[Abstract ] Objective To investigate effect of phloretin on apoptotic of hepatoma carcinoma cells SMMC-7721, and explore its mechanisms.Methods Logarithmic phase of hepatoma carcinoma cells SMMC-7721 were cultured separately with 30, 60, 120 mg/L phloretin, morphological alterations of apoptotic were observed by phase contrast microscopy and AO/EB double fluorescence staining method was used to observe were low, medium and high concentration trentment group, respectively.the cells treated by phloretin.Apoptotic rates, cell cycle progression, mitochondrial trans-membrane potential and intracellular calcium homeostasis were detected by flow cytometry.Results Cells appeared typical apoptosis morphological alterations.Phloretin induced SMMC-7721 cell line apoptosis in a dosage and duration dependent manner.Cell cycle was arrested at G1 phase, mitochondrial trans-membrane potential decreased, intracellular free Ca2 +increased.Conclusion Phloretin induce apoptosis of SMMC-7721 by affecting cell cycle progression, reducing mitochondrial trans-membrane potential and changing intracellular calcium homeostasis.

Objective To investigate proliferative and apoptotic effects of phloretin on hepatoma carcinoma cells, hepatoma carcinoma cells HepG-2 was used as research materials.Methods This research observed morphological alterations using phase contrast microscopy and electron microscopy, cell proliferation were detected by MTT assay, and using flow cytometry detected apoptotic rates, cell cycle progression, mitochondrial trans-membrane potential and intracellular calcium homeostasis.ResuIts Apoptotic cells appeared morphological alterations.Phloretin exerted a inhibitory the proliferation of HepG-2 cell line, and induced its apoptosis in a dosage and duration dependent manner.Cell cycle was arrested at G1 phase, mitochondrial trans-membrane potential dropped, intracellular free Ca2 + increased.ConcIusion Phloretin can induce apoptosis of HepG-2 via arresting cell cycle progression, reducing mitochondrial trans-membrane potential and disturbing intracellular calcium homeostasis.

Objective To investigate the proliferative and apoptotic effects of phloretin on gastric cancer cell andthe possible mechanisms. Methods SGC-7901 were treated with different concentrations of phloretin(40,80,160 mg/L), and the cell morphological alterations were detected by using Hoechst33258 staining, cell activity were detected by MTT assay, cell apoptosis, cell cycle progression, mitochondrial trans-membrane potential and intracellular calcium homeostasis were detected by flow cytometry.ResuIts After treated with different concentrations of phloretin at different times, SGC-7901 cell showed morphological alterations.Phloretin could inhibite the proliferation of SGC-7901 cell line, and induced its apoptosis in a dosage and duration dependent manner.Cell cycle was arrested at G1 phase, mitochondrial trans-membrane potential dropped, intracellular free Ca2 +increased.ConcIusion phloretin can induce apoptosis of SGC-7901 via arresting cell cycle progression, reducing mitochondrial trans-membrane potential and disturbing intracellular calcium homeostasis.

Objective To evaluate the effect of segmental pulmonary veins isolation for atrial fibrillation (AF) and investigate the possible factors that may affect its result. Methods In 120 (105 men; age 50.0?8.6 years) consecutive patients with paroxysmal (n=99) or persistent (n=21) AF, segmental PVs electrical isolation with Lasso mapping catheters was performed. The relationship of the outcome of the initial procedure and factors such as age, sex, type of AF, left atrial diameter, case history, left ventricular ejection fraction and presence of hypertension were analyzed by statistical methods. Results 52 (52.5%) out of the 99 patients with paroxysmal AF and 6 (28.5%) out of the 21 with persistent AF were free of AF after a single ablation procedure. Univariate analysis revealed that left atrial enlargement (P=0.001), persistent AF (P=0.046) and old age (P=0.047) were related to the recurrence of AF after the first procedure. Patients with paroxysmal AF apparently had a better outcome than those with persistent AF after repeat ablation but of no statistical significance (P=0.094). Logistic regression analysis revealed that left atrial enlargement was the only independent risk factor of recurrent AF after the first procedure. Conclusion About 50% of the patients with paroxysmal AF are free of AF after single ablation. Left atrial enlargement is the only independent risk factor of recurrent AF while old age and persistent AF influence the outcome of the first procedure.

0.05).Conclusion The use of domestic clopidogrel in PCI patients with individualized dose is safe and effective which can further reduce bleeding complications.

ObjectiveTo explore regulation effect of miR-340-5p on regulating bone morphogenetic protein 4(BMP4) expression and the differentiation of rat's NSCs.MethodsNSCs of rats were divided randomly into three groups: normal group (Mock),group with nonsense oligonucleotide (Anti-Con) and group with antisense oligonucleotide of miR-340-5p (Anti-miR-340-5p).The qRT-PCR was used to detect the relative expression of miR-340-5p.The expression of NF200 and MAP-2 was detected by immunocytochemical staining and immunofluorescence,respectively.Western blot was used to detect the expression of BMP4 protein.ResultsThe relative levels of miR-340-5p expression were significantly decreased in Anti-miR-340-5p group (0.14±0.01) compared with that of Mock group(1.01±0.17) and Anti-Con group(1.07±0.13) (P<0.01).Immunocytochemical staining indicated that NF200 was positive in cells of Anti-miR-340-5p group.The proportion of MAP2 positive cells was increased in Anti-miR-340-5p group compared with other groups (P<0.05).Western blot showed the increased expression of BMP4 protein in Anti-miR-340-5p group (0.84±0.09) compared with Mock group(0.53±0.04) and Anti-Con group (0.63±0.09) (P<0.05).ConclusionThe miR-340-5p may exert a potential function in regulating differentiation of NSCs into neurons through a negative regulation of BMP4.

Objective To evaluate the influence of successful revascularization by percutaneous coronary intervention(PCI)on heart function of patients with heart dysfunction combined with chronic total occlusion(CTO).Methods The clinical data of 272 patients with heart dysfunction combined with CTO were analyzed.The patients were divided into PCI success group(246 cases)and PCI failure group(26 cases)respectively according to the results of PCI.Six months after PCI,the patients underwent cardiac ultrasound examination to compare the heart function between the two groups.Results Cardiac ultrasound examination was successfully performed in 229 patients in PCI success group and 24 patients in PCI failure group at 6 months after PCI.The left ventricular ejection fraction(LVEF)and left ventricular end-diastolic volume index(LVEDVI)showed no significant difference in PCI failure group at 6 months after PCI compared with that before PCI(P＞0.05).In PCI success group,LVEF and LVEDVI were significantly increased at 6 months after PCI compared with that before PCI and compared with that in PCI failure group at 6 months after PCI[(51±5)％ vs.(43±6)％ and(45±2)％,(77±13)ml/m2 vs.(86±12)ml/m2 and(86±10)ml/m2,P＜0.05].The cardiac functional grading in PCI failure group had no significant difference compared with that before PCI(P＞0.05),but in PCI success group it had significant difference compared with that before PCI and compared with that in PCI failure group at 6 months after PCI(P＜0.05).Conclusion Successful revascularization by PCI can improve heart function in patients with heart dysfunction combined with CTO.

Objective To compare the myocardial damage in patients with severe valvular heart disease undergoing open heart surgery under propofol and sevoflurane combined anesthesia.Methods Thirty-two patients with severe heart valvular disease undergoing open heart surgery were randomized into 3 groups:midazolam group (group M,n =8),propofol group (group P,n =12) and sevoflurane group (group S,n =12).Midazolam 1-5 mg,vecuronium 0.15 mg/kg and fentanyl 10-20 μg/kg were injected intravenously in group M.Propofol 1-2 mg/kg,vecuronium 0.15 mg/kg and fentanyl 10 μg/kg were injected intravenously in group P.In group S,the patients inhaled sevoflurane until the eyelash reflex disappeared,the end-tidal concentration of sevoflurane was 0.5 ％-2.0％,and vecuronium 0.15 mg/kg and fentanyl 10μg/kg were injected intravenously.The patients were mechanically ventilated after tracheal intubation.Anesthesia was maintained with iv infusion of midazolam 0.1 mg· kg-1 · h-1,fentanyl 0.2 μg· kg-1 · min-1,and vecuronium 0.12 mg· kg-1 · h-1 in group M,with iv infusion of propofol 150 μg· kg-1 · min-1 and fentanyl μg· kg-1 · min-1 in group P,or with inhalation of 0.5％-2.0％sevoflurane in group S.CPB was established routinely.The concentration of sevoflurane was 0.5 ％-1.0％ during CPB.Venous blood samples were collected before anesthesia (T1),at 20 min and 2 h after aortic unclamping (T2,3),and at 24 h after operation (T4) for determination of the levels of plasma lactic dehydrogenase (LDH),creatine kinase (CK),creatine kinase MB (CK-MB),cardiac troponin Ⅰ (cTnⅠ),superoxide dismutase (SOD)and tumor necrosis factor (TNF)-α.Myocardial tissues were taken at T2 for determination of heme oxygenase-1 (HO-1) expression and for examination of the myocardial ultrastructure.Results Compared with group M,the levels of plasma LDH,CK-MB,and CK were significantly decreased at T2-4,the levels of plasma SOD and cTnⅠ were significantly increased at T2,3,and the expression of HO-1 was up-regulated at T2 in groups P and S,and the levels of plasma TNF-α were significantly decreased at T2-4 in group P and at T2,3 in group S (P ＜ 0.05).The pathologic changes induced by I/R were less severe in groups P and S than in group M.Conclusion Both propofol and sevoflurane can attenuate the myocardial damage in patients with severe valvular heart disease undergoing open heart surgery and the effects are comparable.

Objective The prognosis of traumatic brain injury is closely associated with the apoptosis of neural cells .This study investigated the anti-apoptosis effect of alpha lipoic acid (α-LA) and its possible mechanism in the mouse model of traumatic brain injury. Methods Seventy-two healthy male ICR mice were randomly divided into four groups of 18 each:sham operation +vehicle, sham operation +α-LA, trauma +vehicle, and trauma +α-LA.The model of traumatic brain injury was made by weight-dropping.The animals in the α-LA groups were treated with intragastric α-LA at 30 minutes after surgery, while those in the vehicle groups with oral dimethyl sulfoxide in corn oil .At 48 hours after treatment , brain samples were collected from the mice for determining brain edema , measuring the expressions of cytochrome c , Bcl-2-associated X protein ( Bax ) , and caspase-3 in the mitochondria and cytosol of the brain tissue by Western blot and immunohistochemistry respectively , and detecting the survival of the neurons and apoptosis of neural cells in the cortical area by Nissl staining and TUNEL , re-spectively. Results The brain water volume , caspase-3 expres-sion, and neural cell apoptosis were markedly higher while the neuron survival remarkably lower in the trauma +vehicle group than in the sham operation +vehicle and sham operation +α-LA groups ( P<0.01).Compared with the mice in the trauma +vehicle group, those in the trauma +α-LA group showed significantly reduced proportion of water in the brain tissue ([79.89 ±0.55] vs [81.71 ± 0.66]%, P<0.05), expression of caspase-3 ([58.40 ±7.31] vs [47.42 ±7.74]%, P<0.05), and apoptosis of neural cells ([59.63 ±8.61] vs [44.86 ±7.32]%, P <0.05), but increased survival rate of neurons ([44.45 ±10.56] vs [57.46 ± 11.01]%, P<0.05).The expression of cytochrome c in the mitochondria was remarkably decreased and that of Bax markedly in -creased in the trauma +vehicle than in the sham operation +vehicle and sham operation +α-LA groups (P<0.01). Conclusion Alpha lipoic acid has a protective effect against traumatic brain injury in mice , probably by inhibiting the apoptosis of neural cells through the mitochondrial pathway .