Zhong Dai

Publications (9)34.9 Total impact

• Article: Stimulation of Calcitonin Gene-Related Peptide Release Through Targeting Capsaicin Receptor: A Potential Strategy for Gastric Mucosal Protection.

  Xiu-Ju Luo, Bin Liu, Zhong Dai, Zhi-Chun Yang, Jun Peng
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  ABSTRACT: Calcitonin gene-related peptide (CGRP) is a predominant neurotransmitter from capsaicin-sensitive sensory nerves, which are widely distributed in the gastrointestinal system. These sensory nerves are reported to be involved in the protection of gastric mucosa against damage by various stimuli, and CGRP is a potential mediator in this process. In addition to increase in gastric mucosal blood flow, the beneficial effects of CGRP on gastric mucosa include inhibition of gastric acid secretion, prevention of cellular apoptosis and oxidative injury. The synthesis and release of CGRP is regulated by the capsaicin receptor which is known as transient receptor potential vanilloid subfamily member 1 (TRPV1) and the agonists of TRPV1 have the potential for gastric mucosal protection. So far, multiple TRPV1 agonists, including capsaicin, capsiate, anandamide and rutaecarpine are reported to exert beneficial effects on gastric mucosal injury induced by various stimuli. Therefore, the TRPV1/CGRP pathway represents a novel target for therapeutic intervention in human gastric mucosal injury.
  Digestive Diseases and Sciences 08/2012; · 2.12 Impact Factor
• Article: Alpha lipoic acid protects heart against myocardial ischemia-reperfusion injury through a mechanism involving aldehyde dehydrogenase 2 activation.

  Lan He, Bin Liu, Zhong Dai, Hong-Feng Zhang, Yi-Shuai Zhang, Xiu-Ju Luo, Qi-Lin Ma, Jun Peng
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  ABSTRACT: Recent studies demonstrate that alpha lipoic acid can prevent nitroglycerin tolerance by restoring aldehyde dehydrogenase 2 (ALDH2) activity and ALDH2-mediated detoxification of aldehydes is thought as an endogenous mechanism against ischemia-reperfusion injury. This study was performed to explore whether the cardioprotective effect of alpha lipoic acid was related to activation of ALDH2 and the underlying mechanisms. In a Langendorff model of ischemia-reperfusion in rats, cardiac function, activities of creatine kinase (CK) and ALDH2, contents of 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) were measured. In a cell model of hypoxia-reoxygenation, the apoptosis, ALDH activity, reactive oxygen species level, 4-HNE and MDA contents were examined. In the isolated hearts, ischemia-reperfusion treatment led to cardiac dysfunction accompanied by an increase in 4-HNE and MDA contents. Pretreatment with lipoic acid significantly up-regulated myocardial ALDH2 activity concomitantly with an improvement of cardiac dysfunction and a decrease in 4-HNE and MDA contents, these effects were blocked by the inhibitor of ALDH2. Similarly, in the cultured cardiomyocytes, hypoxia-reoxygenation treatment induced apoptosis accompanied by an increase in the production of reactive oxygen species, 4-HNE and MDA. Administration of lipoic acid significantly up-regulated cellular ALDH2 activity concomitantly with a reduction in apoptosis, production of reactive oxygen species, 4-HNE and MDA, these effects were reversed in the presence of ALDH2 or PKCε inhibitors. Our results suggest that the cardioprotective effects of lipoic acid on ischemia-reperfusion injury are through a mechanism involving ALDH2 activation. The regulatory effect of lipoic acid on ALDH2 activity is dependent on PKCε signaling pathway.
  European journal of pharmacology 03/2012; 678(1-3):32-8. · 2.59 Impact Factor
• Article: Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release.

  Nian-Sheng Li, Xiu-Ju Luo, Zhong Dai, Bin Liu, Yi-Shuai Zhang, Zhi-Chun Yang, Jun Peng
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  ABSTRACT: Capsiate is a non-pungent analogue of capsaicin from CH-19 Sweet peppers. Capsaicin is reported to trigger calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the oral administration of acidified ethanol. Gastric tissues were collected for analysis of the gastric ulcer index, cellular apoptosis, activities of caspase-3, catalase and superoxide dismutase (SOD), and levels of CGRP, TNF-α, and malondialdehyde (MDA). Our results show that the acute administration of ethanol significantly increased the gastric ulcer index concomitantly with an increase in cellular apoptosis, caspase-3 activity, and TNF-α and MDA levels, as well as a decrease in the activities of catalase and SOD. Pretreatment with 1 mg/kg capsiate attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level, catalase, and SOD activities, and a decrease in caspase-3 activity, and TNF-α and MDA levels. The effects of capsiate were inhibited by capsazepine, an antagonist of TRPV1. These results suggest that capsiate is able to produce beneficial effects on ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1.
  Planta Medica 09/2011; 78(1):24-30. · 2.15 Impact Factor
• Article: Rutaecarpine inhibits hypoxia/reoxygenation-induced apoptosis in rat hippocampal neurons.

  Zhong Dai, Jian Xiao, Si-Yu Liu, Liao Cui, Gao-Yun Hu, De-Jian Jiang
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  ABSTRACT: Our previous studies showed that rutaecarpine (Rut) protected against myocardial ischemia/reperfusion (I/R) injury, which was associated with activation of transient receptor potential vanilloid subtype 1 (TRPV1). Recently, TRPV1 activation was also reported to exert neuroprotective effects. The present study was to investigate the effect of Rut on hypoxia/reoxygenation (H/R)-induced apoptosis in primary rat hippocampal neurons. Three-hour hypoxia (1% O2) and consequent 24-h reoxygenation significantly increased the apoptotic death of hippocampal neurons as evidenced by increases in both TUNEL-positive cell number and caspase-3 activity. However, pretreatment with Rut (1-10microM) or caspase-3 specific inhibitor DEVD-CHO could markedly attenuate H/R-induced apoptosis in neurons. Rut markedly induced the phosphorylation of Akt and PI3K inhibitor LY294002 prevented the survival effect of Rut on neurons. Intracellular oxidative stress was significantly induced after H/R, which was inhibited by Rut and LY294002 as well as antioxidant PDTC. TRPV1 antagonist capsazepine or intracellular Ca2+ chelator BAPTA/AM could abolish these effects of Rut mentioned above. In summary, the present data suggest that Rut inhibits H/R-induced apoptosis of hippocampal neurons via TRPV1-[Ca2+]i-dependent and PI3K/Akt signaling pathway, which is related to inhibiting oxidative stress and caspase-3 activation.
  Neuropharmacology 10/2008; 55(8):1307-12. · 4.81 Impact Factor
• Article: Asymmetric dimethylarginine induces apoptosis via p38 MAPK/caspase-3-dependent signaling pathway in endothelial cells.

  De-Jian Jiang, Su-Jie Jia, Zhong Dai, Yuan-Jian Li
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  ABSTRACT: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), is emerging as a key contributor for endothelial dysfunction and its effects on endothelium are not yet completely defined. The aim of this study was to investigate ADMA-induced apoptosis and its mechanisms in human umbilical vein endothelial cells (HUVECs). Apoptosis was evaluated by in situ terminal uridine nick end labeling (TUNEL) assay and DNA fragmentation analysis. Caspase-3 activity was measured using a colorimetric protease assay kit. Activations of mitogen-activated protein kinases (MAPKs) were characterized by Western blot and immunofluorescence. Intracellular oxidant production was measured using H(2)DCF-DA, an oxidant-sensitive fluorescent indicator. ADMA (3-30 microM) induced apoptosis of HUVECs in a dose- and time-dependent manner. Caspase-3 was activated during apoptosis and its specific inhibitor DEVD-CHO significantly attenuated ADMA-induced apoptosis. Phosphorylation of p38 MAPK was induced by ADMA, and p38 MAPK specific inhibitor SB203580 concentration-dependently prevented ADMA-induced caspase-3 activation and cell apoptosis. ADMA increased intracellular oxidant production, which was significantly suppressed by intracellular antioxidant PDTC, l-arginine or antisense endothelial NOS mRNA. They also markedly prevented ADMA-induced phosphorylation of p38 MAPK and cell apoptosis. In conclusion, our present results demonstrate that ADMA induces apoptosis of endothelial cell via elevation of intracellular oxidant production, which involves p38 MAPK/caspase-3-dependent signaling pathway.
  Journal of Molecular and Cellular Cardiology 05/2006; 40(4):529-39. · 5.17 Impact Factor
• Article: 3,4,5,6-Tetrahydroxyxanthone prevents vascular endothelial cell apoptosis induced by high glucose.

  Zhong Dai, Duan-Fang Liao, De-Jian Jiang, Han-Wu Deng, Yuan-Jian Li
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  ABSTRACT: Apoptosis of endothelial cells may be an important risk factor contributing to the incidence of vascular complications in diabetes. In the present study, we tested the effect of 3,4,5,6-tetrahydroxyxanthone, a synthetic xanthone derivative, on apoptosis induced in human umbilical vein endothelial cells (HUVEC) by a high glucose concentration. Cell apoptosis was detected using DNA ladder formation and flow cytometric techniques. The expression of Bcl-2 protein was analysed using flow cytometric techniques. Lactate dehydrogenase (LDH) activity and malonyldialdehyde (MDA) content in the medium were measured. Cell viability was assayed by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) method. Exposure of HUVEC to a high glucose concentration (30 mM) for 48 h markedly increased LDH release and MDA content in the medium and induced apoptosis and Bcl-2 protein expression in HUVEC. Pretreatment with 3,4,5,6-tetrahydroxyxanthone (1, 3 or 10 microM) or probucol (10 microM) significantly decreased the level of LDH and MDA in the medium, reduced apoptosis and increased the expression of Bcl-2 protein in HUVEC. These results suggest that 3,4,5,6-tetrahydroxyxanthone inhibits high-glucose-induced endothelial cell apoptosis by increasing Bcl-2 protein expression in HUVEC.
  Archiv für Experimentelle Pathologie und Pharmakologie 11/2004; 370(4):314-9. · 2.65 Impact Factor
• Article: 17beta-estradiol preserves endothelial function by reduction of the endogenous nitric oxide synthase inhibitor level.

  Zhong Dai, Hui-Qing Zhu, De-Jian Jiang, Jun-Ling Jiang, Han-Wu Deng, Yuan-Jian Li
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  ABSTRACT: Previous studies have shown that endothelial dysfunction is associated to an increase of endogenous nitric oxide synthase (NOS) inhibitor level and estrogen reduces impairment of the endothelium due to oxidized low-density lipoprotein (LDL). The purpose of the present study was to investigate the effect of estradiol on endothelial dysfunction and the increased level of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, induced by LDL. Male Sprague-Dawley rats were treated with a single injection of native LDL (4 mg/kg) for 48 h. Vasodilator responses to acetylcholine in the aortic rings and serum levels of ADMA and malondialdehyde (MDA) were determined. Treatment with native LDL markedly reduced endothelium-dependent relaxation to acetylcholine in the isolated rat thoracic aortic rings and increased serum levels of ADMA and MDA (P < 0.01). Pretreatment with 17beta-estradiol (0.1 or 0.3 mg/kg) significantly attenuated inhibition of vasodilator responses to acetylcholine and elevation of both ADMA and MDA concentration by LDL (P < 0.01). These results suggest that estradiol possesses a protective effect on the endothelium and the protective effect is related to reduction of ADMA concentration by inhibition of lipid peroxidation.
  International Journal of Cardiology 09/2004; 96(2):223-7. · 7.08 Impact Factor
• Article: 3,4,5,6-Tetrahydroxyxanthone protects against myocardial ischemia-reperfusion injury in rats.

  Zhong Dai, De-Jian Jiang, Gao-Yun Hu, Yan-Hua Du, Jing Yu, Chang-Ping Hu, Dan Luo, Yuan-Jian Li
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  ABSTRACT: In the present study, we tested the protective effect of 3,4,5,6-tetrahydroxyxanthone, a synthetic xanthone derivative, on myocardial ischemia-reperfusion injury in rats. Ischemia-reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts or 30 min coronary artery occlusion and 120 min reperfusion in vivo, respectively. Heart rate, coronary flow (CF), left ventricular pressure (LVP), and its first derivative (+/- dp/dt (max)) were recorded, and the activity of creatine kinase in coronary effluent and tumor necrosis factor-alpha (TNF-alpha) content in myocardial tissues were measured in vitro. The activity of serum creatine kinase, the level of TNF-alpha and interleukin-6 (IL-6), and myocardial infarct size were measured in vivo. 3,4,5,6-tetrahydroxyxanthone (30, 100 or 300 microM) caused a significant improvement of cardiac function (LVP and +/- dp/dt (max)) and a decrease in the release of creatine kinase in coronary effluent as well as the level of TNF-alpha in myocardial tissues in vitro. 3,4,5,6-tetrahydroxyxanthone (0.5 or 1.0 mg/kg, i.v.) also markedly decreased infarct size and the release of creatine kinase and TNF-alpha, and increased serum IL-6 level in vivo. These results suggest that 3,4,5,6-tetrahydroxyxanthone possesses a protective effect on myocardial ischemia-reperfusion injury, and that the protective effects of 3,4,5,6-tetrahydroxyxanthone may be related to inhibition of TNF-alpha production and stimulation of IL-6 generation by inhibition of ROS production.
  Cardiovascular Drugs and Therapy 08/2004; 18(4):279-88. · 3.13 Impact Factor
• Article: Pharmacological effects of xanthones as cardiovascular protective agents.

  De-Jian Jiang, Zhong Dai, Yuan-Jian Li
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  ABSTRACT: Many epidemiological studies indicate that consumption of dietary polyphenolic compounds is beneficial in the prevention of cardiovascular diseases. Xanthones are a class of polyphenolic compounds that commonly occur in plants and have been shown to have extensive biological and pharmacological activities. Recently, the pharmacological properties of xanthones in the cardiovascular system have attracted great interest. Xanthones and xanthone derivatives have been shown to have beneficial effects on some cardiovascular diseases, including ischemic heart disease, atherosclerosis, hypertension and thrombosis. The protective effects of xanthones in the cardiovascular system may be due to their antioxidant, antiinflammatory, platelet aggregation inhibitory, antithrombotic and/or vasorelaxant activities. In particular, the antagonism of endogenous nitric oxide synthase inhibitors by xanthones may represent the basis for improved endothelial function and for reduction of events associated with atherosclerosis.
  Cardiovascular Drug Reviews 02/2004; 22(2):91-102. · 5.21 Impact Factor