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.

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.

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.

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.

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.

[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.

[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.

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.

[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.

Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats.

BACKGROUND AND PURPOSE: Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats. METHODS: Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats. The animals underwent postconditioning consisting of 3 cycles of 15-second/15-second (Post-15/15), 30-second/30-second (Post-30/30), or 60-second/15-second (Post-60/15) reperfusion/reocclusion or 15-second/15-second reperfusion/reocclusion applied after a 45-second reperfusion (Post-45-15/15). RESULTS: Ten minutes of ischemia and 7 days of reperfusion destroyed 85.8% of CA1 hippocampal neurons and 64.1% of parietal cortical neurons. Three cycles of Post-15/15, Post-30/30, and Post-45-15/15 reperfusion/reocclusion markedly reduced neuronal loss after 7 days or 3 weeks of reperfusion and diminished the deficiency in spatial learning and memory. After reperfusion, a period of hyperperfusion followed by hypoperfusion was observed, both of which were blocked by postconditioning. The cytosolic level of cytochrome c increased significantly after 48 hours of reperfusion, and this was inhibited by Post-15/15, Post-30/30, and Post-45-15/15. However, 3 cycles of 60-second/15-second reperfusion/reocclusion failed to protect against neuronal damage, behavioral deficit, or cytochrome c translocation. CONCLUSIONS: Our data provide the first evidence that an appropriate ischemic postconditioning strategy has neuroprotective effects against global cerebral ischemia/reperfusion injury and a consequent behavioral deficit and that these protective effects are associated with its ability to improve disturbed cerebral blood flow and prevent cytochrome c translocation.

Inhibition of superoxide anion-mediated impairment of endothelium by treatment with luteolin and apigenin in rat mesenteric artery.

This study was designed (i) to test the hypothesis that the endothelium-derived hyperpolarizing factor (EDHF) component of ACh-induced vasorelaxation and hyperpolarization of smooth muscle cells (SMCs) are impaired following exposure to superoxide anion, and (ii) to further investigate whether luteolin and apigenin induce vasoprotection at the vasoactive concentrations in rat mesenteric artery. Rat mesenteric arterial rings were isolated for isometric force recording and electrophysiological studies. Perfusion pressure of mesenteric arterial bed was measured and visualization of superoxide production was detected with fluorescent dye. 300 microM pyrogallol significantly decreased the relaxation and hyperpolarization to ACh. Luteolin and apigenin both induced vasoprotection against loss of the EDHF component of ACh-induced relaxation and attenuated the impairment of hyperpolarization to ACh. Oxidative fluorescent microtopography showed that either luteolin or apigenin significantly reduced the superoxide levels. The results suggest that superoxide anion impairs ACh-induced relaxation and hyperpolarization of SMC in resistance arteries through the impairment of EDHF mediated responses. Luteolin and apigenin protect resistance arteries from injury, implying that they may be effective in therapy for vascular diseases associated with oxidative stress.

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.

Opening the calcium-activated potassium channel participates in the cardioprotective effect of puerarin.

The aim of the present study was to determine whether the effective cardioprotection conferred by puerarin against ischemia and reperfusion is mediated by the calcium-activated potassium channel. Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The production of formazan, which provides an index of myocardial viability, was measured by absorbance at 550 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was determined. Pretreatment with puerarin at 0.24 mmol/l for 5 min before ischemia increased myocardial formazan content and reduced LDH release during reperfusion. Administration of paxilline (1 micromol/l), an antagonist of the calcium-activated potassium channel, attenuated the protective effects of puerarin. In isolated ventricular myocytes, pretreatment with puerarin prevented simulated ischemia and reperfusion injury, hydrogen peroxide-induced cell death and the release of reactive oxygen species. Paxilline and chelerythrine (a protein kinase C inhibitor) both attenuated the effects of puerarin. These findings indicate that puerarin protects the myocardium against ischemia and reperfusion injury via opening the calcium-activated potassium channel and activating protein kinase C.

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.

[Cardioprotection of mitoSlo1 channel activation involves mitochondrial permeability transition in ischemia and reperfusion of rat hearts].

OBJECTIVE: To investigate whether the cardioprotection of mitochondrial Slo channel (mitoSlo(1) channel) is associated with mitochondrial permeability transition in isolated rat hearts subjected to ischemia and reperfusion. METHODS: Isolated perfused rat hearts were subjected to 30 min regional ischemia (occlusion of left anterior descending artery) and 120 min reperfusion. The infarct size, lactate dehydrogenase (LDH) release during reperfusion and ventricular hemodynamic parameters were measured. RESULTS: Pretreatment with mitoSlo(1) channel opener, NS1619 10 micromol/L for 10 min reduced the infarct size and LDH release, and improved the recovery of left ventricular developed pressure, left ventricular end-diastolic pressure, maximal rise/fall rate of left ventricular pressure and coronary flow during reperfusion. Administration of atractyloside (20 micromol/L), an opener of mitochondrial permeability transition pore, for 20 min (last 5 min of ischemia and first 15 min of reperfusion) attenuated the reduction of infarct size and LDH release and improvement of left ventricular performance induced by NS1619. In the isolated mitochondria, a significant inhibition of Ca(2+)-induced swelling was observed when mitochondria were incubated with NS1619. CONCLUSION: MitoSlo(1) channel activation by NS1619 protects the myocardium against ischemia and reperfusion injury by inhibiting mitochondrial permeability transition pore opening.

[Interleukin-2 induced endothelium-dependent relaxation of rat thoracic aorta].

Interleukin-2 (IL-2) therapy often results in potentially life-threatening side effects including hypotension. However, the mechanism has not been completely elucidated. In order to determine whether IL-2 modifies vascular tone, we investigated the effect of IL-2 on rat thoracic aorta rings and the underlying mechanisms. Effects of IL-2 on the contraction of high KCl and phenylephrine (PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique. To explore the mechanism, nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl ester (L-NAME), guanylyl cyclase inhibitor methylene blue, and cyclooxygenase inhibitor indomethacin were used. IL-2 (10-1000 U/ml) caused concentration-dependent relaxation of aorta rings preconstricted with PE (10 micromol/L) in endothelium-intact rings, but had no effect on KCl (120 mmol/L) preconstricted rings. Removal of the endothelium, or pretreatment with L-NAME (0.1 mmol/L) or methylene blue (10 micromol/L) or indomethacin (10 micromol/L), inhibited the relaxation of IL-2. The results indicate that the relaxation by IL-2 in rat aorta ring is endothelium-dependent and is possibly mediated by the NO-guanylyl cyclase pathway and cyclooxygenase-dependent pathway.

[Effect of interleukin-2 on the activity of Ca2+ ATPase and Na+/K+ ATPase of sarcoplasmic reticulum and sarcolemma].

The purpose of the present study was to investigate whether interleukin-2 (IL-2) changes the activity of sarcoplasmic reticulum (SR) Ca(2+) ATPase, sarcolemmal Ca(2+)ATPase and Na(+)/K(+) ATPase by measuring the Pi liberated from ATP hydrolysis with colorimetrical methods. It was shown that the activity of Ca(2+)ATPase in SR from IL-2-perfused (10, 40, 200, 800 U/ml) rat heart increased dose-dependently. After incubation of the SR with ATP (0.1 approximately 4 mmol/L), the activity of SR Ca(2+)ATPase increased dose-dependently in the control group. In the SR from 200 U/ml IL-2-perfused hearts, the activity of Ca(2+)ATPase was much higher than that in the control group. On the other hand, incubation of the SR with Ca(2+) (1 approximately 40 micromol/L) increased the activity of SR Ca(2+) ATPase in the control group. The activity of SR Ca(2+)ATPase of IL-2-perfused hearts was inhibited as the function to Ca(2+). Pretreatment with specific kappa-opioid receptor antagonist nor-BNI (10 nmol/L) for 5 min attenuated the effect of IL-2 (200 U/ml) on the activity of SR Ca(2+) ATPase. After pretreatment with pertussis toxin (PTX, 5 mg/L) or U73122 (5 micromol/L), IL-2 failed to increase SR Ca(2+)ATPase activity. The activity of SR Ca(2+)ATPase was not changed by incubation of SR isolated from normal hearts with IL-2. Perfusion of rat heart with IL-2 did not affect the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase. It is concluded that perfusion of rat heart with IL-2 increases the activity of SR Ca(2+)ATPase dose-dependently, which is mainly mediated by cardiac kappa-opioid receptor pathway including a PTX sensitive Gi-protein and phospholipase C. IL-2 increases the activity of SR Ca(2+)ATPase as the function to ATP, but inhibits the activity of SR Ca(2+)ATPase as the function to Ca(2+). IL-2 has no effect on the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase.

[Role of interleukin-2 in the functional myocardial impairment induced by anoxia and reoxygenation].

OBJECTIVE: To investigate the effect of interleukin-2 (IL-2) on myocardial impairment during ischemia/reperfusion or anoxia/reoxygenation. METHODS: Chemical anoxia was introduced in the isolated rat ventricular myocytes by Krebs-Henseleit (K-H) solution containing 10(-3) mol/L sodium dithionite. The video-tracking system and spectrofluorometric method were employed to verify the cell contraction and calcium homeostasis of the single myocyte. Radioimmunoassay was used to analyze the IL-2 levels in myocardium. RESULTS: The levels of IL-2 in myocardium subjected to ischemia/reperfusion were elevated [(14.34+/-5.99 compared with 22.25+/-3.68)ng/g, P<0.01]. During anoxia, cell contraction and the amplitude of electrically induced calcium transient were depressed and the parameters did not return to the pre-anoxia level during reoxygenation. IL-2 at 200 U/L administered during anoxia aggravated the effect of reoxygenation on cell contraction and calcium transient. After perfusion with IL-2, the malondialdehyde content of myocardial mitochondria was elevated. CONCLUSION: Coexistence of IL-2 during anoxia aggravates the effect of reoxygenation on the cell contraction and calcium homeostasis in the isolated rat ventricular myocytes, in which the mitochondrial lipid peroxidation induced by IL-2 is involved.

[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.