Objective: To investigate the effects of electroacupuncture (EA) on the behaviors of rat with anxiety disorder, and the expressions of hippocampal neurotransmitters including 5-hydroxytryptamine (5-HT), norepinephrine (NE) and dopamine (DA), and the expressions of hippocampal B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X (Bax).Methods: Forty-six male Wistar rats were randomly divided into a control group (n=10), a model group (n=12), an EA group (n=12), and a drug group (n=12). Except the control group, the other three groups were established into rat models of anxiety disorder using uncertain empty bottle stimulation. Rats in the EA group and the drug group received corresponding interventions for 15 consecutive days [EA group was given EA at Baihui (GV 20) and Sanyinjiao (SP 6); the drug group was given aqueous solution of alprazolam via intragastric administration]. After intervention, all four groups received open-field test (OFT) and elevated plus-maze (EPM) for behavioral evaluations. The expressions of 5-HT, NE and DA in hippocampus were determined by fluorescence spectroscopy (FS) while the expressions of Bcl-2 and Bax proteins in hippocampus were determined by Western blot (WB). Results: The OFT horizontal scores in the control group, EA group and drug group were significantly higher than that in the model group (all P<0.05), and the difference between the EA group and the drug group was statistically insignificant (P>0.05); the OFT vertical scores in the model group, EA group and drug group were significantly lower than the score in the control group (all P<0.05). The EPM percent of open-arm entries (OE％) in the control group, EA group and drug group was higher than that in the model group (P<0.05), and the differences among these three groups were statistically insignificant (P>0.05); though the percent of open-arm total time (OT％) in the EA group was lower than that in the control group (P<0.05), the difference was statistically insignificant when compared with the drug group (P>0.05), and it was significantly higher than that in the model group (P<0.05). The expression of 5-HT in the EA group was higher than that in the control group (P<0.05); the expression of 5-HT in the EA group was significantly lower than that in the model group (P<0.05); the difference between the EA group and the drug group was statistically insignificantly (P>0.05). The expression of NE in the model group was significantly higher than that in the other three groups (P<0.05), and there was no significant difference among these three groups (P>0.05). The expression of DA in the EA group was significantly higher than that in the control group and the drug group (both P<0.05), while the difference between the EA group and the model group was statistically insignificant (P>0.05). The expression of Bax in the model group was significantly higher than that in the other three groups (all P<0.05), whereas the expression of Bcl-2 in the model group was significantly lower than that in the other three groups (all P<0.05), and the differences in both Bax and Bcl-2 among the other three groups were statistically insignificant (all P>0.05). Bax/Bcl-2 in the EA group was significantly higher than that in the control group (P<0.05) and lower than that in the model group (P<0.05), and the difference was statistically insignificant when compared with the drug group (P>0.05). Conclusion: EA shows promising effects in attenuating rats' anxiety disorder, which may be achieved by the down-regulation of the expressions of 5-HT and NE in the hippocampus and/or inhibition of hippocampal neuronal apoptosis. The efficacy is comparable to that of intervention with alprazolam.

OBJECTIVETo investigate the effects and underlying mechanisms of interferon-alpha (IFN-alpha) on the isolated Langendorff perfused rat hearts and the isolated papillary muscles.

METHODSThe left ventricular developed pressure (LVDP), maximal rise/fall rate of left ventricular pressure (+/-dP/dt(max)), left ventricular end-diastolic pressure (LVEDP), heart rate (HR) and coronary flow (CF) were recorded in isolated Langendorff perfused rat hearts. The average contractile force was measured in the isolated papillary muscles of rat right ventricle.

RESULTIFN-alpha (10 - 10,000 U/ml) induced a concentration-dependent decrease of LVDP and +/-dP/dt(max), and increase of LVEDP and CF in the isolated perfused rat heart (P < 0.05), and decrease of the average contractile force of the papillary muscle (P <0.05). Pretreatment with L-NAME (10(-4) mol/L), an inhibitor of nitric oxide synthase, attenuated the effect of IFN-alpha in the isolated rat hearts and the isolated papillary muscles (P <0.05). Isoproterenol (ISO, 10(-9) - 10(-6)mol/L) increased the contractile force of the rat papillary muscles in a concentration-dependent manner. Perfusion for 10 min with IFN-alpha at 1,000 U/ml attenuated the enhancing effect of ISO. Pretreatment with L-NAME reduced the effects of IFN-alpha on the isolated papillary muscles.

CONCLUSIONIFN-alpha may induce a negative inotropic effect in normal and beta-adrenergic activated cardiac muscles and this effect at least partly be mediated by nitric oxide.

Animals ; Heart ; drug effects ; physiology ; Heart Rate ; drug effects ; In Vitro Techniques ; Interferon-alpha ; pharmacology ; Male ; Myocardial Contraction ; drug effects ; Myocardium ; metabolism ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; antagonists & inhibitors ; metabolism ; Papillary Muscles ; drug effects ; metabolism ; physiology ; Perfusion ; Rats ; Rats, Sprague-Dawley

Objective To explore the changes of the levels of interleukin-17(IL-17),matrix metalloproteinases-9(MMP-9) and immunoglobulin E(IgE) in serum of asthmatic children and analyzing the correlation.Methods Twenty-eight asthmatic children and 14 healthy children were collected to determin the levels of IL-17,MMP-9 by sandwich enzyme linked immunosorbent assay,and the correlation of IL-17,MMP-9 and IgE in serum were analyzed.Results The levels of IL-17,MMP-9 and total IgE in serum of asthmatic children were significantly higher than that of control group(Pa0.05).Conclusions The levels of IL-17 and MMP-9 increase in asthmatic airway inflammation.IL-17 and MMP-9 play an important role in asthmatic airway inflammation and airway rebuilding.

Aged ; CD5 Antigens ; metabolism ; Chromosomes, Human, Pair 11 ; Chromosomes, Human, Pair 14 ; Cyclin D1 ; metabolism ; Diagnosis, Differential ; Female ; Humans ; Liver Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Lymphoma, B-Cell ; metabolism ; pathology ; Lymphoma, Follicular ; metabolism ; pathology ; Lymphoma, Mantle-Cell ; genetics ; metabolism ; pathology ; surgery ; Pseudolymphoma ; metabolism ; pathology ; Translocation, Genetic

The association between atrial fibrillation (AF) after coronary artery bypass grafting (CABG) and the surgical techniques selected has been extensively reported.However,no consistent results were obtained.In the present study,a meta-analysis was conducted by searching the electronic databases PubMed,Embase,Web of Science,and Cochrane to identify the association of post-CABG AF with on-pump (conventional CABG,cCABG) or off-pump CABG (OPCABG).Outcomes from randomized clinical trials (RCTs) and propensity score matching (PSM) trials were pooled by using the fixed-effect or the random-effect modeling method,and verified by the quality-effect modeling method.There were 35 studies with 36 independent reports that met the inclusion criteria and were eventually included in our meta-analysis.The total odds ratio (OR) of the incidence of post-CABG AF between OPCABG and cCABG was 0.80 (95％ CI 0.71-0.91).The 25 randomized clinical trials (RCTs) had an OR of 0.69 (95％ CI 0.56-0.86),while the OR of the 11 PSM trials was 0.88 (95％ CI 0.77-1.00).Twenty-six studies involving the patients at a mean age no more than 65 years showed an OR of 0.76 (95％ CI 0.64-0.90),whereas 10 studies with patients greater than 65 years old showed an OR of 0.90 (95％ CI 0.78-1.05).The results of this meta-analysis suggest that OPCAB surgery may reduce the incidence of post-CABG AF when compared to cCABG and that younger patients may benefit more from OPCAB and have a lower incidence ofpost-CABG AF.

This study investigated the effect of arctigenin (Arc) on the cell activation, cytokines expression, proliferation, and cell-cycle distribution of mouse T lymphocytes. Mouse lymphocytes were prepared from lymph node and treated with Phorbol-12-myristate-13-acetate (PMA)/Ionimycin (Ion) and/or Arc. CD69, CD25, cytokines, proliferation and cell cycle were assayed by flow cytometry. The results showed that, at concentrations of less than 1.00 micromol x L(-1), Arc expressed non-obvious cell damage to cultured lymphocytes, however, it could significantly down-regulate the expression of CD69 and CD25, as well as TNF-alpha, IFN-gamma, IL-2, IL-4, IL-6 and IL-10 on PMA/Ion stimulated lymphocytes. At the same time, Arc could also inhibit the proliferation of PMA/Ion-activated lymphocytes and exhibited lymphocyte G 0/G1 phase cycle arrest. These results suggest that Arc possesses significant anti-inflammatory effects that may be mediated through the regulation of cell activation, cytokines expression and cell proliferation.
Animals ; Anti-Inflammatory Agents ; isolation & purification ; pharmacology ; Antigens, CD ; metabolism ; Antigens, Differentiation, T-Lymphocyte ; metabolism ; Arctium ; chemistry ; Cell Cycle Checkpoints ; drug effects ; Cell Proliferation ; drug effects ; Cytokines ; metabolism ; Female ; Furans ; isolation & purification ; pharmacology ; Interferon-gamma ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-2 ; metabolism ; Interleukin-2 Receptor alpha Subunit ; metabolism ; Interleukin-4 ; metabolism ; Interleukin-6 ; metabolism ; Ionomycin ; pharmacology ; Lectins, C-Type ; metabolism ; Lignans ; isolation & purification ; pharmacology ; Lymphocyte Activation ; drug effects ; Mice ; Mice, Inbred BALB C ; Plants, Medicinal ; chemistry ; T-Lymphocytes ; cytology ; drug effects ; immunology ; Tetradecanoylphorbol Acetate ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

AIMTo determine whether the cardioprotection of puerarin (Pue) against ischemia/reperfusion (I/R) is mediated by mitochondrial transmembrane pore or channels.

METHODSMale Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Formazan, a product of 2,3,5-triphenyltetrazolium 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.

RESULTSThe pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased formazan content of myocardium, reduced LDH release, improved the recovery of the left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure, left ventricular end-diastolic pressure and rate pressure product (left ventricular developed pressure multiplied by heart rate) and attenuated the decrease of coronary flow during reperfusion. Administration of atractyloside (20 micromol/L), an opener of mitochondrial permeability transition pore, for 20 min (first 20 min of reperfusion) and 5-hydroxydecanoate (100 micromol/L), the mitochondrial specific K(ATP) blocker, for 20 min before ischemia attenuated the protective effects of Pue.

CONCLUSIONThe findings indicate that in the isolated rat heart, Pue protects myocardium against ischemia/ reperfusion injury via the opening of mitochondrial ATP-sensitive potassium channel and the inhibition of mitochondrial permeability transition pore opening.

Animals ; Decanoic Acids ; metabolism ; Hydroxy Acids ; metabolism ; Isoflavones ; pharmacology ; Male ; Mitochondria, Heart ; drug effects ; metabolism ; Mitochondrial Membrane Transport Proteins ; drug effects ; Myocardial Reperfusion Injury ; metabolism ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the inhibitory effect of the deep peroneal nerve (DPN) on the cardiovascular responses induced by excitation of the paraventricular nucleus of hypothalamus (PVN) and the role of central nucleus of amygdala (CeA) in this effect.

METHODSCeA was injected by L-glutamate or Kainic acid (KA). The femoral arterial pressure, mean arterial pressure (MAP), electrocardiogram (ECG) and heart rate (HR) of SD rats were recorded while PVN or DPN was electrically stimulated.

RESULTSIt showed that MAP increased when PVN was activated by electrical stimulation. Stimulating contralateral DPN inhibited this pressor response. Ten minutes after microinjection of KA(0.02 mol/L, 100 nl) into ipsilateral CeA, MAP increased for (13.8 +/- 3.2) mmHg when PVN was stimulated. Microinjection of KA into CeA could not only reduce the pressor response elicited by stimulation of PVN for (6.6 +/- 1.6) mmHg (P < 0.05), but also the inhibitory effect of DPN from 51.5% to 32.0% .

CONCLUSIONThe results suggest that central nucleus of amygdala partly mediate the central pressor response induced by stimulation of PVN. The neurons in central nucleus of amygdala are involved in the inhibitory effect of DPN on the above pressor response.

Afferent Pathways ; Amygdala ; physiology ; Animals ; Blood Pressure ; Central Nervous System ; physiology ; Hypothalamus ; physiology ; Paraventricular Hypothalamic Nucleus ; physiology ; Peroneal Nerve ; physiology ; Rats ; Rats, Sprague-Dawley

AIMTo determine whether activation of kappa-opioid receptor with U50,488H, a selective kappa-opioid receptor agonist, produces any changes in electrical uncoupling during prolonged ischemia and whether these changes in electrical uncoupling is associated with the cardioprotection induced by kappa-opioid receptor activation, and to explore the possible mechanism.

METHODS(1) To observe the effect of U50,488H (10(-7), 10(-6), 3 x10(-6) and 10(-5) mol/L), a selective kappa-opioid receptor agonist, or with a selective kappa-opioid receptor antagonist nor-BNI (5 x 10(-6) mol/L), or with a mitochondrial K(ATP) channel inhibitor 5-HD on myocardium during ischemia/reperfusion in isolated perfused rat heart. Parameters of measurements include hemodynamic data, formazan content, heart rate, coronary flow, and lactate dehydrogenase (LDH). (2) To examine the effect of U50,488H of different concentration on electrical coupling parameters (including onset of uncoupling, plateau time, slope, and fold increase in r1) during 70 min myocardial ischemia in isolated perfused rat heart.

RESULTS(1) Pretreatment with U50,488H concentration dependently increased formazan content and reduced LDH release induced by 30 min of ischemia and 120 min of reperfusion. (2) The onset of electrical uncoupling and plateau time during prolonged ischemia was delayed by kappa-opioid receptor activation with U50,488H. (3) Linear regression analysis shown that the increase in formazan content and decrease in LDH release produced by kappa-opioid receptor activation was associated with delayed electrical uncoupling during prolonged ischemia. (4) The effects of U50,488H on formazan content, LDH release and on electrical coupling were abolished by nor-BNI, or 5-HD.

CONCLUSIONThis results demonstrate that the onset of electrical uncoupling during prolonged ischemia is delayed by kappa-opioid receptor activation with a selective kappa-opioid receptor agonist U50,488H, and that delayed electrical uncoupling is associated with the cardioprotection induced by kappa-opioid receptor activation with U50,488H. These effects of kappa-opioid receptor activation with U50,488H are mediated by mitochondrial K(ATP) channels.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ; pharmacology ; Animals ; Antihypertensive Agents ; Heart ; drug effects ; physiopathology ; In Vitro Techniques ; Male ; Myocardial Ischemia ; physiopathology ; Myocardium ; metabolism ; Naltrexone ; analogs & derivatives ; pharmacology ; Potassium Channels ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa ; agonists

OBJECTIVETo investigate the role of mitochondrial calcium uniporter in cardioprotection elicited by ischemic postconditioning (Postcond).

METHODSMale Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Left ventricular developed pressure (LVDP), maximal rise/fall rate of left ventricular pressure (± dP/dtmax) were measured. The level of lactate dehydrogenase (LDH) in the coronary effluent was measured spectrophotometrically, the content of formazan of myocardium was also measured at the end of reperfusion.

RESULTCompared to I/R group, Postcond had an significant increase in the mechanical function of the left ventricle, with LDH release reduced and the content of formazan increased. Spermine, the opener of mitochondrial calcium uniporter, deteriorated the mechanical function of left ventricle and decreased the formazan content, and increased LDH release. Ruthenium red, the inhibitor of mitochondrial calcium uniporter, increased the mechanical function of the left ventricle, decreased the LDH release, but the content of formazan was not increased.

CONCLUSIONThe inhibition of mitochondrial calcium uniporter is involved in the mechanisms of ischemic postconditioning.

Animals ; Calcium Channels ; metabolism ; physiology ; Disease Models, Animal ; Formazans ; analysis ; Heart ; physiopathology ; Ischemic Postconditioning ; L-Lactate Dehydrogenase ; analysis ; Male ; Myocardial Reperfusion Injury ; metabolism ; physiopathology ; prevention & control ; Rats ; Rats, Sprague-Dawley