Zhong Dai

Central South University, Changsha, Hunan, China

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Publications (7)26.64 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Protein‑coding genes and small non‑coding microRNAs involved in the guidance of differentiation in mesenchymal stem cells (MSCs) into osteoblasts have been extensively investigated in previous studies. However, long non‑coding RNAs (lncRNAs), which account for a large proportion of the genomic sequences in numerous species, have not yet been reported. In the present study, the lncRNA expression profile was analyzed using the Arraystar lncRNA array in C3H10T1/2 MSCs undergoing early osteoblast differentiation and 116 differentially expressed lncRNAs were identified between BMP‑2 treated and untreated groups. Among these lncRNAs, 59 were upregulated and 57 were downregulated in BMP‑2 treated groups. In addition, 24 cooperatively differentially expressed lncRNAs and nearby mRNA pairs were found. For example, mouselincRNA0231 and its nearby gene, EGFR, were downregulated, while lncRNA NR_027652 and its nearby gene, DLK1, were upregulated. These observations may be part of the regulatory mechanisms of lncRNAs in the control of osteoblast differentiaton. In conclusion, results of the present study indicate that lncRNA expression profiles are significantly altered in C3H10T1/2 undergoing early osteoblast differentiation and these results may provide insight into the mechanisms responsible for osteoblast differentiation.
    Molecular Medicine Reports 06/2013; · 1.17 Impact Factor
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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. · 4.11 Impact Factor
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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. · 5.15 Impact Factor
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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. · 2.15 Impact Factor
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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. · 6.18 Impact Factor
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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. · 2.67 Impact Factor
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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

Publication Stats

117 Citations
26.64 Total Impact Points


  • 2004–2008
    • Central South University
      • School of Pharmaceutical Sciences
      Changsha, Hunan, China
  • 2006
    • Guangdong Medical College
      • Department of Pharmacology
      Tsamkong, Guangdong, China