured cardiomyocytes of Sprague-Dawley rats were divided into control, hypoxic reoxygenation (HR) and different concentrations of Pio-P group. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (?m). RESULTS: The injury of mitochondrial structure in IR group was severer than that in Pio-P group, while the difference between 5-HD+Pio group and IR group was not evident. Flameng score in Pio-P group(1.62?0.60) was significantly lower than that in IR group (2.75?1.09), P0.05). CONCLUSION: Pioglitazone protects the heart from ischemia reperfusion/ hypoxia reoxygenation injury evidenced by improving mitochondrial ultrastructure and lessening the loss of mitochondrial membrane potential, and decreasing apoptosis. The cardioprotective effects can be inhibited by the blocker of mitochondrial ATP-sensitive potassium channels.

AIM: To study the effect of adrenomedullin (ADM) on L-type calcium currents (I Ca,L) and its signaling transduction process in guinea-pig ventricular myocytes. METHODS: By using whole-cell patch clamp technique, the effect of ADM(1-100 nmol?L -1) on I Ca,Lmyocyte. Furthermore, the possible signaling transduction process of ADM on I Ca,L was investigated by observing the effects of ADM 22-52 (a specific ADM-receptor antagonist,100 nmol?L -1)+ADM(100 nmol?L -1), H-89 (a specific protein kinase A inhibitor, 10 ?mol?L -1) + ADM(100 nmol?L -1), PKC 19-36 (a specific protein kinase C inhibitor, 10 ?mol?L -1) + ADM(100 nmol?L -1) and PMA (a specific protein kinase C activator, 1 ?mol?L -1) on I Ca,L, respectively. RESULTS: ADM at the concentrations of 1-100 nmol?L -1 decreased I Ca,L in a dose-dependent manner (P

Objective To investigate the change of transmembrane potential during Noradrenaline's early preconditioning phase and probe the mechanism of action.Methods Primary culture myocardial cell of neonate rat were divided into three groups at random.GroupⅠ is control group,Group Ⅱis treatment group by hypoxia,Group Ⅲ is treatment group by NA.Group Ⅰ didn't give any drug to culture for 40minutes;Group Ⅱ treated for 40minutes by hypoxia,Group Ⅲ exposed to Noradrenaline(0.2?g/ml)for 10 minutes then treated with hypoxia for 40 minutes.The fluorescence intensity of rhodamine-123 marked mitochondria were detected by flow cytometry.Results The fluorescence intensity of three Group were test by analysis of variance(F=461.3,P

This study examined the effect of artesunate (Art) on the proliferation, DNA replication, cell cycles and apoptosis of vascular smooth muscle cells (VSMCs). Primary cultures of VSMCs were established from aortas of mice and artesunate of different concentrations was added into the medium. The number of VSMCs was counted and the curve of cell growth was recorded.The activity of VSMCs was assessed by using MTT method and inhibitory rate was calculated.DNA replication was evaluated by [3 H]-TdR method and apoptosis by DNA laddering and HE staining. Flowmetry was used for simultaneous analysis of cell apoptosis and cell cycles. Compared with the control group, VSMCs proliferation in Art interfering groups were inhibited and [3H]-TdR incorprating rate were decreased as well as cell apoptosis was induced. The progress of cell cycle was blocked in G0/G1 by Art in a dose-dependent manner. It is concluded that Art inhibits VSMCs proliferation by disturbing DNA replication, inducing cell apoptosis and blocking cell cycle in G0/G1 phase.

Objective To investigate the protective effect and mechanism of epigallocatechin-3-gallate against myocardial ischemia and reperfusion injury in rats.Methods The Sprague-Dawley rats underwent 30min of left anterior descending(LAD)coronary occlusion and 6 hours reperfusion to make ischemia/repefusion(I/R)injury model in vivo.Sixty male rats were randomly divided into 3 groups:sham group,I/R group,epigallocatechin-3-gallate group.Creatine kianse isoenzyme-MB(CK-MB)and the activity of Caspase-3 and the apoptotie index(AI)by TUNEL staining were measured in each group,I/R and EGCG group were measured the infarcted size(IS/AAR%).In addition,pathologic changes of myoeardial tissue were observed under electron microscopy.Results Compared with I/Rgroup,EGCG group markedly decreasedthe activity of CK-MB in serum[(951.57±123.71)vs(1826.38±205.32),P＜0.01]and the activity of Caspase-3 in myocardiaI tissue[(0.56±0.17)vs(0.81±0.20),P＜0.01],the value of IS/AAR% in EGCG group was lower than that in I/R group[(26.73±5.22)vs(41.56±6.81),P＜0.01].AI were significantly decreased in EGCG group compared with I/R group[(7.39±2.43)vs(15.62±4.28),P＜0.01].The electron microscopic examination showed that pathologic changes of myocardiocytes in the EGCG group were significantly milder than that of the I/R group.Conclusion Epigallocatechin-3-gallate has protective effect against myocardial ischemia and reperfusion injury in rats,and the protective mechanism may be related to decreasing the cardiomyocytes apoptosis by inhibition the activity of Caspase-3.

AIM: To investigate the effects of homocysteine (Hcy) on apoptosis and expression of caspases-3 in cultured human vascular smooth muscle cells (HVSMCs). METHODS: HVSMCs were cultured in vitro. The rate of apoptosis in HVSMCs was detected by flow cytometry. The expression of caspases-3 mRNA in HVSMCs was detected by reverse-transcription polymerase chain reaction (RT-PCR). RESULTS: The rates of apoptosis in HVSMCs incubated with 500 ?mol/L Hcy for 0 h, 6 h, 12 h, 24 h and 48 h were 2.39%?0.47%, 2.45%?0.64%, 7.58%?1.02%, 13.37%?4.71% and 17.69%?3.13%, respectively. The ratio of the absorbance of caspases-3 mRNA/GAPDH was 0.24?0.08, 0.29?0.10, 0.89?0.26, 1.37?0.24 and 1.82?0.53,respectively, suggesting that Hcy induces the apoptosis and expression of caspases-3 mRNA in HVSMCs in a time-dependent manner. The rates of apoptosis in HVSMCs incubated with 0, 100, 200, 500 or 1 000 ?mol/L Hcy for 24 h were 2.68%?0.23%, 2.79%?0.12%, 8.45%?2.41%, 13.37%?4.71% and 23.75%?5.56%, respectively, revealing that Hcy induced the apoptosis in HVSMCs in a concentration-dependent manner. CONCLUSION: Hcy induces the apoptosis in HVSMCs by regulating the expression of caspases-3, which may be one of the mechanisms involved in atherosclerotic effects of Hcy.