Effect of imatinib on myocardial fibrosis in DOCA-salt hypertensive rats

AIM: To investigate the effects of imatinib (IMA), one of platelet-derived growth factor receptor (PDGFR) inhibitors, on myocardial fibrosis in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. METHODS: Sixty male uninephrectomized SD rats were treated with 1% NaCl and 0.2% KCl in the drinking water for 4 weeks and assigned to 3 groups: vehicle control group (control group), DOCA treatment group (DOCA group), DOCA and IMA treatment group (DOCA+IMA group). Systolic blood pressure (SBP) was measured using the tail-cuff method. Myocardial tissue inflammation was analyzed by hematoxylin-eosin staining. Collagen volume fraction (CVF) and perivascular collagen area (PVCA) were analyzed by Sirius red staining. Ectodermal dysplasia-1 (ED-1) was analyzed by immunohistochemistry. Expression levels of platelet-derived growth factors (PDGF-A and PDGF-C), PDGF receptor α (PDGFRα) and phosphorylated PDGFRα (p-PDGFRα) were detected by Western blotting. RESULTS: SBP in DOCA group and DOCA+IMA group were signficantly higher than that in control group. No significant difference of SBP between DOCA group and DOCA+IM group was observed. In DOCA group, severe myocardial fibrosis was found, and CVF and PVCA were higher than those in control group. The differences of the CVF and PVCA between DOCA+IMA group and control group were detected, but the CVF and PVCA in DOCA+IMA group were significantly lower than those in DOCA group. Compared with control group, different degrees of myocardial tissue inflammation and monocyte/macrophage infiltration were observed in DOCA group and DOCA+IMA group. The expression levels of PDGF-A, PDGF-C and PDGFRα in DOCA group and DOCA+IMA group were much higher than those in control group, but the expression of p-PDGFRα in DOCA+IMA group were signficantly lower than that in DOCA group. CONCLUSION: Mineralocorticoid-induced myocardial fibrosis is related to cardiac tissue inflammatory response, excessive monocyte/macrophage infiltration and expressions of PDGF-A,PDGF-C and PDGFRα. Imatinib has an inhibitory effect on the myocardial fibrosis. The mechanisms may be associated with the inhibition of PDGFRα activity on the surface of fibroblast, thus interrupting PDGFs signaling-induced fibroblast division and proliferation.     

Effect of bFGF on promoting angiogenesis in infarct area and improving myocardial fibrosis in mouse myocardial infarction model

AIM: To investigate the protective effect of basic fibroblast growth factor (bFGF) on the heart of mice with myocardial infarction and its mechanism. METHODS: The model of myocardial infarction was established by the ligation of left anterior descending artery of C57/B6 mice (8~12 weeks old) after lateral thoracotomy. The mice were divided into sham operation group, myocardial infarction group and bFGF administration group. bFGF at 0.5 μg was intraperitoneally injected on alternate days after myocardial infarction for 7 d. Cardiac Doppler ultrasonography was used to detect cardiac function after myocardial infarction for 28 d, and left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction and left ventricular shortening fraction (LVFS) were used to evaluate cardiac function. After myocardial infarction for 28 d, the mice were sacrificed and the hearts were collected for preparing pathological sections. The degrees of myocardial fibrosis and angiogenesis in the myocardial infarction area were observed. Western blot was used to detect the indicators of angiogenesis. RESULTS: The results of Masson staining showed that bFGF administration significantly reduced myocardial fibrosis at 28 d after myocardial infarction. Cardiac ultrasound data showed that cardiac functions in myocardial infarction group were poorer than those in sham group, and bFGF administration significantly improved cardiac functions. Immunofluorescence staining showed that neovascularization in myocardial infarction area of bFGF administration group was more than that in myocardial infarction group. The results of Western blot showed that bFGF activated AKT/HIF-1α/VEGF signaling pathway. CONCLUSION: Intraperitoneal injection of bFGF reduces myocardial fibrosis and improves cardiac function in myocardial infarction mice. bFGF may promote angiogenesis by activating AKT/HIF-1α/VEGF signaling pathway.     

Effect of Shenshuguanxin granula on coronary circulation in rats with myocardial infarction

AIM：To explore the effect of traditional Chinese medicine Shenshuguanxin granula on coronary circulation in a rat model of myocardial infarction (MI). METHODS：SD rats (n=50, SPF grade) were randomly divided into 5 groups (n=10):sham group, MI group, and high-dose, middle-dose and low-dose Shenshuguanxin granula treatment groups. The rat MI model was established by ligation of the coronary artery. The cardiac markers, small and medium-sized blood vessels ［microvessel count (MVC) value］ in the infarct zone, and platelet endothelial cell adhesion mo-lecule 1 (PECAM-1) and vascular endothelial growth factor (VEGF) expression in the infarct border zone were measured. RESULTS：After 4 weeks of coronary artery ligation, the significant increases in MVC in the infarct zone, and the expression of PECAM-1 and VEGF in the infarct border zone were detected compared with sham group (P<0.05). The differences of cardiac markers between MI group and other groups were insignificant (P>0.05). CONCLUSION:Shenshuguanxin granula improves coronary circulation in the rats with myocardial infarction by increasing the expression of PECAM-1 and VEGF, and promoting small and medium-sized angiogenesis.     

Effect of fluvastatin on left ventricular remodeling after myocardial infarction in rats

AIM: To clarify the protective effect of long-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on ventricular remodeling after myocardial infarction (MI) in rats and its mechanisms. METHODS: Myocardial infarction were established by ligated left coronary anterior artery in SD rats, 24 hours after the operation, the survival rats were treated by gavage fluvastatin (20 mg·kg^-1·d^-1) or distilled water for 8 weeks. Doppler echocardiography, homodynamic and cardiac histomorphometry were used to assess the ventricular remodeling and cardiac function. The plasma levels of total cholesterol (Tch), creatinine (Cr), glutamic-oxal (o) acetic transaminase (AST), lipid peroxidation (LPO), glutathione perioxidase (GSH-PX), nitrogen monoxide (NO₂^-/NO₃^-) were detected. RESULTS: The Tch, Cr and AST were not significant difference in groups. Left ventricular end-diastole pressure, right relative weight, left ventricular posterior wall thickness, collagen volume fraction and the lung weight were decreased in AMI+fluvastatin group compared to AMI group (P＜0.05, P<0.01); The levels of LPO, NO₂^-+NO₃^- in plasma and LPO in myocardium decreased, but plasma GSH-PX level increased in AMI+fluvastatin group (P＜0.05). CONCLUSION: Fluvastatin ameliorates the ventricular structural remodeling in a rat model of infarction, and delays the development of heart failure. The anti-oxidation mechanism of fluvastatin may take part in this process.     

Early-phase changes of parameters related to myocardial fibrosis in acute myocardial infarction

AIM:To investigate the changes in parameters related to myocardial fibrosis of H2 relaxin (H2RLX) and procollagen type I C-terminal peptide (PICP), transforming growth factor-β1 (TGF-β1) level in the plasma after acute anterior myocardial infarction.METHODS:Forty-one patients with anterior myocardial infarction (MI) and 10 controls with normal coronary vessels were selected.Plasma H2RLX, PICP, and TGF-β1 levels were determined by enzyme linked immunosorbent assay (ELISA) in 10 control subjects and 41 post-MI patients at day 3 and 7 post-MI.RESULTS:(1) H2RLX level at day 3 post-infarct had no difference between the patients and the controls.No marked change in H2RLX at day 3 versus day 7 post-infarct was observed.（2）The level of PICP at day 3 post-infarct was markedly increased followed by a fall at day 7 post-infarct, but was still higher than that in control.(3) TGF-β1 level, which was similar at day 3 and 7 post-infarct, was higher than that in control.(4) At day 7 post-infarct, the level of H2RLX was positively correlated with the fasting blood glucose in MI group.CONCLUSION:In early period of acute MI, profibrotic factors such as TGF-β1 expression and collagen expression increase.However, antifibrotic relaxin has no change.     

Effect of leonurine on expression of miR-1 in rats with myocardial fibrosis induced by isoproterenol

AIM: To investigate effect of leonurine on the expression of microRNA-1 (miR-1) in rats with myocardial fibrosis induced by isoproterenol (ISO). METHODS: SD rats (n=10) were used as normal control group, and 80 rats were given ISO by intraperitoneal injection daily for 2 weeks to establish the model of myocardial fibrosis. The model rats were randomly divided into 5 groups:model group, low-dose (7.5 mg·kg^-1·d^-1) leonurine group, middle-dose (15 mg·kg^-1·d^-1) leonurine group, high-dose (30 mg·kg^-1·d^-1) leonurine group and p38 mitogen-activated protein kinase (p38 MAPK) inhibitor (0.3 mg·kg^-1·d^-1) group. After the treatment for 2 weeks, the ultrastructure of left ventricular myocardial tissues was observed under electron microscope. Masson staining was used to detect collagen fibrosis, and the expression of collagen I and collagen Ⅲ was determined by the method of immunohistochemistry. The contents of endothelin-1 (ET-1) and angiotensin Ⅱ (Ang Ⅱ) were measured by ELISA. The expression of miR-1 and ET-1 mRNA was detected by real-time PCR, and the protein expression of p38 MAPK, β-myosin heavy chain (MHC) and α-MHC was determined by Western blot. RESULTS: Compared with model group, the ultrastructure of left ventricular myocardial tissues in high-dose leonurine group was attenuated, and the expression of miR-1 and the protein expression of α-MHC in left ventricular myocardial tissues of high-dose leonurine group were increased (P<0.05). Collagen volume fraction, collagen I, collagen Ⅲ, the ratio of collagen Ⅰ/collagen Ⅲ, the contents of ET-1 and Ang Ⅱ, the mRNA expression of ET-1, and the protein expression of p38 MAPK and β-MHC in high-dose leonurine group were lower than those in model group (P<0.05). CONCLUSION: Leonurine attenuates myocardial fibrosis in the rats induced by ISO, and it is potentially associated with affecting the expression of miR-1, and inhibiting ET-1/p38 MAPK signaling pathway.     

Effect of fluvastatin on left ventricular remodeling and caspase-3 expression after myocardial infarction in rats

AIM: To observe the effect of fluvastatin (FV) on left ventricular remodeling and expression of caspase-3 after myocardial infarction (MI) in rats. METHODS: Rats were divided into 4 groups: group Ⅰ (sham), group Ⅱ (sham+FV), group Ⅲ (MI) and group Ⅳ (MI+FV). group Ⅱ and Ⅳ were treated with FV (10 mg·kg^-1·d^-1) for 4 weeks. The left ventricular structure, echocardiography and hydroxyproline were observed. The expression of caspase-3 was measured by immunohistochemistry and RT-PCR. RESULTS: Compared with MI group, there was a improvement of ultrastructure and index of left ventricular remodeling, and decrease in hydroxyproline in MI+FV group (all P<0.05). The number of caspase-3 positive cells also decreased in MI+FV group, and RT-PCR showed the level of caspase-3 mRNA expression was lower than that in MI group (P<0.05). CONCLUSION: Fluvastatin improves left ventricular remodeling after myocardial infarction, decreases the expression of caspase-3 and inhibits apoptosis.     

Effects of pioglitazone on myocardial energy metabolism and hemodynamics in rats with myocardial infarction

AIM: To observe the effects of pioglitazone on myocardial energy metabolism and hemodynamics in rats with heart failure after myocardial infarction (MI). METHODS: The model of MI was established by ligation of left anterior descending artery. The 20 surviving rats were randomly divided into MI group (n=10) and pioglitazone intervention group (P group,n=10, pioglitazone 3 mg·kg^-1·d^-1 orally). The sham-operated rats (SH, n=10) served as controls. Hemodynamic parameters were measured. The ratio of left ventricular weight to body weight (LVW/BW) and the ratio of right ventricular weight to body weight (RVW/BW) were calculated after 8-week treatment. The expression of PPARγ was examined by Western blotting. Mitochondrial respiratory function was determined by Clark oxygen electrodes. The size of adenine acid pool (ATP, ADP and AMP) in mitochondria was measured by HPLC. The adenine nucleotide translocator(ANT) activity was detected by the atractyloside-inhibitor stop technique. RESULTS: Compared with SH group, the protein expression of PPARγ was significantly decreased in MI group (P<0.01). The mitochondrial respiratory activity, the transport activity of ANT and the high-energy phosphate content were decreased in MI group (P<0.01), and the hemodynamic parameters were in disorder (P<0.01). Compared with MI group, the protein expression of PPARγ in P group was significantly increased. The mitochondrial respiratory activity, the high-energy phosphate content, the transport activity of ANT were improved (P<0.01). However, the hemodynamic parameters were not significantly changed.CONCLUSION: Pioglitazone increases the protein expression of PPARγ and improves myocardial energy metabolism in the development of heart failure in the rat model of myocardial infarction, but dose not change the hemodynamic parameters significantly.     

Autoimmune reaction mediates myocardial injury after acute myocardial infarction in rats

AIM: The study was designed to explore the autoimmune mechanism of myocardial injury and ventricular remodeling after acute myocardial infarction (AMI). METHODS: An experimental animal model of AMI was adopted in Wistar rats. After 6 weeks, splenocytes were freshly transferred to syngeneic inbred rats. Four weeks later, these recipient rats were anesthetized for hemodynamics analysis by catheter technique. Serum antibody against cardiac myosin heavy chanin (MHC) was screened by ELISA. Histopathological studies were performed on all hearts. The phenotypes of T lymphocytes in myocardium were analyzed by histocytochemistry stain. RESULTS: Histopathological studies showed the lymphocytes infiltration in non-infarction myocardium in AMI rats and the organ specific inflammation of myocardium in all succedent recipient (AMI-T) rats. Histocytochemistry stain revealed the predominant CD4+T cells infiltration in myocardium. The antibody against MHC was examined in 8/22 cases of AMI rats and AMI-T rats, but none in sham-T rats. The left ventricular dysfunction was found in AMI-T rats, which was characterized by slight decline of +dp/dtmax. CONCLUSIONS: The study showed inflammatory response of non-infarction myocardium in AMI rats and demonstrated the lymphocytes-mediated myocardial injury and cardiac dysfunction by adoptive transfer of splenocytes of AMI rats. The autoimmune-mediated myocardial injury might be a novel mechanism of ventricular remodeling after AMI.     

Short-term cardioprotective effects of trimetazidine on acute myocardial infarction in rats

AIM: To observe the myocardial protective effects of trimetazidine on myocardial infarction (MI) in Sprague-Dawley (SD) rats. METHODS: Ninety SD rats were randomly assigned to 3 groups (n=30 each): myocardial infarction group (MI group), MI+trimetazidine group (MT group) and sham group (S group). By permanently ligating the left anterior descending artery, the MI model was set up in the rats in MI group and MT group. Before and after setting up the MI model, normal saline was given to the rats in MI and S group by gavage. On the other hand, trimetazidine (3 mg/kg,twice per day) was given to the rats in MT group by gavage. At 8 h, 24 h and 48 h after applying trimetazidine, the serum level of cardiac troponin I (cTnI) was measured. At the 1st week, 2nd week and 4th week after treated with trimetazidine, the size of myocardial infarction, the maximum rising rate of the left ventricular systolic pressure (+dp/dt_max) and the maximum descending rate of the left ventricular diastolic pressure (-dp/dt_max) were measured. Also at the 1st week after applying trimetazidine, the cardiomyocyte apoptotic index was detected. RESULTS: Compared with MI group 2 weeks after applying trimetazidine, +dp/dt_max significantly increased in MT group , and -dp/dt_max also significantly increased in MT group . Four weeks after applying trimetazidine, +dp/dt_max significantly increased in MT group , and -dp/dt_max also significantly increased in MT group . At 8 h and 48 h after applying trimetazidine, no statistically significant difference (P＞0.05) of serum cTnI between MI group and MT group was observed. However, at 24 h after applying trimetazidine, the serum level of cTnI decreased in MT group as compared with MI group . Aditionally, trimetazidine significantly decreased the infarction size of myocardium in MT group (0.248±0.052) as compared with MI group (0.362±0.082, P<0.01). CONCLUSION: Trimetazidine has short-term cardioprotective effects on the rats with acute MI by improving myocardial systolic and diastolic functions, reducing infarct size and inhibiting apoptosis.     

Progress in monocytes/macrophages regulating cardiac fibrosis after myocardial infarction

Myocardial fibrosis is the main pathophysiology following myocardial infarction, which leads to cardiac remodeling and heart failure ultimately. The inflammatory response of monocyte/macrophage recruitment is essential to heart repair after myocardial infarction. However, macrophages in different periods after myocardial infarction are multifaceted, and participate in the process of myocardial fibrosis. This article mainly elucidates the relationship between monocytes/macrophages and cardiac fibrosis after myocardial infarction.     

Effect of atorvastatin on myocardial fibrosis induced by aldosterone

AIM: To investigate the effects and mechanisms of atorvastatin on myocardial fibrosis induced by aldosterone in SD rats. METHODS: Forty male uninephrectomized SD rats were limited to drink 1% NaCl water for 4 weeks and assigned to the follow groups: vehicle control rats (CON group); aldosterone treated rats (ALD group); spironolactone + aldosterone treated rats (SPI+ALD group); atorvastatin + aldosterone treated rats (ATO+ALD group). Blood pressure was measured by catheterization. Expression of platelet-derived growth factor (PDGF-A, PDGF-B), platelet-derived growth factor receptor (PDGFR-α, PDGFR-β) and ectodermal dysplasia-1 (ED-1) were analyzed by immunohistochemistry. Collagen volume fraction (CVF) and perivascular collagen area (PVCA) were analyzed by Sirius-Red staining. Myocardium osteopontin protein was detected by Western blotting analysis. RESULTS: Mean arterial blood pressure in ALD group, SPI+ALD group and ATO+ALD group was elevated, and significant difference was observed between the three groups and vehicle control group (P<0.01 or P<0.05). Myocardial fibrosis was observed in ALD group. Compared to other three groups, the index of CVF and PVCA was increased significantly (P<0.01 or P<0.05). No significant difference of the index of CVF and PVCA between ATO+ALD group and SPI+ALD group was observed (P>0.05). Compared to other groups, the levels of PDGF-A, PDGF-B, PDGFR-α, ED-1 and OPN in ALD group were significantly increased (P<0.01 or P<0.05). The levels of PDGF-A, PDGF-B, PDGFR-α and OPN were no significant difference between ATO+ALD group and SPI+ALD group (P<0.01 or P<0.05). However, the level of ED-1 in ATO+ALD group was significantly decreased compared to SPI+ALD group (P<0.05). No significant difference of PDGFR-β level among four groups was found (P>0.05). CONCLUSION: These results suggest that atorvastatin may attenuate myocardial fibrosis induced by aldosterone. The mechanisms concern with reduction of macrophage infiltration, expression of inflammatory cytokines OPN, partially inhibition of platelet-derived growth factor and its receptor expression.     

Effects of granulocyte colony-stimulating factor on the myocardial infarction in experimental rats

AIM: To investigate the effects of granulocyte colony-stimulating factor (G-CSF) on the myocardial infarction in experimental rats. METHODS: Rats were randomly divided into GT group and saline control group (SC).The rats of GT group were treated with G-CSF (10 μg/kg) once a day subcutaneously for 5 days and those of SC group were received saline.On the third day, both groups were injected with isoprenaline (ISO) interaperitoneally to develop acute ischemic model. The hearts were harvested from 2 weeks to 4 weeks after administration of ISO for histopathological examination. RESULTS: Compared with saline control group, G-CSF treatment group significantly reduced the scar size (P<0.05). We also found the regeneration of myocytes, smooth muscle and endothelial cells. CONCLUSION: G-CSF treatment could be benefical to the regeneration of infarcted myocardium and significantly reduce scar size and it could be used for therapeutic intervention of the acute myocardial infarction.     

Combinational effects of trimetazidin and parecoxib on acute myocardial infarction in rats

AIM: To investigate the protective effects and mechanisms of combinational use of trimetazidine(TMZ) and parecoxib sodium on acute myocardial infarction (AMI) in rats. METHODS: Sixty-six Sprague-Dawley rats were randomly divided into 5 groups: sham group; AMI group; AMI+TMZ group; AMI+parecoxib group; AMI+TMZ+parecoxib group. All rats were sacrificed and cardiac functions (HR, LVSP, LVEDP, +dp/dt_max,-dp/dt_max) were measured with a Pclab-3804 biological signal processing system on the 8th day. The infarct size in each group was checked up by TTC staining method. RT-PCR was employed to detect the bax mRNA and bcl-2 mRNA. The protein levels of COX-2, Bax, Bcl-2 and cleaved caspase-3 in myocardium were determined by Western blotting. The activity of caspase-3 in each group was measured by colorimetric assay kit, and the apoptotic rates were detected with DNA ladder kit.RESULTS: Compared with sham group, increased expression of COX-2 protein (P<0.01) was observed in AMI group. The expression of COX-2 protein in parecoxib group was lower than that in AMI group (P<0.01). Compared with AMI group, the combinational use of trimetazidin and parecoxib improved contractile functions (LVSP and +dp/dt_max), reduced the infarct size and lowered the apoptotic rates remarkably. Specifically, the combinational use of trimetazidin and parecoxib showed better effects than use of trimetazidin or parecoxib alone. Reduced expression of Bax/Bcl-2 mRNA and protein, the reduced caspase-3 activity and cleaved caspase-3 expression were also found in combinational group as compared with other groups (P<0.05).CONCLUSION: The combinational use of trimetazidin and parecoxib effectively improves cardiac functions and reduces infarct size. The mechanism of the protective effect is probably associated with inhibiting apoptosis of cardiac myocytes.     

Expression of endostatin in ischemic myocardium of myocardial infarction rats

AIM: To study the expression of endostatin in ischemic myocardium of myocardial infarction (MI) rats in various periods and the correlation with VEGF expression and microvascular density (MVD).METHODS: Thirty-two male Sprague-Dawley rats after myocardial infarction were randomly divided into 7, 14, 21 and 28 days group.The sham group was normal control group (eight rats in each group).The expression of endostatin, VEGF and MVD in ischemic myocardium were observed by immunohistochemistry.RESULTS: The expression of endostatin significantly increased in the ischemic myocardium after MI, peaked at 7 days, then gradually decreased at 14, 21 and 28 days.The endostatin level at 28 days was the same as the shams.The changing trends of expression of endostatin in ischemic myocardium after MI were similar to that of VEGF and were significantly correlated with the MVD.CONCLUSION: The expression of endostatin increased in ischemic myocardium of myocardial infarction rats.The changing trends of endostatin were similar to that of VEGF and positively correlated with the MVD.These data suggest that endostatin may modulate ischemic myocardium angiogenesis after myocardial infarction.     

Effect of arsenic trioxide on bleomycin-induced pulmonary fibrosis in rats

AIM: To observe the effect of arsenic trioxide (ATO) on bleomycin-induced pulmonary fibrosis in rats. METHODS: Pulmonary fibrosis was induced in Sprague-Dawley (SD) rats by intratracheal instillation of bleomycin (BLM). The rats in ATO treatment group, steroid treatment group and model group were intraperitoneally injected with ATO, dexamethasone or normal saline (NS), respectively, while the control rats received NS both intratracheally and intraperitoneally. The effects of ATO were evaluated by analyzing the median survival time, hydroxyproline level in the lung, semi-quantitative grading of alveolitis and pulmonary fibrosis, and quantitative analysis of the collagen in lung tissue (Masson’s trichrome staining). Apoptosis index (AI) of the lung was detected by using the terminal transferase dUTP-digoxygenin nick end-labeling (TUNEL) method. The results of immunohistochemical staining for some cytokines were quantitatively analyzed. RESULTS: ATO (1) prolonged the median survival time of rats with BLM-induced pulmonary fibrosis at some extent; (2) attenuated the alveolitis and pulmonary fibrosis, reduced hydroxyproline level and collagen deposition in the lung tissue; (3) increased the AI of lung tissue at a certain phase; and decreased the levels of transforming growth factor-β1 (TGF-β1) and tissue inhibitor of metalloproteinase-1 (TIMP-1), increased the content of interferon-γ (IFN-γ), but did not influence the concentration of matrix metalloproteinase-9 (MMP-9) significantly. CONCLUSION: ATO might attenuate BLM-induced pulmonary fibrosis in rats via increasing the AI in the lung tissue.     

Effects of atorvastatin on release of endothelial microparticles and myocardial apoptosis in rats with acute myocardial infarction

AIM: To investigate the effect of atorvastatin(AT) on the release of endothelial microparticles(EMP) and myocardial apoptosis in the rats with myocardial infarction. METHODS: SD male rats(n=24) were randomly divided into 3 groups:sham operation(sham) group, myocardial infarction(MI) group and MI+AT group. The rat model of acute myocardial infarction was prepared by coronary artery ligation. At 2 h and 24 h after modeling, the peripheral blood was collected to detect creatine kinase-MB(CK-MB) and cardiac troponin T(cTnT). The circulating levels of EMP were measured by flow cytometry. The myocardial apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay. RESULTS: At 2 h after modeling, the level of CK-MB was significantly increased in MI group compared with sham group, and the level of EMP and the myocardial apoptotic rate were significantly increased in MI group and MI+AT group compared with sham group. At 24 h after modeling, the level of EMP was significantly increased in MI group compared with sham group. The levels of CK-MB, cTnT, EMP and the myocardial apoptotic rate were significantly decreased in MI+AT group compared with MI group. Moreover, the level of CK-MB in MI group was significantly increased at 24 h compared with that at 2 h after modeling. The levels of CK-MB, cTnT and EMP were significantly decreased in MI+AT group at 24 h compared with those at 2 h after modeling. CONCLUSION: Ator-vastatin may reduce the level of EMP and the myocardial apoptotic rate in the rats with acute myocardial infarction, indicating that atorvastatin plays a role in protecting endothelium.     

Effect of lentinan on myocardial impairment in diabetic rats

AIM:To study the protective effect of lentinan against myocardial impairment in diabetic rats.METHODS:Morphology of myocardium from streptozocin induced diabetic rats treated with lentinan was observed under light microscopy(LM) and transmission electron microscopy(TEM). Activity of superoxide dismutase(SOD), nitric oxide synthase (NOS) and contents of malondialdehyde (MDA) and nitric oxide (NO) were detected biochemically in myocardial homogenate.RESULTS:Vacuolar degeneration, local lysis of myocardium and interstitial proliferation under LM and expansion of mitochondria, shortening of mitochondrial crest, lysis of myofibril and proliferation of interstitial collogenous fiber under TEM were observed. The activity of SOD decreased and the activity of NOS, the contents of NO, MDA increased, but the morphological change became slight in LNT-treatment group. Activity of SOD increased while activity of NOS and contents of MDA, NO decreased in LNT-treated rats compared with diabetic rats.CONCLUSION:LNT protectes diabetic myocardium, and the anti-lipid peroxidation and decreasing of NO level may be involved in it.