Jin-Cheng Liu

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (13)36.37 Total impact

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    ABSTRACT: Motilin is a 22-amino-acid gastrointestinal polypeptide that was first isolated from the porcine intestine. We identified that motilin receptor is highly expressed in GABAergic interneurons in the basolateral nucleus (BLA) of the amygdala, the structure of which is closely involved in assigning stress disorder and anxiety. However, little is known about the role of motilin in BLA neuronal circuits and the molecular mechanisms of stress-related anxiety. Whole-cell recordings from amygdala slices showed that motilin depolarized the interneurons and facilitated GABAergic transmission in the BLA, which is mimicked by the motilin receptor agonist, erythromycin. BLA local injection of erythromycin or motilin can reduce the anxiety-like behavior in mice after acute stress. Therefore, motilin is essential in regulating interneuron excitability and GABAergic transmission in BLA. Moreover, the anxiolytic actions of motilin can partly be explained by modulating the BLA neuronal circuits. The present data demonstrate the importance of motilin in anxiety and the development of motilin receptor non-peptide agonist as a clear target for the potential treatment of anxiety disorders.
    Molecular Neurobiology 01/2013; DOI:10.1007/s12035-012-8383-5 · 5.29 Impact Factor
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    ABSTRACT: One of the leading cause of death in the world is ischemia/reperfusion (I/R) -mediated acute myocardial infarction (AMI).There are a lot of Chinese traditional patent medicines, such as Xin'an Capsules, Xin Xuening Tablet and so on, which have the protective effects on myocardial I/R injury and have been routinely used in treating cardiac diseases for a long time in China. Hyperoside (Hyp) is the chief component of these medicines. This study investigated the action of Hyp in isolated myocardial I/R injury, as well as its possible mechanisms.Using the Langendorff model, isolated Sprague-Dawley rat hearts were subjected to 30min of global ischemia and 50min of reperfusion. Cardiac function was measured, and infarct size was evaluated by triphenyltetrazolium chloride staining at the end of the reperfusion. Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK). Myocardium was also measured for the activity of total superoxide dismutase (T-SOD) and the content of Malonaldialdehyde (MDA). Phosphorylation of extracellular signal-regulated protein kinase (ERK) was analyzed by Western blotting.We reported for the first time that administration of Hyp before/ after I/R significantly improved heart contraction and limited the infarct size, CK and LDH leakage from the damaged myocardium after I/R. The activity of SOD and the content of MDA remarkably changed in the presence of Hyp as well. Phosphorylation of ERK was significantly increased in Hyp-treated hearts when compared to controls (p<0.01). Hyp-induced ERK phosphorylation was inhibited by PD98059. We therefore conclude that Hyp can protect cardiomyocytes from I/R-induced oxidative stress through the activation of ERK-dependent signaling.
    Free Radical Biology and Medicine 01/2013; 57. DOI:10.1016/j.freeradbiomed.2012.12.023 · 5.71 Impact Factor
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    ABSTRACT: The G-protein coupled estrogen receptor 30 (GPR30) is a seven-transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was to investigate the effects of GPR30 on vascular responsiveness in diabetic ovariectomized (OVX) rats and elucidate the possible mechanism involved. The roles of GPR30 were evaluated in the thoracic aorta and cultured endothelial cells. The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. Dose-dependent vasoconstrictive responses to phenylephrine were attenuated significantly in the rings of the thoracic aorta following the acute G1 administration in the diabetic OVX rats. This effect of G1 was abolished partially by L-NAME and G15. The acute administration of G1 increased significantly the eNOS activity and the concentration of NO in the endothelial cells exposed to high glucose. G1 treatment induced an enhanced endothelium-dependent relaxation to acetylcholine (Ach) in the diabetic OVX rats. Further examination revealed that G1 induced vasodilation in the diabetic OVX rats by increasing the phosphorylation of eNOS. These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats.
    PLoS ONE 06/2012; 7(6):e38787. DOI:10.1371/journal.pone.0038787 · 3.53 Impact Factor
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    ABSTRACT: Hyperoside (Hyp) is a flavonoid compound isolated from Rhododendron ponticum L. leaves that elicits vascular protective effects in vitro. Treatment with Hyp has been found to attenuate endothelial cell damage induced by oxidative stress, but its mechanisms of action remain unclear. This study investigated the action of Hyp in an endothelial injury model induced by hydrogen peroxide (H(2)O(2)), as well as its possible mechanisms. Human umbilical vein endothelial cells (HUVECs) were treated with H(2)O(2) alone or in combination with Hyp. The protective effects of Hyp against H(2)O(2) were evaluated, and the activation of extracellular signal-regulated protein kinase (ERK) in Hyp was assayed in HUVECs. Loss of cell viability as well as excessive cell apoptosis and death were observed in HUVECs after 18 h of challenge with H(2)O(2) (400μM); however, both cell apoptosis and death were attenuated in the Hyp-pretreated cells. Western blot analysis revealed that Hyp increased the expression of Bcl-2 but decreased that of Bax. In addition, Hyp induced the phosphorylation of ERK1/2 in HUVECs. These observations provide preliminary evidence that Hyp protects HUVECs against H(2)O(2) damage, at least partially, by activating the ERK signaling pathway.
    Journal of ethnopharmacology 11/2011; 139(2):388-94. DOI:10.1016/j.jep.2011.11.020 · 2.94 Impact Factor
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    ABSTRACT: To evaluate the feasibility and short-term results of transcatheter aortic valve implantation (TAVI) using a new transcatheter valve. Twenty healthy adult sheep received general anesthesia. Under the guidance of X-ray and transthoracic echocardiography (TTE), the new anti-calcification transcatheter valve was released from delivery system and implanted at the level of native aortic annulus via left common carotid artery. Position and function of the new anti-calcification transcatheter valve were evaluated by angiography and TTE immediately after intervention. Thirty day survival rate of animals was obtained. New transcatheter valves were implanted in all sheep. Fifteen sheep (75%) survived up to 30 days and post-operative examination showed that the transcatheter valve was in optimal position without migration and mitral valve impingement. The native coronary artery was patent in these animals. There was a slight paravalvular leak in 5 sheep. Postoperative echocardiography showed reflux percentage was significantly increased (P < 0.05) compared pre-intervention. Effective orifice area, aortic systolic pressure, diastolic aortic pressure, mean aortic pressure, left ventricular systolic pressure, left ventricular end diastolic pressure and heart rate were similar between post and pre-intervention (all P < 0.05). Five sheep died after TAVI within 30 days, including one fatal ventricular fibrillation occurred immediately after releasing the transcatheter valve and another sheep died of acute myocardial infarction due to left main coronary artery occlusion evidenced by angiography. Two sheep died of severe mitral regurgitation at 8 and 12 hours post-operation and one died of infective endocarditis at 26 days after intervention. Our favorable preliminary results showed that it was feasible to perform TAVI using the new transcatheter valve.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 11/2011; 39(11):1005-10.
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    ABSTRACT: To evaluate the safety and efficacy of staged hybrid approach in treating ventricular septal defect (VSD) patients combined with patent ductus arteriosus (PDA) and pulmonary artery hypertension (PAH). From July 2004 to July 2009, 22 VSD patients with PDA and PAH were enrolled and received staged hybrid approach treatment (transcatheter PDA occlusion and elective open surgery for VSD several days after PDA occlusion). All patients were followed up to examine rhythm change, residual shunt, shape of occlude, possible valve regurgitation, and aortic stenosis by echocardiography. After transcatheter PDA occlusion, pulmonary arterial systolic pressure decreased from (76.2 ± 25.8) mm Hg (1 mm Hg = 0.133 kPa) to (55.4 ± 20.6) mm Hg (P = 0.005), mean pulmonary artery pressure decreased from (53.5 ± 23.5) mm Hg to (36.2 ± 17.8) mm Hg (P = 0.049), total pulmonary resistance decreased from (8.2 ± 4.9) wood units to (6.9 ± 4.3) wood units (P = 0.037), and pulmonary-to-systemic flow ratio (Qp/Qs) increased from 2.8 ± 2.3 to 3.4 ± 1.7 (P = 0.045) post transcatheter interventional PDA occlusion. After VSD repair, pulmonary arterial systolic pressure decreased from (64.5 ± 22.3) mm Hg to (43.1 ± 18.9) mm Hg (P = 0.001) and mean pulmonary artery pressure decreased from (40.2 ± 18.7) mm Hg to (29.5 ± 15.8) mm Hg (P = 0.040). There was no death or right heart failure during the follow-up. Staged hybrid approach is an effective and safe strategy for treating VSD patients with PDA and PAH.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 02/2011; 39(2):128-31.
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    CardioVascular and Interventional Radiology 11/2010; 34(1). DOI:10.1007/s00270-010-0043-4 · 1.97 Impact Factor
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    ABSTRACT: 1. Serotonin (5-hydroxytryptamine; 5-HT) plays important roles in the development of cardiac hypertrophy via activation of 5-HT receptors. The aim of the present study was to investigate the role of 5-HT(2B) receptors in the development of cardiomyocyte apoptosis and hypertrophy associated with noradrenaline (NA) overload. 2. Cardiac hypertrophy was induced in rats by intraperitoneal injection of 1.5 mg/kg NA for 4 weeks. Starting from Day 15, 5-HT2B receptor antagonist SB 204741 (i.p., 0.5 or 2 mg/kg) or SDZ SER 082 (i.p., 1 mg/kg) was injected twice daily for another 14 days. Whole-cell patch-clamp techniques were used to record ionic currents in freshly isolated ventricular cardiomyocytes. Western blot and terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling (TUNEL) assays were used to assess myocardial apoptosis. 3. Expression of 5-HT(2B) receptors was enhanced in the hypertrophic left ventricle induced by NE overload in vivo. The 5-HT(2B) receptor antagonist SB 204741 partially reversed cardiac hypertrophy induced by NE overload (P < 0.05) and decreased L-type calcium currents in ventricular cardiomyocytes (P < 0.05). In addition, SB 204741 notably attenuated myocardial apoptosis, as evidenced by downregulation of Bax and caspase 3 (P < 0.05) and upregulation of the anti-apoptotic Bcl-2 protein (P < 0.05). 4. In conclusion, the data suggest an involvement of 5-HT(2B) receptors in the generation of apoptotic events associated with cardiac remodelling during increased adrenergic stimulation.
    Clinical and Experimental Pharmacology and Physiology 03/2010; 37(7):e145-51. DOI:10.1111/j.1440-1681.2010.05388.x · 2.41 Impact Factor
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    ABSTRACT: The aim of the present study was to determine whether U50,488H, a selective kappa-opioid receptor agonist, inhibits the remodeling of the pulmonary artery (PA). In addition, changes in the concentrations of nitric oxide (NO), endothelin (ET) and angiotensin II (AngII) in hypoxic pulmonary hypertensive (HPH) rats were investigated to explore the mechanisms underlying the effects of U50, 488H on HPH. We found that intraperitoneal administration of U50,488H (every other day) during hypoxia depressed mean pulmonary arterial pressure (mPAP) and attenuated right ventricular pressure (RVP) and right ventricular hypertrophy, at the same time it inhibited remodeling of the PA compared with hypoxia for 2 wk. Moreover, U50,488H also inhibited proliferation of the pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia for 48 h in a dose-dependent manner. Compared with the 2 wk hypoxia group, U50,488H increased the concentration of NO and decreased the production of ET and AngII (P<0.01). In addition, acute intravenous administration of U50,488H after hypoxia for 4 wk decreased mPAP. Our results suggest that effects of anti-remodeling of the PA and anti-proliferation of the PASMC, and regulation of the vasomotor factors in both blood and pulmonary tissues of HPH rats may be critical mechanisms underlying the preventive and therapeutic effects of U50,488H in HPH rats.
    Vascular Pharmacology 04/2009; 51(2-3):72-7. DOI:10.1016/j.vph.2009.03.003 · 4.62 Impact Factor
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    ABSTRACT: Gentiopicroside is one of the secoiridoid compound isolated from Gentiana lutea. It exhibits analgesic activities in the mice. The anterior cingulate cortex (ACC) is a forebrain structure known for its roles in pain transmission and modulation. Painful stimuli potentiate the prefrontal synaptic transmission and induce glutamate NMDA NR2B receptor expression in the ACC. But little is known about Gentiopicroside on the persistent inflammatory pain and chronic pain-induced synaptic transmission changes in the ACC. The present study was undertaken to investigate its analgesic activities and central synaptic modulation to the peripheral painful inflammation. Gentiopicroside produced significant analgesic effects against persistent inflammatory pain stimuli in mice. Systemic administration of Gentiopicroside significantly reversed NR2B over-expression during the chronic phases of persistent inflammation caused by hind-paw administration of complete Freunds adjuvant (CFA) in mice. Whole-cell patch clamp recordings revealed that Gentiopicroside significantly reduced NR2B receptors mediated postsynaptic currents in the ACC. Our findings provide strong evidence that analgesic effects of Gentiopicroside involve down-regulation of NR2B receptors in the ACC to persistent inflammatory pain.
    Neuropharmacology 07/2008; 54(8):1175-81. DOI:10.1016/j.neuropharm.2008.03.007 · 4.82 Impact Factor
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    ABSTRACT: The modulation of beta-adrenoceptor signaling in the hearts of hindlimb unweighting (HU) simulated weightlessness rats has not been reported. In the present study, we adopted the rat tail suspension for 4 wk to simulate weightlessness; then the effects of simulated microgravity on beta-adrenoceptor signaling were studied. Mean arterial blood pressure (ABP), left ventricular pressure (LVP), systolic function (+dP/dtmax), and diastolic function (-dP/dtmax) were monitored in the course of the in vivo experiment. Single rat ventricular myocyte was obtained by the enzymatic dissociation method. Hemodynamics, myocyte contraction, and cAMP production in response to beta-adrenoceptor stimulation with isoproterenol or adenylyl cyclase stimulation with forskolin were measured, and Gs protein was also determined. Compared with the control group, no significant changes were found in heart weight, body weight and ABP, while LVP and +/-dP/dtmax were significantly reduced. The ABP decrease, LVP increase, and +/-dP/dtmax in response to isoproterenol administration were significantly attenuated in the HU group. The effects of isoproterenol on electrically induced single-cell contraction and cAMP production in myocytes of ventricles in the HU rats were significantly attenuated. The biologically active isoform, Gsalpha (45 kDa) in the heart, was unchanged. Both the increased electrically induced contraction and cAMP production in response to forskolin were also significantly attenuated in the simulated weightlessness rats. Above results indicated that impaired function of adenylyl cyclase causes beta-adrenoceptor desensitization, which may be partly responsible for the depression of cardiac function.
    Journal of Applied Physiology 06/2008; 105(2):569-74. DOI:10.1152/japplphysiol.01381.2007 · 3.43 Impact Factor
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    ABSTRACT: Surgical repair and endovascular stent-graft placement are both therapies for thoracic aortic dissection. A combination of these two approaches may be effective in patients with type A dissection. In this study, we evaluated the prognosis of this combined technique. From December 2003 to December 2006, 15 patients with type A dissection were admitted to our institute; clinical data were retrospectively reviewed. Follow-up was performed at discharge and approximately 12 months after operation. Endovascular stent-graft placement by interventional radiology and surgical repair for reconstruction of aortic arch was performed in all patients. Total arch replacement for distal arch aneurysm was carried out under deep hypothermia with circulatory arrest; antegrade-selected cerebral perfusion was used for brain protection. Four patients concomitantly received a coronary artery bypass graft. Hospital mortality rate was 6.7%; the patient died of cerebral infarction. Neural complications developed in two patients. Multi-detector-row computed tomography scans performed before discharge revealed complete thrombosis of the false lumen in six patients and partial thrombosis in eight patients. At the follow-up examination, complete thrombosis was found in another three patients, aortic rupture, endoleaks or migration of the stent-graft was not observed and injuries of peripheral organs or anastomotic endoleaks did not occur. For patients with aortic type A dissection, combining intervention and surgical procedures is feasible, and complete or at least partial thrombosis of the false lumen in the descending aorta can be achieved. This combined approach simplified the surgical procedures and shortened the circulatory arrest time, minimizing the necessity for further aortic operation.
    International Journal of Surgery (London, England) 05/2008; 6(2):151-6. DOI:10.1016/j.ijsu.2008.02.004 · 1.65 Impact Factor
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    ABSTRACT: Optimal management of muscular ventricular septal defects (MVSDs) remains controversial. Left ventriculotomy is the cornerstone of surgical repair but is frequently complicated by residual shunts, left ventricular dysfunction, apical aneurysm, or arrhythmias. In this study, we evaluated the long-term outcomes of surgical repairs in infants with isolated MVSDs. We retrospectively analyzed clinical data from 56 children with MVSDs (31 males, 25 females). Follow-up by questionnaire and Doppler echocardiography was performed at discharge and between 2 and 124 months after surgery. Patient age was 2 to 40 months (median, 21 months) and weight was 3.0 to 15.3 kg (median, 5.3 kg). Two patients died after surgery (hospital mortality, 3.57%). One patient with MVSDs died of low cardiac output caused by the long duration of cardiopulmonary bypass. Another patient with Swiss cheese MVSD received a single patch closure but died of low cardiac output immediately after cardiopulmonary bypass. Immediate complications such as a third-degree atrial-ventriclar block occurred in 2 patients, but they recovered before discharge and showed no residual shunt. No deaths occurred during follow-up, but a residual shunt was found in 1 patient. Delayed complete heart block requiring a pacemaker occurred in 1 patient. One patient showed paroxysmal supraventricular tachycardia that was treated with amiodarone. The left ventricular ejection fraction was 0.45-0.55 in 8 patients and 0.55-0.73 in 46 patients. No apical aneurysm was found. All the surviving patients returned to normal school life. Our results indicate that surgery is a suitable treatment option in infants and children with isolated MVSDs and that preoperative diagnosis is crucial to a successful outcome. Infants can tolerate a left ventriculotomy incision for MVSDs in the lower or apical ventricular septum.
    Heart Surgery Forum 02/2008; 11(2):E78-81. DOI:10.1532/HSF98.20071202