Cobalt vacancy-originated TiMnCoCN compounds with a self-adjusting ability for the high-efficiency acidic oxygen evolution reaction.

Oxygen evolution reaction (OER) electrocatalysts in acidic media, except for precious IrO2, have difficulty realizing good electrocatalytic activity and high electrochemical stability simultaneously. However, the scarcity of IrO2 as an acidic OER electrocatalyst impedes its large-scale application in hydrogen generation, organic synthesis, nonferrous metal production and sewage disposal. Herein, we report the design and fabrication of a nanoporous TiMnCoCN compound based on the nanoscale Kirkendall effect, possessing an intriguing self-adjusting capability for the oxygen evolution reaction (OER) in a 0.5 M H2SO4 solution. The nanoporous TiMnCoCN compound electrode for the acidic OER displays a low overpotential of 143 mV for 10 mA cm-2 and exhibits no increase in potential over 50,000 s, which is ascribed to the self-adjusting ability, Carbon/nitrogen (C/N) incorporation and nanoporous architecture. The concentration of inert TiO2 on the reconstructed surface of the compound can self-adjust with the change in OER potential via a cobalt-dissolved vacancy approach according to the stabilization requirement. In this work, the self-reconstruction law of surface structure was discovered, providing a novel strategy for designing and fabricating nonnoble OER electrocatalysts with superior catalytic performance and robust stability in acidic media.

Bicontinuous Nanoporous Nitrogen/Carbon-Codoped FeCoNiMg Alloy as a High-Performance Electrode for the Oxygen Evolution Reaction.

The kinetics of the oxygen evolution reaction (OER) in aqueous electrolytes is relatively slow, which seriously limits the energy efficiency of electricity-to-hydrogen conversion. Herein, a bicontinuous nanoporous FeCoNiMg alloy is prepared by high heat sintering method based on the nanoscale Kirkendall effect and the surface is codoped with nitrogen and carbon elements by the nitrocarburizing method (denoted NC-FeCoNiMg). The three-dimensional (3D) nanoporous NC-FeCoNiMg alloy electrode achieves superior electrocatalytic performance for the OER in alkaline media, delivering a low Tafel slope (34.6 mV dec-1) and small overpotentials (235 and 290 mV at 10 and 100 mA cm-2, respectively). Under consecutive high current densities, the NC-FeCoNiMg electrode still exhibits excellent long-term stability, and the OER activity even increases after testing for 100 h at a high current density of 1000 mA cm-2. Comprehensive studies reveal that the N/C codoping of the inner and outer surfaces dramatically improves the electrocatalytic activity of the NC-FeCoNiMg electrode. This work demonstrates an efficient nanoarchitectural construction and a surface modulation strategy to increase the electrocatalytic activity and stability of transition-metal-based electrodes for the OER, holding great promise for fulfilling the requirements for the large-scale production of clean hydrogen energy.

Self-supported nickel-doped molybdenum carbide nanoflower clusters on carbon fiber paper for an efficient hydrogen evolution reaction.

Developing an efficient, stable and low-cost noble-metal-free electrocatalyst for the hydrogen evolution reaction (HER) is an effective way to alleviate the energy crisis. Herein, we report a simple and facile approach to synthesize self-supported Ni-doped Mo2C via a molten salt method. By optimizing the content of Ni, the concentration of Ni(NO3)2, and the annealing time, self-supported nanoflower-like electrocatalysts composed of ultrathin nanosheets on carbon fiber paper (CFP) can be achieved. Such a fluffy and porous nanoflower-like structure has a large specific surface area, which can expose many active sites, and promote charge transfer; moreover, all of the above is beneficial for improving the HER performance. Density functional theory (DFT) calculations reveal that the doping of Ni leads to a down shift of the value of the d band center (εd), so that the adsorbed hydrogen (Hads) is easier to desorb from the catalyst surface, thus leading to an enhanced intrinsic catalytic activity of Ni doped Mo2C based catalysts. As a result, Mo2C-3 M Ni(NO3)2/CFP with a nanoflower-like structure prepared at 1000 °C for 6 h exhibits the best electrocatalytic performance for the HER in 0.5 M H2SO4, with a low overpotential of 56 mV (at j = 10 mA cm-2) and a Tafel slope (27.4 mV dec-1) comparable to that of commercial Pt/C (25.8 mV dec-1). The excellent performance surpasses most of the noble-metal-free electrocatalysts. In addition, the outstanding long-term durability of Mo2C-3 M Ni(NO3)2/CFP is demonstrated by showing no obvious fluctuations during 35 h of the HER testing. This work provides a simple and facile strategy for the preparation of nanoelectrocatalysts with high specific surface areas and high catalytic activities, both of which promote an efficient HER.

Strain in a platinum plate induced by an ultrahigh energy laser boosts the hydrogen evolution reaction.

The ligand and the strain near the active sites in catalysts jointly affect the electrocatalytic activity for the catalytic industry. In many cases, there is no effective strategy for the independent study of the strain effect without the ligand effect on the electrocatalytic activity for the hydrogen evolution reaction (HER). Laser shock peening (LSP) with a GW cm-2 level power density and a 10-30 ns short pulse is employed to form compressive strain on the surface and in the depth direction of a platinum (Pt) plate, which changes the inherent interatomic distance and modifies the energy level of the bonded electrons, thereby greatly optimizing the energy barrier for the HER. The crystal lattice near the surface of the LSP Pt plate is distorted by the strain, and the interplanar spacing decreases from 0.225 nm in the undeformed region to 0.211 nm in the deformed region. The specific activity of the LSP Pt has an increase of 2.9 and 6.4 times in comparison with that of the pristine Pt in alkaline and acidic environments, respectively. This investigation provides a novel strategy for the independent study of the strain effect on the electrocatalytic activity and the improvement of electrocatalysts with high performance in extensive energy conversion.

Enhanced mechanical properties of 4H-SiC by epitaxial carbon films obtained from bilayer graphene.

Graphene exhibits excellent mechanical properties under atomically thin thickness, which made it very suitable for nanoelectromechanical systems that had high requirements for the thickness of coatings. The epitaxial bilayer graphene on the 4H-SiC (0001) surface presents high stiffness and hardness comparable to diamond. However, due to structural transition occurring at the nanoscale, it is difficult to elucidate reinforcement mechanisms using experimental methods. Here, we applied molecular dynamics simulations to study nanoindentation of epitaxial carbon-film-covered 4H-SiC (0001) surfaces. Because a weak interaction potential existed between graphene layers at indentation depth (h < 0.8 Å) that far smaller than interlayer distance, the epitaxial bilayer graphene does not allow the 4H-SiC to exceed its intrinsic stiffness. When the indentation depth h ≥6.45 Å, the sp3 hybridized bonds formed on the interlayer of graphene, which leads to fewer amorphous atoms in the sample of 4H-SiC and exhibits stronger stiffness, in comparison with bare 4H-SiC. This strongly suggests the existence of sp3 bonds contributing to the surface strengthening. Meanwhile, we found that the comprehensive mechanical properties of nanocomposites with hydrogenated diamond-like films were superior to those of nanocomposites with other carbon films at high temperatures.

One-Step and One-Precursor Hydrothermal Synthesis of Carbon Dots with Superior Antibacterial Activity.

Discovering efficient antibacterial materials is crucial in the area of increasing drug resistance. Herein, we synthesized carbon dots (C-dots) with superior antibacterial activity through a simple one-step hydrothermal method. In this method, p-phenylenediamine serves as not only the carbon source but also the origin for the functional group anchored on the obtained C-dots. The antibacterial activity of the obtained C-dots was tested against Staphylococcus aureus and Escherichia coli. The minimum bactericidal concentrations of the synthesized C-dots against S. aureus and E. coli were 2 and 30 µg/mL, respectively, which are lower than that of previously reported C-dots. The antibacterial mechanism was investigated, and the results indicated that a large number of -NH3+ groups on the C-dots' surface enhanced their antibacterial activity. Besides, the C-dots exhibited negligible cytotoxicity.

Cobalt-Iron Oxide Nanoarrays Supported on Carbon Fiber Paper with High Stability for Electrochemical Oxygen Evolution at Large Current Densities.

Here, we demonstrate that nonprecious CoFe-based oxide nanoarrays exhibit excellent electrocatalytic activity and superior stability for electrochemical oxygen evolution reaction (OER) at large current densities (>500 mA cm-2). Carbon fiber paper (CFP) with three-dimensional macroporous structure, excellent corrosion resistance, and high electrical properties is used as the support material to prevent surface passivation during the long-term process of OER. Through a facile method of hydrothermal synthesis and thermal treatment, vertically aligned arrays of spinel Co xFe3- xO4 nanostructures are homogeneously grown on CFP. The morphology and the Fe-doping content of the CoFe oxide nanoarrays can be controlled by the Fe3+ concentration in the precursor solution. The arrays of CoFe oxide nanosheets (NSs) grown on CFP (Co2.3Fe0.7O4-NSs/CFP) deliver lower Tafel slope (34.3 mV dec-1) than CoFe oxide nanowire (NW) arrays grown on CFP (Co2.7Fe0.3O4-NWs/CFP) in alkaline solution, owing to higher Fe-doping content and larger effective specific surface area. The Co2.3Fe0.7O4-NSs/CFP electrode exhibits excellent stability for OER at large current densities in alkaline solution. Moreover, the morphology and structure of CoFeO nanoarrays are well preserved after long-term testing, indicating the high stability for OER.

Morphology-Controllable Synthesis of Cobalt Telluride Branched Nanostructures on Carbon Fiber Paper as Electrocatalysts for Hydrogen Evolution Reaction.

Cobalt telluride branched nanostructures on carbon fiber paper (CFP) with two different morphologies were synthesized via solution-based conversion reaction. Both the CoTe2 with nanodendrite and CoTe with nanosheet morphologies on the CoTe2 nanotube (CoTe2 NDs/CoTe2 NTs and CoTe NSs/CoTe2 NTs) supported by CFP exhibit high activities toward hydrogen evolution reaction (HER). Particularly, the CoTe NSs/CoTe2 NTs only require an overpotential of 230.0 mV to deliver the current density of 100 mA cm(-2) in acid solution. After cycling for 5000 cycles or 20 h continual electrolysis, only a small performance loss is observed.

Endothelium-dependent and -independent vasorelaxant actions and mechanisms induced by total flavonoids of Elsholtzia splendens in rat aortas.

Elsholtzia splendens (ES) is, rich in flavonoids, used to repair copper contaminated soil in China, which has been reported to benefit cardiovascular systems as folk medicine. However, few direct evidences have been found to clarify the vasorelaxation effect of total flavonoids of ES (TFES). The vasoactive effect of TFES and its underlying mechanisms in rat thoracic aortas were investigated using the organ bath system. TFES (5-200mg/L) caused a concentration-dependent vasorelaxation in endothelium-intact rings, which was not abolished but significantly reduced by the removal of endothelium. The nitric oxide synthase (NOS) inhibitor N(ω)-nitro-l-arginine methyl ester (100µM) and the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,2-α]quinoxalin-1-one (30µM) significantly blocked the endothelium-dependent vasorelaxation of TFES. Meanwhile, NOS activity in endothelium-intact aortas was concentration-dependently elevated by TFES. However, indomethacin (10µM) did not affect TFES-induced vasorelaxation. Endothelium-independent vasorelaxation of TFES was significantly attenuated by KATP channel blocker glibenclamide. The accumulative Ca(2+)-induced contraction in endothelium-denuded aortic rings primed with KCl or phenylephrine was markedly weakened by TFES. These results revealed that the NOS/NO/cGMP pathway is likely involved in the endothelium-dependent vasorelaxation induced by TFES, while activating KATP channel, inhibiting intracellular Ca(2+) release, blocking Ca(2+) channels and decreasing Ca(2+) influx into vascular smooth muscle cells might contribute to the endothelium-independent vasorelaxation conferred by TFES.

[Effects of total flavones of Elsholtzia splendens in isolated ischemia/reperfusion rat hearts].

OBJECTIVE: To investigate the influence of total flavonoids of Elsholtzia splendens (TFES) on isolated ischemia/reperfusion rat hearts and its underlying mechanisms. METHODS: Hearts isolated from male SD rats were perfused on the Langendorff apparatus and subjected to global ischemia for 30 min followed by 120 min of reperfusion. The cardiac infarct size was measured by TTC staining. Hemodynamic parameters and the level of lactate dehydrogenase (LDH) in the coronary effluent were measured. Absorbance at 520 nm was determined in isolated cardiac mitochondria exposed to 200 micromol/L CaCl2 to detect the opening of the mitochondrial permeability transition pore. RESULTS: Pretreatment with TFES (1, 10, 100 microg/ml) for 5 min decreased infarct size and LDH release and improved the recovery of the left ventricular developed pressure. In mitochondria, the decrease of absorbance at 520 nm evoked by CaCl2 was greatly inhibited by TFES. CONCLUSION: TFES prevents myocardial ischemia/reperfusion injury, and this cardioprotective effect is probably via inhibiting mitochondrial permeability transition pore opening.

[Expression and function of autophagy after ischemia/reperfusion in rats hippocampus neuron].

OBJECTIVE: To explore the expression of autophagy after ischemia/reperfusion and its possible function in rats hippocampus neurons. METHODS: After 2 hours oxygen-glucose deprivation and different periods time of reperfusion (OGD/R) treatment in primary hippocampal neurons, neuron viability was evaluated by MTT assay, specific structure of autophagosome and specific protein of autophagy microtubule-associated protein 1 light chain 3 B (LC3B) were detected by transmission electron microscope and immunofluorescence respectively. The inhibitor of autophagy 3-Methyladenine (3-MA) was also used to exam the viability of neurons. RESULTS: Treatment by OGD/R markedly reduced neuronal viability. Compared to the control group, autophagy existed in different time periods after OGD/R shown both in transmission electron microscope and immunofluorescence. Application of 3-MA significantly reduced neuronal viability. CONCLUSION: Oxygen-glucose deprivation can activate autophagy in rat hippocampus neurons, which may resist the injury during ischemia/reperfusion.

[Effect of S-allyl-L-cysteine on isolate heart subject to ischemia/reperfusion].

OBJECTIVE: To investigate the effect of S-allyl-L-cysteine (SAC) on isolated rat heart subject to ischemia/reperfusion(I/R) injury and the mechanisms. METHODS: The isolated perfused rat hearts on a Langendorff apparatus were subjected to global ischemia for 30 min and followed by 120 min of reperfusion. Hemodynamic index, the production of formazan and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. Superoxide dismutase (SOD) and reactive oxygen species (ROS) in myocardial homogenates were measured. RESULTS: Compared with I/R group, the hemodynamics were greatly improved, the production of formazan was increased, and LDH level in effluent was reduced in SAC group. SAC improved the SOD activity and significantly decreased the level of ROS. In addition, threonine (Thr) attenuated the protective effect of SAC significantly. CONCLUSION: SAC has protective effect against myocardial ischemia/reperfusion injury on rats. The possible mechanism is that SAC be transported into the cell through alanine-serine-cysteine-transporter 1 (ASCT-1) improves SOD activity and reduces the level of ROS.

[Luteolin reduces cardiac dysfunctions in streptozotocin-induced diabetic rats].

OBJECTIVE: To investigate the effects of luteolin (Chinese Traditional Medicine) on cardiac functions and mitochondrial oxidative stress in streptozotocin (STZ)-induced diabetic rats. METHODS: Male SD rats were randomly divided into a normal control group, a luteolin control group, a diabetic group, and diabetic groups orally administered with a low dose (10 mg/(kg x d)) or a high dose of luteolin (100 mg/ (kg x d)) for eight weeks. The body weight, blood glucose, cardiac functions, left ventricular weight, myocardial collagen and reactive oxygen species (ROS) levels were assayed. The cardiac mitochondrial ROS level, superoxide dismutase (SOD) activity and the mitochondrial swelling were measured. RESULTS: Treatment with luteolin had no effect on the blood glucose but reduced the losing of body weight in diabetic rats. High dose of luteolin markedly reduced the ratio of ventricular weight and body weight, increased the left ventricular develop pressure, and decreased the left ventricular end diastolic pressure in diabetic rats. The myocardial levels of ROS and collagen, the cardiac mitochondrial ROS level, and the mitochondrial swelling in diabetic rats were all markedly reduced by high dose of luteolin. Furthermore, high dose of luteolin significantly increased the mitochondrial SOD activity in diabetic rat hearts. CONCLUSION: Treatment with luteolin for 8 weeks markedly improves the cardiac function, which may be related to reducing mitochondrial oxidative stress and mitochondrial swelling in diabetic rats.

[Partial endothelium-dependent vasorelaxation of crocetin and its mechanism].

OBJECTIVE: To investigate the vasorelaxation effect of crocetin (CCT) and its mechanism. METHODS: Isolated aortic rings from Sprague-Dawley rats were mounted in the organ bath system. The tension of the aorta was recorded. RESULT: CCT significantly provoked concentration-dependent relaxation in both endothelium-intact and-denuded aortic rings pre-constricted by phenylephrine (10⁻5 mol/L), and the vasorelaxation in endothelium-intact aortic rings was stronger than that in endothelium-denuded ones. CCT had no significant effects on aortic rings pre-constricted with KCl (6 × 10⁻² mol/L). Pretreatment with eith L-NAME (10⁻4 mol/L), an inhibitor of nitric oxide synthase (NOS), or indomethacin (10⁻5 mol/L), an inhibitor of cyclooxygenase, for 30 min significantly attenuated the relaxation of endothelium-intact aortic rings induced by CCT. Besides, both tetraethylammonium (a Ca²(+)-activated K(+) channel inhibitor, 5 × 10⁻³ mol/L) and 4-aminopyridine (a voltage-sensitive K(+) channel inhibitor, 10⁻³ mol/L), but not the ATP-sensitive K(+) channel inhibitor glibenclamide (3 × 10⁻6 mol/L), significantly attenuated CCT-induced relaxation in endothelium-denuded aortic rings. CONCLUSION: CCT had partial endothelium-dependent relaxation in rat aortas, which may be mediated by activating the endothelial NOS-NO and cyclooxygenase-prostacyclin pathways. The endothelium-independent relaxation in rat aortas induced by CCT may be mediated by Ca²(+)-activated K(+) channels and voltage-sensitive K(+) channels.

[Electrophysiological effect of atorvastatin on isolated rat hearts injured by ischemia/reperfusion].

OBJECTIVE: To investigate the myocardial electrophysiological effect and its underlying mechanisms of atorvastatin (Ator) on isolated rat hearts injured by ischemia/reperfusion (I/R). METHODS: Isolated SD rat hearts were mounted on Langendorff system, and a local I/R was induced by ligation (30 min) and release (15 min) of the left anterior descending artery. During the reperfusion period, the effect of Ator on diastolic excitation threshold (DET), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) on rat heart were measured. RESULT: Compared with the control group, medium concentration of Ator prolonged the ERP in normal rat hearts; low, medium and high concentration of Ator significantly inhibited the decrease of DET, ERP and VFT induced by I/R. However, pretreatment with L-NAME cancelled these cardiac electrophysiological effects of Ator. CONCLUSION: Ator reduced electrophysiological alteration induced by I/R in isolated rat hearts, which may be mediated by activating nitric oxide pathway to enhance the myocardial electrophysiological stability.

[Auricularia auricular polysaccharide protects myocardium against ischemia/reperfusion injury].

OBJECTIVE: To determine whether auricularia auricular polysaccharide (AAP) protects heart against ischemia/reperfusion (1/ R) injury and its underlying mechanisms. METHODS: Male Sprague-Dawley rats, pretreated with AAP (50, 100, 200 mg/(kg x d), gastric perfusion) for 4 weeks, were used for Langendorff isolated heart perfusion. The hearts were subjected to global ischemia for 30 min followed by 120 min of reperfusion and the left ventricular hemodynamic parameters were measured. Formazan, a product of 2, 3, 5-triphenyl-tetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. The cardiac malondialdehyde (MDA), a product of lipid peroxidation, and superoxide dismutase (SOD) activity were determined after myocardial I/R. RESULTS: The pretreatment with AAP at 50, 100, 200/(kg d) for 4 weeks before I/R increased myocardial formazan content, reduced LDH release, improved the recovery of the left ventficular developed pressure, maximal rise rate of left ventricular pressure, and rate pressure product (left ventricular developed pressure multiplied by heart rate) attenuated the decrease of coronary flow during reperfusion. The cardiac protective effect of high dose AAP was more potent than that of compound radix salviae miltiorrhizae (CRSM, 4 ml/(kg x d), gastric perfusion for 4 weeks). Pretreatment with AAP (100 mg/(kg x d)) markedly inhibited the increase of MDA level and the decrease of SOD activity induced by I/R in myocardium. CONCLUSION: The findings indicate that in the isolated rat heart, AAP protects myocardium against ischemia/reperfusion injury via enhancing the activity of SOD and reducing lipid peroxidation in heart.

[Myocardial protective effect of acetylcholine against ischemia/reperfusion injury and its underlying mechanism].

OBJECTIVE: To determine whether the caidioprotection of acetylcholine (ACh) against ischeniia/reperftision (I/R) injury is re-kited to mitochondrial permeability transition pore (MEW) and mitochondrial AW-sensitive potassium channel (mitoK(ATP)). METHODS: Male Sprague-Dawley rats were used for Langendorif isolated bean perkision. The hearts were subjected to global ischemia for 30 mm followed by 120 rein of reperfusion and the left ventricular hemodynaniic parameters were measured. Formazan, a product of 2,3, 5-triphenyl-tetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. RESULTS: The pretreatment with ACh (0.1 mol/L, 5 mm) before I/R markedly increased myocardial formazan content, reduced LDH release, improved the recovery of the left veritficular developed pressure, +/- dP/dtmax, and rate pressure product (left ventricular developed pressure multiplied by hean rate) and attenuated the decrease of coronary flow during reperfusion. The opener of MPTP, atiractyloside (20 mmoL/L) or the inhibitor of mitoK(ATP), 5-hydroxydecanoate (100 micromol/L) abolisbed the beneficial effect of ACh. CONCLUSION: In the isolated rat bean, ACh protects myocardium against ischemia/reperfusion injury via inhibiting the opening of MPTP and increasing the opening of mitoKATP in heart.

Mitochondrial pores modulate the protective effect of acetylcholine on ventricular myocytes during ischemia/reperfusion injury.

In this study, we investigated the cardioprotective effect of acetylcholine (ACh) via modulation of mitochondrial permeability transition pore (MPTP) opening through the mitochondrial ATP-sensitive potassium channel (mitoK(ATP) channel). In isolated ventricular myocytes from male Sprague-Dawley rats, 0.1 micromol/L ACh was administered for 6 min, before 30 min of simulated ischemia and 30 min of reperfusion (I/R). A mitoK(ATP) inhibitor (5-hydroxydecanoate, 5-HD) and an MPTP opener (atractyloside, Atr) were used to analyze the underlying mechanisms. Myocyte contractile function, myocyte viability, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) and mitochondrial membrane potential were assayed. During reperfusion, the amplitudes of contraction, +/-dL/dt(max), and end-diastolic length of myocytes were decreased, which were markedly improved by pretreatment with ACh. However, such effects of ACh were reversed by 100 micromol/L 5-HD for 20 min before ischemia, or 20 micromol/L Atr for 20 min at the beginning of reperfusion. Pretreatment with ACh markedly reduced I/R-induced cell death, LDH release, ROS signals and mitochondrial membrane potential dissipation, all of which were reversed by 5-HD or Atr. In conclusion, ACh may protect ventricular myocytes from I/R injury by inhibiting MPTP opening and stabilizing the mitochondrial membrane potential through activating the mitoK(ATP) channel.

[Study of the effects of Auricularia auricular polysaccharide on local ischemia/reperfusion injury in rat].

OBJECTIVE: To investigate the influence of Auricularia Auricular polysaccharide (APP) on acute cerebral injury induced by ischemia/reperfusion in rats and its underlying mechanism. METHODS: Adult male SD rats were intragastrically pretreated with AAP at a low (50 mg/kg) or high (100 mg/kg) dose once a day for 20 days before operation. Rats intraperitoneally injected with ginkgo biloba extract (EGb671) were taken as positive control. Focal ischemia was achieved by middle cerebral artery occlusion (MCAO) on the right side for 60 min. After 24 hrs of reperfusion, the nerve function defects were recorded by Longa's score and the brain infarct sizes were measured by 2,3,5-Triphenyl-tetrazolium-chlor (TTC) staining. Apoptotic neurons were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining after 48 h of reperfusion. The levels of oxidative stress was determined via the mitochondria-generated reactive oxygen species (ROS). RESULTS: AAP treatment decreased Longa's score, brain infarct size, apoptotic neurons and mitochondria-generated ROS in a dose-dependent manner. AAP at 100 mg/kg gave a better performance compared with EGb671 on all parameters examined. CONCLUSION: AAP treatment protected rat brain from focal ischemia/reperfusion injury by its anti-oxidative effect and worked better than EGb671.

[Antiarrhythmic effect of ethyl acetate extract from Chrysanthemum Morifolium Ramat on rats].

OBJECTIVE: To investigate the effect of ethyl acetate extract from Chrysanthemum Morifolium Ramat (CME) on experimental arrhythmia induced by ischemia/reperfusion or aconitine in rats and to explore its underlying mechanisms. METHODS: Arrhythmia model in intact rat was induced by aconitine (30 microg/kg body weight, i.v.). In isolated Langendorff perfused rat hearts, regional ischemia and reperfusion was induced by ligation and release of left anterior descending artery. The ventricular fibrillation threshold (VFT), effective refractory period (ERP), and diastolic excitation threshold (DET) in the isolated heart were measured. The action potentials of papillary muscle in rat right ventricle were recorded by conventional glass microelectrode technique. RESULTS: Compared with control group CME significantly decreased the number and duration of ventricular tachycardia (VT); delayed the occurrence of ventricular premature beats (VPB) and VT induced by aconitine. Arrhythmia score of the CME group was lower than that in aconitine-treated group. CME markedly prolonged the ERP and increased the VFT in the isolated perfused rat hearts during ischemia and reperfusion. CME prolonged action potential duration at 50% and 90% repolarization of the right ventricular papillary muscles and decreased the maximal rate of rise of the action potential upstroke, but did not affect the resting potential, amplitude of action potential. CONCLUSION: CME can reduce myocardial vulnerability and exerts its antiarrhythmic effects induced by aconitine or ischemia/reperfusion, which may be related to its prolongation of action potential duration and effective refractory period that enhance the electrophysiological stability of myocardiaium.