The effect of poly(lactic-co-glycolic acid) conduit loading insulin-like growth factor 1 modified by a collagen-binding domain on peripheral nerve injury in rats.

Peripheral nerve injury (PNI) exists widely and seriously affects patients' daily lives. However, the effect of nerve repair is still limited, and only 50% of patients can recover useful functions. To overcome these obstacles, collagen-coated poly(lactic-co-glycolic acid) (PLGA) conduits loaded with CBD-IGF-1 were designed and tested in vitro and in vivo. The physical characterization of the conduit was tested by scanning electron microscopy, and the static water contact angle, release rate, and nerve regeneration ability of the conduit were verified in a rat sciatic nerve injury model. The results showed that the PLGA/col/CBD-IGF-1 conduit had a rough surface and good hydrophilicity. CBD-IGF-1 could be released slowly from the PLGA/col/CBD-IGF-1 conduit. In the in vivo experiment, gait analysis and electrophysiological evaluation showed that the sciatic functional index and electrophysiological parameters were best in the group treated with the PLGA/col/CBD-IGF-1 conduit. The pathological examination results for the sciatic nerve and gastrocnemius muscle in the group treated with the PLGA/col/CBD-IGF-1 conduit were better than those in the other three groups. In short, this study demonstrated the beneficial effects of CBD-IGF-1 in nerve regeneration. The PLGA/col/CBD-IGF-1 conduit has therapeutic potential for use in the treatment of PNI.

Prevention of enzymatic browning of Chinese yam (Dioscorea spp.) using electrolyzed oxidizing water.

In this study, the effects of electrolyzed oxidizing water (EOW) on the prevention of enzymatic browning of fresh-cut "Jiu Jinhuang" Chinese yam were investigated. The yams were immersed in the inhibitors for 25 min at 20 °C. Compared with the tap water (TW) treatment, the chromatic attributes were significantly different after 72 h of storage (P < 0.05). The activities of polyphenol oxidase (PPO, EC 1.10.3.1), peroxidase (POD, EC 1.11.1.7), and L -phenylalanine ammonia lyase (PAL, EC 4.3.1.5) were inhibited when measured at 24 h. The contents of phenolic acids, including gallic and chlorogenic acid, in the group treated with the slightly acidic electrolyzed water (SAEW) were higher than those treated with TW and neutral electrolyzed water (NEW). The group treated with NEW had the highest total phenol content (P < 0.05, at 24 h), while the group treated with SAEW had the highest flavonoid content (P < 0.05) during storage. Without being treated with inhibitors, the Km and Vmax values of yam PPO were 0.0044 mol/L and 0.02627 U/min, respectively, and the Ki of samples treated with SAEW and citric acid (CA) were 15.6607 and 2.3969 µmol/L, respectively. These results indicate that EOW is beneficial as a browning inhibitor.

Thorombolytic therapy with rescue percutaneous coronary intervention versus primary percutaneous coronary intervention in patients with acute myocardial infarction: a multicenter randomized clinical trial.

BACKGROUND: Although thrombolytic therapy with rescue percutaneous coronary intervention (PCI) is a common treatment strategy for ST-segment elevation acute myocardial infarction (STEMI), scant data are available on its efficacy relative to primary PCI, and comparison was therefore the aim of this study. METHODS: This multicenter, open-label, randomized, parallel trial was conducted in 12 hospitals on patients (age < or = 70 years) with STEMI who presented within 12 hours of symptom onset (mean interval > 3 hours). Patients were randomized to three groups: primary PCI group (n = 101); recombinant staphylokinase (r-Sak) group (n = 104); and recombinant tissue-type plasminogen activator (rt-PA) group (n = 106). For all patients allocated to the thrombolytic therapy arm, coronary angiography was performed at 90 minutes after drug therapy to confirm infarct-related artery (IRA) patency; rescue PCI was performed in cases with TIMI flow grade < or = 2. Bare-metal stent implantation was planned for all patients. RESULTS: After randomization it required an average of 113.4 minutes to start thrombolytic therapy (door-to-needle time) and 141.2 minutes to perform first balloon inflation in the IRA (door to balloon time). Rates of IRA patency (TIMI flow grade 2 or 3) and TIMI flow grade 3 were significantly lower in the thrombolysis group at 90 minutes after drug therapy than in the primary PCI group at the end of the procedure (70.5% vs. 98.0%, P < 0.0001, and 53.0% vs. 85.9%, P < 0.0001, respectively). Rescue PCI with stenting was performed in 117 patients (55.7%) in the thrombolytic therapy arm. Rates of patency and TIMI flow grade 3 were still significantly lower in the rescue PCI than in the primary PCI group (88.9% vs. 97.9%, P = 0.0222, and 68.4% vs. 85.0%, P = 0.0190, respectively). At 30 days post-therapy, mortality rate was significantly higher in the thrombolysis combined with rescue PCI group than in primary PCI group (7.1% vs. 0, P = 0.0034). Rates of death/MI and bleeding complications were significantly higher in the thrombolysis with rescue PCI group than in the primary PCI group (10.0% vs. 1.0%, P = 0.0380, and 28.10% vs. 8.91%, P = 0.0001, respectively). CONCLUSIONS: Thrombolytic therapy with rescue PCI was associated with significantly lower rates of coronary patency and TIMI flow grade 3, but with significantly higher rates of mortality, death/MI and hemorrhagic complications at 30 days, as compared with primary PCI in this group of Chinese STEMI patients with late presentation and delayed treatments.

Blockade of AT1 receptor partially restores vasoreactivity, NOS expression, and superoxide levels in cerebral and carotid arteries of hindlimb unweighting rats.

Previous studies have demonstrated activation of the local renin-angiotensin system in hindlimb unweighting (HU) rat vasculature. The present study intended to identify the effects of blockade of angiotensin II (ANG II) type 1 (AT(1)) receptors with losartan on vascular reactivity, nitric oxide synthase (NOS) expression, and superoxide anion (O(2)(*-)) levels in 3-wk HU rat cerebral and carotid arteries. Three weeks later, vasoconstriction, vasodilatation, endothelial NOS (eNOS) and inducible NOS (iNOS) protein, as well as O(2)(*-) levels in rat cerebral and carotid arteries were examined. We found that HU enhanced maximal response to KCl/5-hydroxytryptamine (P < 0.01) in basilar arteries and KCl/phenylephrine (P < 0.05) in common carotid arteries from HU rats. Acetylcholine induced concentration-dependent vasodilatation in all the artery rings, but with significantly smaller amplitude in basilar (P < 0.01) and common carotid (P < 0.05) arteries from HU rats than those from control rats. Chronic treatment with losartan partially restored response to vasoconstrictors and acetylcholine-induced vasodilatation in basilar (P < 0.01) and common carotid (P < 0.05) arteries from losartan-treated HU rats. Furthermore, iNOS content in cerebral arteries and eNOS/iNOS content in carotid arteries were significantly (P < 0.01) increased in HU rats. Meanwhile, HU increased O(2)(*-) levels in all the layers of these arteries. However, losartan restored NOS content and O(2)(*-) levels toward normal. These results suggested that the HU-induced enhancement of vasoconstriction and reduction in endothelium-dependent relaxation involved alterations in O(2)(*-) and NOS content through an ANG II/AT(1) receptor signaling pathway.

DIDS attenuates staurosporine-induced cardiomyocyte apoptosis by PI3K/Akt signaling pathway: activation of eNOS/NO and inhibition of Bax translocation.

AIMS: 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), a non-selective chloride channel blocker, has been shown to prevent cell apoptosis, however, the underlying mechanisms remain undefined, thus the present study was to explore whether phosphatidylinositol 3'-kinase (PI3K)/Akt and its downstream molecules are involved in the cytoprotective effect of DIDS. METHODS: Neonatal rat cardiomyocytes were exposed to staurosporine (STS) in the presence or absence of DIDS. Cell viability, apoptosis and expressions of Akt, phospho-Akt (p-Akt), eNOS, phospho-eNOS (p-eNOS), Bcl-2/Bax and nitric oxide (NO) production were determined, and Bax translocation was assessed by double immunofluorescence labeling and Western blotting. RESULTS: DIDS markedly improved cell viability and exerted an anti-apoptotic effect on STS-exposed cardiomyocytes. DIDS resulted in a 2.1-fold increase of p-Akt over control levels, prevented the reduction in eNOS expression and phospho-eNOS levels induced by STS and significantly increased NO production (all P<0.01 vs. STS alone). Treatment with LY294002, a selective PI3K inhibitor, abolished DIDS-induced increases in p-Akt, eNOS, p-eNOS and NO production, and completely abrogated the DIDS-induced anti-apoptotic effect (P<0.01). Treatment with L-NAME, a non-selective NOS inhibitor similarly inhibited the increased NO but only partly abolished protective effects of DIDS (P<0.05). In addition, DIDS effectively inhibited STS-induced Bax translocation to mitochondria, which was also reversed by LY294002. CONCLUSION: DIDS protects cardiomyocytes against STS-induced apoptosis via activating PI3K/Akt signaling pathway, including increasing eNOS phosphorylation and the subsequent NO production and inhibiting Bax translocation.

Nitric oxide induces heat shock protein 72 production and delayed protection against myocardial ischemia in rabbits via activating protein kinase C.

BACKGROUND: Nitric oxide (NO) is a biologically active molecule which has been reported to protect the heart against ischemia and reperfusion injury in different species. This study aimed to test the hypothesis that nitric oxide may induce the expression of heat shock protein 72 (HSP72) which may protect the heart against ischemia. METHODS: Rabbits were given intravenous saline or S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, or Zaprinast, an inhibitor of cyclic guanosine monophosphate (GMP)-phosphodiesterase, which may increase myocardial cyclic GMP content. Twenty-four hours later, the rabbits were either sampled to measure HSP72, or induced with a 30-minute coronary occlusion followed by a 120-minute reperfusion, and then the infarct size was measured. Meanwhile, chelerythrine (CHE, an inhibitor of protein kinase C) was given intravenously 5 minutes before SNAP injection and the effect on HSP72 expression and infarct size was determined. RESULTS: Twenty-four hours after pretreatment, immunoblotting showed HSP72 expression increased in the SNAP group compared with control groups, and this was blocked by CHE. Myocardial infarct size in the SNAP group was smaller than that of the control group ((32.4 +/- 5.8)% vs (51.1 +/- 4.7)%, P < 0.05). Pretreated with CHE abolished the infarct size-limiting effect of SNAP ((46.0 +/- 5.1)%). Pretreatment with Zaprinast neither induced HSP72 expression nor reduced infarct size ((55.4 +/- 5.4)%). CONCLUSION: NO induced HSP72 expression and a delayed protection to the heart via the activities of protein kinase C by a cyclic GMP-independent pathway.

Safety and efficacy of the CYPHER Select Sirolimus-eluting stent in the "Real World"--clinical and angiographic results from the China CYPHER Select registry.

OBJECTIVE: This post-marketing surveillance registry is aimed at determining the safety and reliability of the CYPHER Select Sirolimus-eluting stent (SES) in routine clinical practice. BACKGROUND: Little information and angiographic follow-up data in large-scale "real world" registry is available for the CYPHER Select SES, an advanced-generation SES. METHODS: This was a prospective multicenter (20 centers) registry. 1189 consecutive patients who received at least 1 CYPHER Select SES during daily clinical practice were enrolled. Patients who underwent emergency stenting for acute myocardial infarction were excluded. RESULTS: The procedure's success rate was 98.3% for CYPHER Select SES implantation, and follow-up rates were 98% with 100% data auditing. Target lesion revascularization (TLR) at 12 months occurred in 60 (5.14%) cases, cardiac death in 13 cases (1.11%), Q wave myocardial infarction (MI) in 5 cases (0.43%), non-Q-MI in 9 cases (0.77%), target vessel revascularization (TVR) in 67 cases (5.74%), and MACE defined as cardiac death, nonfatal MI and TLR in 76 cases (6.51%). MACE-free survival rate at 12 months was 93.7%. Angiographic follow-up at 9 months was performed in 418 (68.3%) lesions treated by CYPHER Select SES. The binary restenosis rate was 4.8% in-stent and 9.6% in-segment. Subgroup analysis showed diabetes, bifurcation lesion and combined use of different stents were independent risk factors of cumulative MACE. In-segment MLD

Alpha-linolenic acid attenuates high glucose-induced apoptosis in cultured human umbilical vein endothelial cells via PI3K/Akt/eNOS pathway.

OBJECTIVE: High glucose-induced apoptosis in vascular endothelial cells contributes to the acceleration of atherosclerosis associated with diabetes. We hypothesized that alpha-linolenic acid (ALA) might attenuate high glucose-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were cultured at 5.5 and 33 mmol/L for 72 h. ALA with different concentrations was added with defatted bovine serum albumin as a carrier for 18 h before incubation with high glucose. RESULTS: Exposure of HUVECs to high glucose media for 72 h significantly increased the number of apoptotic cells compared with normal glucose control, as evaluated by flow cytometry and terminal deoxyuridine triphosphate nick end labeling assay. Pretreatment with low concentrations of ALA (10, 50, and 100 micromol/L) significantly attenuated high glucose-induced apoptosis of HUVECs, but increasing ALA to 200 micromol/L exerted the opposite effect. Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose. Pretreatment with phosphatidylinositol 3' -kinase kinase inhibitor LY294002 and eNOS inhibitor N(G)-nitro-arginine methyl ester eliminated ALA' antiapoptotic effect. CONCLUSION: ALA exerts an antiapoptotic effect by the phosphatidylinositol 3'-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications.

The opposite-direction modulation of CD4+CD25+ Tregs and T helper 1 cells in acute coronary syndromes.

Different subsets of T lymphocytes have different functions in atherosclerosis advancement. T helper 1 cells and T regulatory 1 cells have been demonstrated to play opposite roles in rupture of atherosclerotic lesion. However, the role of novel subset of T regulatory cells, known as CD4+CD25+Foxp3+ T cells, remains largely unknown in coronary artery disease (CAD). In this study, we investigated the peripheral CD4+CD25+Foxp3+ T cells of patients with CAD and controls. The patients submitted were divided into three groups: stable angina pectoris (SA) group, unstable angina pectoris (UA) group and acute myocardial infarction (AMI) group. We analyzed the frequencies of peripheral CD4+CD25+Foxp3+ T cells and T helper 1/T helper 2 cells, expression of Foxp3 in CD4+CD25+ T subsets and cytokines pattern in patients and controls. We found that the reduction of CD4+CD25+Foxp3+ T lymphocytes was consistent with the expansion of Th1 cells in patients with unstable CAD. The reversed development between CD4+CD25+ Tregs and Th1 cells might contribute to plaque destabilization.

Acute hyperglycemia exacerbates myocardial ischemia/reperfusion injury and blunts cardioprotective effect of GIK.

There is a close association between hyperglycemia and increased risk of mortality after acute myocardial infarction (AMI). However, whether acute hyperglycemia exacerbates myocardial ischemia/reperfusion (MI/R) injury remains unclear. We observed the effects of acute hyperglycemia on MI/R injury and on the cardioprotective effect of glucose-insulin-potassium (GIK). Male rats were subjected to 30 min of myocardial ischemia and 6 h of reperfusion. Rats were randomly received one of the following treatments (at 4 ml.kg(-1).h(-1) iv): Vehicle, GIK (GIK during reperfusion; glucose: 200g/l, insulin: 60 U/l, KCL: 60 mmol/l), HG (high glucose during ischemia; glucose:500 g/l), GIK + HG (HG during I and GIK during R) or GIK + wortmannin (GIK during R and wortmannin 15 min before R). Blood glucose, plasma insulin concentration and left ventricular pressure (LVP) were monitored throughout the experiments. Hyperglycemia during ischemia not only significantly increased myocardial apoptosis (23.6 +/- 1.7% vs. 18.8 +/- 1.4%, P < 0.05 vs. vehicle), increased infarct size (IS) (45.6 +/- 3.0% vs. 37.6 +/- 2.0%, P < 0.05 vs. vehicle), decreased Akt and GSK-3beta phosphorylations (0.5 +/- 0.2 and 0.6 +/- 0.1% fold of vehicle, respectively, P < 0.05 vs. vehicle) following MI/R, but almost completely blocked the cardioprotective effect afforded by GIK, as evidenced by significantly increased apoptotic index (19.1 +/- 2.0 vs. 10.3 +/- 1.2%, P < 0.01 vs. GIK), increased myocardial IS (39.2 +/- 2.8 vs. 27.2 +/- 2.1%, P < 0.01 vs. GIK), decreased Akt phosphorylation (1.1 +/- 0.1 vs. 1.7 +/- 0.2%, P < 0.01 vs. GIK) and GSK-3beta phosphorylation (1.4 +/- 0.2 vs. 2.3 +/- 0.2%, P < 0.05 vs. GIK). Hyperglycemia significantly exacerbates MI/R injury and blocks the cardioprotective effect afforded by GIK, which is, at least in part, due to hyperglycemia-induced decrease of myocardial Akt activation.

[The effect of alendronate on arterial calcification in rat model].

OBJECTIVE: To study the effect of alendronate on artery calcification in rats. METHODS: (1) 4-week SD male rats were randomly divided into 3 groups: alendronate group (AL, n = 6), calcification group (CA, n = 6) and normal group (N, n = 6). In AL and CA group, artery calcification of rat was established by subcutaneous injection of vitamin D3 (300,000 U x kg(-1) x d(-1) for 3 days) and Warfarin (15 mg x 100 g(-1) x 12 h(-1) for 4 days); In AL group, at 4 days before establishment of artery calcification, alendronate (1 mg x kg(-1) x 24 h(-1)) was administered with subcutaneous injection and continued to be given to the end of the study. Abdominal aortae were collected for paraffin section and stained with von Kossa staining to observe the area of calcification. (2) Rat aortic vascular smooth muscle cells (VSMC) were cultured in vitro with tissue explant. All cells were divided into 5 groups: normal group, calcification group (control group), and alendronate 10(-9), 10(-7) and 10(-5) mol/L group. Before inducing calcification, alendronate 10(-9), 10(-7) and 10(-5) mol/L group were individually pre-treated with final concentrations of 10(-9), 10(-7) and 10(-5) mol/L alendronate for 24 hours. Beta-glycerophosphate were then added in the calcification group and in all the alendronate groups to induce VSMC calcification. All cells were cultured for 14 days. Cell crawling slice was applied to Alizarin red S staining to observe VSMC calcification. Colorimetric method was applied to measure the contents of Ca2+, cell proteins, and ALP activity. The ratio of contents of Ca2+ and cell proteins was cell calcium deposits. Cell proliferation was measured with tetrazolium salt (MTT) method. RESULTS: (1) With von Kossa staining the black deeply stained structure was found to be decreased in AL group. (2) As compared with the control group, in all the alendronate groups, showed that the number of calcium nodules [(6.8 +/- 2.7, 6.2 +/- 4.2, 5.3 +/- 2.4) % vs (7.4 +/- 3.8)%], and cell calcium depositions [(5.2 +/- 1.2, 4.8 +/- 1.7, 3.5 +/- 1.8)% vs (5.6 +/- 1.6)%], cell ALP activity and cell proliferation decreased significantly and dose-dependently. CONCLUSION: Alendronate can inhibit the artery calcification in rats.

Cardioprotective effect of resvaratrol pretreatment on myocardial ischemia-reperfusion induced injury in rats.

OBJECTIVE: The major objective of the present study was to examine the cardioprotective effect of resveratrol, an antioxidant presents in red wine, in the rat after ischemia-reperfusion (I/R). DESIGN: The left coronary artery was in occlusion for 30 min followed by a 120 min reperfusion in anesthetized rats. Animals were pretreated with and without resveratrol before occlusion. The post-ischemic ventricular function (left ventricle maximum systolic pressures and the maximal first derivative of developed pressure) and myocardial infarct size and myocardial nitric oxide (NO) and malonaldehyde (MDA) content were compared. RESULTS: Resveratrol pretreatment had dramatic cardioprotective effects on post-ischemic ventricular functional recovery and decreasing myocardial infarct size. Resveratrol pretreatment also increased NO and decreased MDA content in myocardium. CONCLUSIONS: Resveratrol has cardioprotective properties in I/R rats. The cardioprotective effects in the I/R rats may be correlated with its antioxidant activity and upregulation of NO production.

[Effect of nanoparticle with vascular endothelial growth factor gene transferred into ischemic myocardium: experiment with rabbits].

OBJECTIVE: To evaluate the possibility and efficiency of nanoparticle as a new vector in vascular endothelial growth factor (VEGF) gene transference, and investigate the efficacy of direct gene transfer of nanoparticle with VEGF(165) gene into ischemic myocardium. METHODS: Nanoparticle-VEGF (Np/VEGF) complex was prepared with poly (D, L-lactide-co-glycolide) (PLGA) loading VEGF(165) gene and the envelopment efficiency and size of the complex were determined. The Np/VEGF was transfected into the cultured myocardial cells, RT-PCR and ELISA were used to evaluate the transfection of VEGF. Suspension of Np/VEGF was injected into the myocardial tissue of 4 rabbits. 96 hours after operation myocardial tissue was obtained, made into sections, and observed with electron microscope. New Zealand White rabbits underwent thoracotomy followed by ligation of left anterior descending coronary artery to establish ischemic models. The New Zealand White rabbits were divided into 3 groups: Np/VEGF group (n = 12, nanoparticle with VEGF(165) were injected into the cordial myocardium), blank plasmid group (n = 12, injected with blank VEGF(165) plasmid), and control group (n = 8, injected with normal saline). Ultrasonography and immunohistochemistry with factor VIII related antigen were conducted to evaluate the cardiac function and the collateral circulation of the occluded artery. One month later the rabbits were killed to observe the vascularization of capillaries in the ischemic myocardium. RESULTS: The envelopment efficiency of the Np/VEGF complex thus prepared, 50 - 300 nm in size, were 1.87% y. RT-PCR and ELISA showed that VEGF gene had been successfully transfected into myocardial cells by the nanoparticles. A great number of nanoparticles were observed in the myocardial cytoplasm and nuclei. One month after operation, the ventricular wall motor amplitude of the Np/VEGF group was 1.87 mm +/- 0.32 mm, significantly larger than those of the blank plasmid group (1.59 mm +/- 0.24 mm, P < 0.05) and control group (0.93 mm +/- 0.40 mm, P < 0.05); and the left ventricular ejection fraction of the Np/VEGF group was 60% +/- 10%, significantly higher than those of the blank plasmid group (50% +/- 6%, P < 0.05) and control group (40% +/- 8%, P < 0.05). The capillary density at low power field (x 100) of the Np/VEGF group was 57 +/- 12, significantly higher than those of the VEGF group (41 +/- 14) and control group (24 +/- 8). CONCLUSION: Nanoparticle can act as a vector to transfect specific gene in vitro and in vivo. Direct gene transfer of nanoparticle with DNA encoding VEGF into the ischemic rabbit myocardium can increase capillary number; therefore it may be a novel therapeutic approach for myocardial ischemia.

[Cardiomyocyte-like differentiation of human bone marrow mesenchymal stem cells after exposure of 5-azacytidine in vitro].

To investigate the potential of adult mesenchymal stem cells (hMSCs) derived from human bone marrow to undergo cardiomyogenic differentiation after exposure of 5-azacytidine in vitro. A small bone marrow aspirate was taken from the iliac crest of human volunteers, and hMSCs were isolated by 1.073 g/mL Percoll and cultured in the right cell culturing medium as previously described. The phonotypes of hMSCs were identified by flow cytometry. The stem cells were cultured in cell culture medium (as control) and medium mixed with 5-azacytidine (5-aza, 3, 5, 10 micromol/L) (n=5, respectively) for cellular differentiation. We examined respectively with immunohischemistry at 21 days of inducement on desmin, cardiac-specific cardiac troponin I (cTnI), GATA4 & connexin43. The ultrastructures of induced cells were examined by transmission electron microscope. The results indicated that the hMSCs showed a fibroblast-like morphology with vortex distribution in their peak propagation, and express high level of CD44 but negative for CD34 and CD45. 20%-30% cells grown after 5, 10 microl/L 5-aza treatment connected with adjoining cells and coalesced into myotube structures after 14 days. After 21 days of culturing, immunohistochemistry revealed expression of desmin, GATA4, cTnI and connexin43 in 5, 10 micromol/L showed positive, but no cardiac specific protein were found in neither 3 micromol/L nor in control group. The ratio of cTnI positive stained cells in 10 micromol/L group were higher than that in 5 micromol/L group (65.3+/-4.7% vs 48.2+/-5.4%, p<0.05). Electron microscopy revealed myofilaments were formed. The results indicated that purified hMSCs from adult bone marrow can be differentiated into cardiac-like muscle cells with 5-aza inducement in vitro and the differentiation is in line with the 5-aza concentration.