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Bao-feng Yang

Publications and source records attributed to Bao-feng Yang.

At least 19 recordsLinked to original sources
PubMed2006

Involvement of calcium-sensing receptor in ischemia/reperfusion-induced apoptosis in rat cardiomyocytes.

The calcium-sensing receptor (CaR) is a seven-transmembrane G-protein coupled receptor, which activates intracellular effectors, for example, it causes inositol phosphate (IP) accumulation to increase the release of intracellular calcium. Although intracellular calcium overload has been implicated in the cardiac ischemia/reperfusion (I/R)-induced apoptosis, the role of CaR in the induction of apoptosis has not been fully understood. This study tested the hypothesis that CaR is involved in I/R cardiomyocyte apoptosis by increasing [Ca2+]i. The isolated rat hearts were subjected to 40-min ischemia followed by 2 h of reperfusion, meanwhile GdCl3 was added to reperfusion solution. The expression of CaR increased at the exposure to GdCl3 during I/R. By laser confocal microscopy, it was observed that the intracellular calcium was significantly increased and exhibited a Deltapsim, as monitored by 5,5',6,6'-tetrachloro-1,1',3,3'- tetraethylbenzimidazolcarbocyanine iodide (JC-1) during reperfusion with GdCl3. Furthermore, the number of apoptotic cells was significantly increased as shown by TUNEL assay. Typical apoptotic cells were observed with transmission electron microscopy in I/R with GdCl3 but not in the control group. The expression of cytosolic cytochrome c and activated caspase-9 and caspase-3 was significantly increased whereas the expression of mitochondrial cytochrome c significantly decreased in I/R with GdCl3 in comparison to the control. In conclusion, these results suggest that CaR is involved in the induction of cardiomyocyte apoptosis during ischemia/reperfusion through activation of cytochrome c-caspase-3 signaling pathway.

Animals↗
PubMed2006

[The cardioprotective effect and mechanism of lumbrokinase].

AIM: To investigate the protective effect of lumbrokinase against myocardial ischemia and to further explore its underlying mechanisms. METHODS: The effect of lumbrokinase on myocardial ischemia was observed by a model of acute myocardial infarction due to permanent ligation of the left anterior descending coronary artery in rats. Patch-clamp technique and laser scanning confocal microscopy were utilized to study the action of lumbrokinase on L-type calcium current (ICa-L) and intracellular calcium concentration ([Ca2+]i). RESULTS: Lumbrokinase decreased the infarct size of myocardium in a dose-dependent manner. The inhibitory rate of lumbrokinase at the dose of 20, 40 and 80 mg x kg(-1) was 7.7%, 34.6% and 46.2%, respectively. The electrophysiological studies displayed that, at + 10 mV, the ICa-L was markedly reduced from (-14.42 +/- 1.53) pA/pF to (-11.33 +/- 1.40) pA/pF (decreased by 21.4%, P <0.01) and (-9.92 +/- 1.31) pA/pF (decreased by 36.5%, P <0.01) by lumbrokinase (10 and 50 micromol x L(-1)), respectively. Confocal experiments showed that 10 micromol x L(-1) lumbrokinase showed no obvious effects on [Ca2+]i at resting states (P > 0.05). However, the increase of [Ca2+]i induced by 60 mmol x L(-1) KCl was distinctly limited by 10 micromol x L(-1) lumbrokinase (P <0.01). Within 240 s, the no obvious peak value of fluorescent intensity (FI) was shown. CONCLUSION: Lumbrokinase showed protective action against myocardial infarction in rats. The possible mechanisms of anti-ischemia could be attributed to decreasing ICa-L and [Ca2+] of ventricular myocytes in rats.

Animals↗
PubMed2006

[The diagnosis and treatment of polycythemia rubra vera manifesting as acute cerebral stroke].

OBJECTIVE: To analyze the particularities of diagnosis and treatment of acute cerebral stroke secondary to polycythemia vera (PV). METHODS: To track and evaluate the clinical parameters, the manifestations of CT/MRI, the data of laboratory examinations, the therapeutic responses and the prognosis of acute cerebral stroke secondary to PV. Twenty-two cases of PV with initial presentation as acute stroke were analyzed. RESULTS: (1) 55.0% of the patients with stroke as the initial presentation of to PV had multiple lacuna infarction. (2) 37.5% of the patients had a temporary symptom aggravation after receiving a therapeutic regimen of blood-letting and chemotherapy, whereas, the stroke symptoms improved and became stable when treated with blood-letting combined with hemodilution and chemotherapy simultaneously. (3) Six cases received homoharringtonine treatment and all of them reached complete remission (CR). However, 3 of them showed ST segment and T-wave changes in electrocardiogram and 2 of them had bone marrow depression. Four cases received arsenic trioxide and obtained CR, but the relapse rate reached 50.0%. Nine cases were treated with hydroxycarbamide and all of them obtained CR. CONCLUSIONS: (1) Stroke secondary to PV should be treated with stroke regimen as well as PV therapy, and hydroxycarbamide might have stable benefit and few side effects. (2) Hematocrit assay should be used as a routine item in stroke patients with frequently relapsed.

Adult↗
PubMed2005

M3-R/IK(M3)--a new target of antiarrhythmic agents.

AIM: To investigate the relationship between M3-R/IK(M3) and arrhythmia in order to find a new target for antiarrhythmic agents. METHODS: Using the acute ischemic model of rats and patch-clamp techniques, the effects of the M3 receptor on the occurrence of arrhythmias and its possible mechanisms were studied. RESULTS: In acute ischemic model of rats, the M3 receptor antagonist 4-diphenylacetoxy-N-methylpiperidine-methiodide (4DAMP) increased the occurrence of arrhythmias, and the M3 receptor agonist choline suppressed the onset and the development of arrhythmias (P < 0. 01). No change was observed after treatment with other receptor antagonists (M1, M2, and M4). With patch-clamp techniques, it was found that choline induced K+ current could be inhibited by 4DAMP. Antagonists toward M1, M2, and M4 receptors all failed to alter the current. CONCLUSION: Choline modulates the cellular electrical properties of the heart, probably by activating a K+ current via stimulation of the M3 receptor. M3-R/IK(M3) may act as a new target for antiarrhythmic agents.

Animals↗
PubMed2005

[Vitexicarpin, a flavonoid from Vitex trifolia L., induces apoptosis in K562 cells via mitochondria-controlled apoptotic pathway].

AIM: To investigate the inhibitory effect of vitexicarpin on the proliferation of human cancer cells and its mechanism of action. METHODS: The inhibitory effect of vitexicarpin on the proliferation of human cancer cells was evaluated by the SRB method and its apoptosis-inducing effect was demonstrated by morphological observation under light microscope, flow cytometric analysis and agarose gel electrophoresis. The proteins related to apoptosis were examined by Western blotting analysis. RESULTS: Vitexicarpin significantly inhibited the proliferation of human cancer cells, A2780, HCT-15, HT-1080 and K562, with the IC50 values of (19.1 +/- 2.4) micromol x L(-1) for A2780(48 h), (0.66 +/- 0.10) micromol x L(-1) for HCT-15(48 h), (0.44 +/- 0.06) micromol x L(-1) for HT-1080 (48 h) and (0.28 +/- 0.14) micromol x L(-1) for K562 (24 h). The cells treated with vitexicarpin showed characteristic morphology typical for apoptosis and gave dose-dependent sub-G0/G1 peak in the flow cytometric analysis and DNA ladder on agarose gel electrophoresis. In Western blotting analysis, the cleavage of PARP and caspase-3, the release of cytochrome c from mitochondria into the cytosol, the decrease of Bcl-2 expression level, and the down-regulation of the ratio of Bcl-2/Bax expression level were examined in the K562 cells treated with vitexicarpin. CONCLUSION: Vitexicarpin induces apoptosis in K562 cells via mitochondria-controlled apoptotic pathway.

Antineoplastic Agents, Phytogenic↗
PubMed2005

[Inhibitory effects of chloride channel blockers NPPB on proliferation of human glomerular mesangial cells].

AIM: To investigate the effects of NPPB, a chloride channel blocker, on proliferation of mesangial cells. METHODS: Cell proliferation was determined by measuring cell number and 3H-thymidine incorporation. The LDH activity released from these cells was measured as evaluation of cell viability. The phase of cell cycle was detected by flow cytometry. RESULTS: Cell proliferation assays showed that treatment with both NPPB (50 and 25 micromol x L(-1)) and in hypertonic media (100% increased osmolarity with D-mannitol ) significantly reduced the number of human MC and 3H-thymidine incorporation in a dose-dependent manner. But the LDH activity was not significantly altered in the treatment with 50 micromol x L(-1) NPPB. Flow cytometry experiments showed that 50 and 25 micromol x L(-1) NPPB arrested (84.2 +/- 2.4) % and (80.8 +/- 2.9) % of cells at G0/G1 stage, versus (70.5 +/- 1.4) % of control cells. Conclusion NPPB suppresses cell proliferation and produces growth arrest at G0/G1 phase in human MC by a mechanism probably associated with changes in cell volume.

Cell Cycle↗
PubMed2004

[Clinical observation and following up of two administration methods of arsenic trioxide in treatment of acute promyelocytic leukemia].

OBJECTIVE: To assess the effectiveness and security of two arsenic trioxide (As(2)O(3)) administration methods in treatment of acute promyelocytic leukemia (APL). METHODS: Forty-eight APL cases were treated with As(2)O(3) with the total daily dosage of 0.16 mg/kg that was divided into two equal doses diluted in 250 ml of 5% glucose given twice in the morning and evening respectively by intravenous infusion' at a speed of 8 drops/min with an interval of 2-3 hours. Forty-eight sex- and age-matched APL cases were treated with As(2)O(3) with the same total daily dosage of 0.16 mg/kg given according to the routine method: infused intravenously once a day with a duration of at most 2 hours. Serum was collected at different time points to examine the arsenic concentration. The remission rate and side effects were observed. RESULTS: The remission rate was 93.8% in the patients treated by the new method, and was 83.3% in the patients treated by the routine method 28 days after the treatment. The lasting duration of effective arsenic level was at least 18.4 +/- 3.3 hours in the new method group, and was 9.4 +/- 1.6 hours in the routine method group. The average time from the initiation of treatment to complete remission (CR) in the new method group was 26.4 +/- 2.4 days, and was 35.7 +/- 4.8 days in the routine method group. No late liver functional lesion and bone marrow depression was found in the two groups during the 6 months followed up. CONCLUSION: The 'multi-times and slowing intravenous infusion' method relieves the side effects of As(2)O(3) treatment, increases the CR rate in treatment of APL.

Adolescent↗
PubMed2004

Effects of tacrolimus on infection of Friend murine leukemia virus to Fv-4 gene heterozygous mice.

AIM: To investigate the effect of tacrolimus (FK506) on the infection of Friend murine leukemia virus (Friend MuLV) in vivo. METHODS: Three kinds of mice were used including Friend MuLV-sensitive BALB/c mice, Friend MuLV-resistant Fv-4 gene-homozygous mice (Fv-4 mice), and Friend MuLV-resistant Fv-4 gene-heterozygous mice (F1 mice). Tacrolimus was administrated i.p. to those mice in every 2 d. Those treated mice were inoculated i.p. with Friend MuLV once on d 3. The symptoms and viral proliferations in those mice were observed to recognize the Friend MuLV infection. The expression and genotype of Fv-4 gene that resistant against the infection of Friend MuLV were analyzed to confirm the genomic background and related mechanism of the resistance. RESULTS: BALB/c mice and F1 mice, but not Fv-4 mice, appeared obvious early death, spleenomegaly, and viral proliferation after both treatments of viral inoculation and tacrolimus administration, whereas the expression and genotype of Fv-4 gene was not changed in F1 mice and Fv-4 mice with treatment of tacrolimus. Compared to the virus-inoculated control, the Friend MuLV-sensitivity of tacrolimus-treated BALB/c mice and the Friend MuLV-resistance of tacrolimus-treated Fv-4 mice were the same as the controls, but only F1 mice became the symptoms and viral proliferation after both treatments. It suggested the Friend MuLV-resistant F1 mice could be converted to be Friend MuLV-sensitive by treatment of tacrolimus, and this conversion was not depended on the expression and genotype of Fv-4 gene. CONCLUSION: Tacrolimus could not inhibit the infection of Friend MuLV in all mice, furthermore, it could enhance the infection of Friend MuLV in F1 mice. The enhancement may be related to the immunosuppressive effect of tacrolimus.

Animals↗
PubMed2004

[Clinical and experimental study of cardiac effects of conventional dosage arsenic trioxide in APL patients].

OBJECTIVE: To investigate cardiac effects of arsenic trioxide (As(2)O(3)) at conventional dosage in acute promyelocytic leukemia (APL) patients. METHODS: The basical heart rate, electrocardiograph, plasma As(2)O(3) concentration of APL patients were dynamically monitored. The action potential duration and current of I(Ca-L) in guinea pig cardiac ventricular myocytes were assayed by patch clamp technique, and the elevated cytosolic [Ca(2+)]i of guinea pig ventricular myocytes induced by As(2)O(3) by laser confocal microscopy. RESULTS: Approximately 52.5% - 35% of 40 APL patients manifested poor cardiac effects of different degree when As(2)O(3) intravenous infused at conventional doses in the initial 1 or 2 weeks with fast heart rate or prolonged QT interval. As(2)O(3) at concentration of 1, 2, 5 micro mol/L prolonged action potential duration from (563.0 +/- 55.8) ms to (737.7 +/- 131.7), (842.4 +/- 115.6) and (1103.2 +/- 96.3) ms respectively (P < 0.05, P < 0.01, P < 0.01), and increased I(Ca-L) of guinea pig cardiac ventricular myocytes as well as the respectively cytosolic [Ca(2+)]i. Calcium channel blocking agent can cut-out the effect. CONCLUSION: As(2)O(3) intravenous infusion at conventional doses can cause tachycardia and prolong QT interval. The probable mechanism might be that As(2)O(3) affects the ion channels and cytosolic calcium.

Adult↗
PubMed2004

[Association between subacute combined degeneration, vitamin B12 deficiency and megaloblastic anemia].

OBJECTIVE: To investigate the association between subacute combined degeneration (SCD) and vitamin B(12) (VB(12)) deficiency and megaloblastic anemia (MA). METHODS: The serum level of VB(12), severity of anemia and lesions in CNS were analysed in 36 cases diagnosed as SCD. In addition, MRI neuro-electrophysiologic examination and CSF myelin basic protein (MBP) concentration were monitored dynamically. The prognosis of SCD was evaluated in relation to the time of the initiation of therapy. RESULTS: Average ferrohemoglobin level in patients was (77.1 +/- 11.2) g/L and the average blood serum level of VB(12) was (87.0 +/- 21.4) ng/L before treatment with an abnormality rate of 47.2%. However, there was no linear correlation between the severity of lesions in CNS and ferrohemoglobin level or level of serum VB(12) (correlation coefficient: r = -0.1917, 0.0926, P > 0.5; r = 0.207, 0.101, P > 0.5, respectively). The comprehensive abnormal rate of evoked potential was 100%, which might occur prior to the clinical symptoms of SCD. The abnormal rate of MRI was 71.4%, and some lesions could diminish or disappear after treatment. The MBP levels in CSF were (3.96 +/- 1.66) ng/L, and (2.25 +/- 1.66) ng/L before and 3 months after the treatment. No significant improvement of symptoms and signs were seen when the treatment was initiated 6 months after the diagnosis. CONCLUSION: SCD is associated with VB(12) deficiency and often accompanied by MA, but there is no linear correlation. Lesions of SCD in spinal cord or brain can be demonstrated in MRI. Evoked potential is critical for early diagnose and identification of silent cases of SCD. The level of MBP in CSF can reflect the severity of the lesion and prosthetic state of myelin sheath. Early diagnosis and treatment play an important role in decreasing the degree of the permanent dysfunction of CNS in SCD.

Adolescent↗
PubMed2004

[Effects of emodin on the intracellular calcium concentration ([Ca2+]i) and L-type calcium current of the single ventricular mytocytes from guinea pig].

AIM: To study the effects of emodin on intracellular calcium concentration ([Ca2+]i) and L-type calcium current of the single ventricular myocytes from guinea pig. METHODS: Enzymatic dissociation was used to isolate single ventricular myocytes from adult guinea pig. They were loaded with Ca2(+)-sensitive fluorecent indicator Fluo-3/AM. [Ca2+]i represented by fluorescent intensity (FI) was measured by laser scanning confocal microscope. Whole cell patch clamp technique was used to record ICa-L. RESULTS: At resting status, [Ca2+]i was not affected by emodin (1-100 mumol.L-1). Emodin at the concentration of 1 mumol.L-1 was shown to increase the [Ca2+]i induced by 60 mmol.L-1 KCl. The peak value of fluorescent intensity was increased from 1,877 +/- 551 to 2,905 +/- 739 (n = 8, P < 0.05). Emodin at the concentration of 10 mumol.L-1 had no effect on the increase of [Ca2+]i induced by 60 mmol.L-1 KCl. However, the increase of [Ca2+]i induced by KCl was reduced to 1,214 +/- 335 (n = 8, P < 0.05) by 100 mumol.L-1 emodin. The density of ICa-L was increased from (-6.2 +/- 1.3) pA/pF to (-8.3 +/- 0.3) pA/pF (n = 6, P < 0.05) by 1 mumol.L-1 emodin at the test pulse of 0 mV. The current was not altered by 10 mumol.L-1 emodin. But it was inhibited from (-6.6 +/- 1.0) pA/pF to (-3.80 +/- 0.16) pA/pF (n = 6, P < 0.05) by 100 mumol.L-1 emodin at the test pulse of +10 mV. CONCLUSION: Emodin has two-way regulation on [Ca2+]i and ICa-L of cardiomyocytes in guinea pig.

Animals↗
PubMed2004

Inactivation gating determines drug potency: a common mechanism for drug blockade of HERG channels.

AIM: To determine the mechanisms of interactions between different drugs and HERG channels. METHODS: Various antiarrhythmic (dofetilide, quinidine, azimilide, RP58866) and non-antiarrhythmic (terfenadine, nicotine) agents were used on HERG channels expressed in Xenopus oocyte. Whole-cell voltage-clamp techniques were used. RESULTS: All drugs produced concentration-dependent block of HERG current. The inhibition was markedly facilitated with voltage protocols favoring channel inactivation (eg, less negative holding potentials). Maneuvers that weakened channel inactivation (eg, elevation of external K+), relieved HERG blockade by all drugs. Moreover, the inhibitory potency was reduced by at least 20-300 fold with varying compounds when rapid C-type inactivation was removed by a mutation located between the transmembrane domains 5 and 6 (S631A). CONCLUSION: The inactivation gating of HERG channels determines the blocking potency of drugs. This mechanism might be common to drugs of various classes.

Animals↗
PubMed2004

[The ion targets of arrhythmias induced by ouabain and aconitine in guinea pig and rat ventricular myocytes].

AIM: To observe the effects of ouabain and aconitine on APD and ion channels in isolated guinea pig and rat ventricular myocytes; to elucidate the action mechanisms of these two drugs and set up new arrhythmic models on cellular level. METHODS: In isolated ventricular myocytes of guinea pig and rat, the effects of ouabain and aconitine on APD, ICa-L, Ik, Ito and Ik1 were observed using the whole cell patch clamp technique. RESULTS: Ouabain (5 micromol x L(-1)) obviously prolonged the APD90, increased ICa-L, decreased Ik and Ik1 in guinea pig ventricular myocytes. Aconitine (1 micromol x L(-1)) lengthened the APD90, increased ICa-L, decreased Ito and increased Ik1 in rat ventricular myocytes. CONCLUSION: The targets on ouabain- and aconitine-induced arrhythmias included APD, ICa-L, Ik, Ito, and Ik1. APD, ICaL, Ik and Ito must be the powerful ones, both in arrhythmic and antiarrhythmic courses. The ouabain- and aconitine- induced arrhythmic models on cellular level were built to study the antiarrhythmic mechanisms of chemicals and evaluate new drugs. These two new-type models in vitro were stable, liable, repeatable and economic, which were superior to those typical models in vivo.

Aconitine↗
PubMed2004

[Relationship between M3 receptor and myocyte apoptosis induced by acute myocardial infarction].

AIM: To explore the effects of M3 receptor on myocyte apoptosis induced by acute myocardial infarction in rats. METHODS: Rat model was induced by ligation of the anterior branch of the left coronary artery. All animals were divided into four groups: sham-operated group, occlusion group, choline group (10 mg x kg(-1), iv), and 4DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) group (0.12 mg x kg(-1), iv). The serum malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. The infarct size areas on the myocardium were identified by TTC staining. The apoptosis in cardiomyocyte was detected by TUNEL assay and apoptosis-related proteins in Bcl-2 and Fas expression were measured by immunohistochemistry assay. RESULTS: M3 receptor agonist choline reduced serum MDA content and increased SOD activity. The myocardial expression of Bcl-2 was increased, whereas the expression of Fas was decreased by choline. However, blockade of M3 receptor by 4DAMP completely inhibited these effects of choline on cardiac myocytes. CONCLUSION: Activation of M3 receptor has protective effect on myocyte apoptosis induced by acute myocardial infarction in rat, and this effect might be related to modulating the expression of some immediateearly genes including Bcl-2 and Fas.

Animals↗