Xu-Yun Li

Zhejiang University, Hangzhou, Zhejiang Sheng, China

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Publications (10)5.55 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Elsholtzia splendens (ES) is, rich in flavonoids, used to repair copper contaminated soil in China, which has been reported to benefit cardiovascular systems as folk medicine. However, few direct evidences have been found to clarify the vasorelaxation effect of total flavonoids of ES (TFES). The vasoactive effect of TFES and its underlying mechanisms in rat thoracic aortas were investigated using the organ bath system. TFES (5-200mg/L) caused a concentration-dependent vasorelaxation in endothelium-intact rings, which was not abolished but significantly reduced by the removal of endothelium. The nitric oxide synthase (NOS) inhibitor N(ω)-nitro-l-arginine methyl ester (100μM) and the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,2-α]quinoxalin-1-one (30μM) significantly blocked the endothelium-dependent vasorelaxation of TFES. Meanwhile, NOS activity in endothelium-intact aortas was concentration-dependently elevated by TFES. However, indomethacin (10μM) did not affect TFES-induced vasorelaxation. Endothelium-independent vasorelaxation of TFES was significantly attenuated by KATP channel blocker glibenclamide. The accumulative Ca(2+)-induced contraction in endothelium-denuded aortic rings primed with KCl or phenylephrine was markedly weakened by TFES. These results revealed that the NOS/NO/cGMP pathway is likely involved in the endothelium-dependent vasorelaxation induced by TFES, while activating KATP channel, inhibiting intracellular Ca(2+) release, blocking Ca(2+) channels and decreasing Ca(2+) influx into vascular smooth muscle cells might contribute to the endothelium-independent vasorelaxation conferred by TFES.
    Environmental toxicology and pharmacology. 08/2014; 38(2):453-459.
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    ABSTRACT: To evaluate the effect of water channel aquaporin 4 (AQP4) on bleomycin-induced lung fibrosis in mice. METHODS: In wild type and AQP4 gene knockout (AQP4-/-) mice, lung fibrosis was induced by injection of bleomycin (3 mg/kg) into the trachea and saline injection was used as a control. At d3,7,14,28 after bleomycin-treatment, mice were randomly sacrificed in batch and the lung coefficient was determined. Serum levels of TGF-β1 and TNF-α were measured by ELISA and hydroxyproline contents in lung tissue were determined by Alkaline hydrolysis method. H-E staining and Masson's staining were performed to examine the pathological changes of lung tissues after bleomycin-treatment. RESULTS: On d14 after bleomycin-treatment, the lung coefficients in wild type mice and AQP4-/- mice were 1.9-fold (12.69 ± 6.05 vs 6.80 ± 0.82,q=4.204,P<0.05) and 2.3-fold (14.05 ± 5.82 vs 6.05± 0.58, q=5.172,P<0.01) of that in control, respectively, but no significant difference was found between wild type and AQP4-/- mice in the lung coefficient value (P>0.05). The hydroxyproline contents in the lung increased after bleomycin-treatment; on d28, the lung hydroxyproline contents in wild type and in AQP4-/- mice were 1.55-fold (0.85 ± 0.22 g/mg vs 0.55 ± 0.14 μg/mg, q=4.313,P<0.05) and 1.4-fold (0.84 ± 0.13 μg/mg vs 0.60 ± 0.14μg/mg, q=4.595,P<0.05) of that in control, respectively, but no significant difference was noticed between wild type and AQP4-/- mice in lung hydroxyproline contents. There was a tendency that serum TGF-β1 and TNF-α levels increased in bleomycin-treated mice, but no significant difference was found between wild type and AQP4-/- mice. AQP4-knockout showed no effects on pathological changes of lung tissues with H-E staining and Masson's staining in mice with bleomycin-induced lung fibrosis. CONCLUSION: AQP4 might not be involved in bleomycin-induced lung fibrosis in mice.
    05/2014; 43(3):281-6.
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    ABSTRACT: To investigate the protective effects of carnosine against experimental closed head injury (CHI) in mice. The CHI model was established by free-falling weight-drop. Carnosine (250 mg/kg or 500 mg/kg) was administered intraperitoneally 30 min before brain trauma, then q.d for 7 d; while normal saline was administrated for control group. The neurological defect was evaluated by neurological severity score (NSS) within 7 d; the survival rate and the histological alternations were observed. Carnosine prevented the body weight loss of mice at dose of 500 mg/kg; significantly increased the survival rate, and reduced the neurological defect and histological damage at dose of 250 and 500 mg/kg. Carnosine can attenuate closed head injury in mice.
    Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 05/2013; 42(3):291-296.
  • Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 11/2010; 26(4):450-2, 480.
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    ABSTRACT: To investigate the vasorelaxation effect of crocetin (CCT) and its mechanism. Isolated aortic rings from Sprague-Dawley rats were mounted in the organ bath system. The tension of the aorta was recorded. 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. 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.
    Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 11/2010; 39(6):559-65.
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    ABSTRACT: To determine the role of the phospholipase D (PLD) pathway in injury and survival of alveolar epithelial cells, A549 cells were exposed to H(2)O(2) (500 microM) which resulted in time-dependent injury and bi-phasic increase of PLD activity at 5 min and at 3 h, respectively. n-Butanol (0.5%) inhibited PLD activation, attenuated cell injury at 5 min of H(2)O(2) exposure, but enhanced injury at 3h of exposure. This activation was inhibited by treatment with catalase (500 units/ml). Exogenous phosphatidic acid mimicked the effects of PLD activation, and diphenyliodonium (NADPH oxidase inhibitor) reversed the decline in cell viability induced by H(2)O(2) exposure. Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H(2)O(2)-induced PLD activation but reversed H(2)O(2)-induced injury. We speculate that PLD activation at the initiation of H(2)O(2) exposure predominantly results in NAPDH oxidase activation, which mediates A549 cell injury, but turns to mediating cell survival as the H(2)O(2) attack continues, which might be mainly due to the accumulation of intracellular phosphatidic acid.
    Toxicology Letters 07/2010; 196(3):168-74. · 3.15 Impact Factor
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    ABSTRACT: To investigate the effect of intranasal administration of low dosage recombinant human erythropoietin (r-HuEPO) on seizure in rats. After intranasal or intraperitoneal administration of r-HuEPO, the behavioral and electroencephalographic changes were observed in pentylenetetrazol (PTZ) and maximal electroshock (MES) induced seizure or electrical amygdaloid-kindled seizure of rats. Intranasal administration of low dosage r-HuEPO increased the seizure latency, and decreased the seizure grade and duration, and the number of convulsive episodes in PTZ induced seizure, with the most potential dosage of 2.4 IU. Intraperitoneal administration of r-HuEPO (3 000, 4 000 IU/kg) only decreased the seizure duration and number of convulsive episodes. The seizure grade, forelimb or hindlimb extension duration were decreased in MES-induced seizure by intranasal administration of 2.4 IU r-HuEPO. In addition, intranasal administration of 2.4 IU r-HuEPO decreased the seizure grade, generalized seizure duration and afterdischarge in electrical amygdaloid-kindled rats stimulated with generalized seizure threshold. Intranasal administration of low dosage r-HuEPO can inhibit the seizure in rats.
    Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 11/2009; 38(6):565-71.
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    ABSTRACT: 1. The aim of the present study was to investigate the mechanism underlying biochanin A-induced relaxation of the aorta in spontaneously hypertensive rats (SHR). 2. The tension in isolated ring preparations of thoracic aortas from normotensive (Wistar-Kyoto (WKY) rats) and SHR at 5 and 10 weeks of age was measured isometrically. 3. Biochanin A (10(-7) to 10(-4) mol/L) induced a concentration-dependent relaxation in aortic rings from both strains at the age of 5 and 10 weeks and the relaxation was greater in rings from 10-week-old SHR compared with age-matched WKY rats. The vasorelaxation induced by biochanin A was significantly reduced by denudation of the endothelium in aortic rings from SHR, but not WKY rats. Treatment with either indomethacin, a cyclo-oxygenase inhibitor, or N(omega)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, had little effect on the relaxation induced by biochanin A in aortic rings from either strain. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, significantly attenuated the relaxation induced by biochanin A in aortic rings from both strains, although the extent of reduction was greater in WKY rats than SHR. Conversely, treatment with 4-aminopyridine, a selective inhibitor of voltage-dependent potassium channels, or tetraethylammonium, an inhibitor of calcium-activated potassium channels, significantly reduced the vasorelaxation induced by biochanin A in rings from SHR but not WKY rats. 4. The greater vasorelaxation produced by biochanin A in aortic rings from 10-week-old SHR is endothelium dependent. Different mechanisms underlie the relaxant effects of biochanin A in aorta from SHR and WKY rats. The mechanisms of biochanin A-induced vasorelaxation in thoracic aortas from both normotensive and hypertensive rats involve ATP-sensitive potassium channels and, in addition, in rings from the hypertensive strain at 10 weeks of age, an endothelium-derived activation of smooth muscle cell potassium channels contributes to the vasorelaxation observed.
    Clinical and Experimental Pharmacology and Physiology 10/2006; 33(9):802-7. · 2.41 Impact Factor
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    ABSTRACT: To examine the effect of cinobufacini on rat thoracic aorta and its mechanism. Isolated rat thoracic aorta was perfused and isometric tension was recorded by organ bath technique before and after cinobufacini treatment. Cinobufacini induced contraction of isolated thoracic aorta with or without endothelium in a concentration-dependent manner (at concentration of 2.5,5.0,7.5,10.0 g/L). The vasoconstriction effect of cinobufacini was more potent in endothelium-denuded aorta ring [(16.3+/-3.39)%, (52.5+/-7.70)%, (60.9+/-8.84)%, (69.2+/-11.34)%] than in endothelium-intact aorta ring [(6.2+/-2.07)%, (14.7+/-4.91), (17.6+/-5.86)%, (20.3+/-6.78)% (P<0.01)]. Its contractile effect was attenuated in Ca(2+)-free solution (about 1/10 of that in buffer with 1.25 mmol/L CaCl(2)) or by the treatment with verapamil (10(-7)mol/L), an L-type calcium channel antagonist. Cinobufacini induced contraction on the endothelium-intact rat aorta was augmented by pretreatment with L-NAME (10(-4)mol/L), a nitric oxide synthase inhibitor. Cinobufacini contracts rat thoracic aorta by opening the voltage-dependent Ca(2+) channel and increasing Ca(2+) influx into vascular smooth muscle. Cinobufacini can also stimulate the release of vascular relaxant factor, nitric oxide, from the endothelium and thus antagonize cinobufacini-induced contraction.
    Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 03/2006; 35(2):178-81.
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    ABSTRACT: Epidemiological data suggest that the incidence of cardiovascular disease is reduced in people who have a high intake of phytoestrogens. The plant-derived estrogen biochanin A is known to cause vasodilation, but its mechanisms of action remain unclear. This study was undertaken to investigate the effects and mechanisms of biochanin A on rat thoracic aorta. Isolated aortic rings were suspended in individual organ baths and isometric tension was measured. Biochanin A induced significant relaxation in rings with or without endothelium. Contractile responses induced by phenylephrine (PE), KCl and CaCl 2 were antagonized by 10<sup>-7</sup>~10<sup>-4</sup>mol/L biochanin A. The transient contraction elicited by PE was significantly attenuated by 10<sup>-5</sup>mol/L biochanin A in Ca<sup>2+</sup>-free medium. The relaxant effect of biochanin A was significantly inhibited by pretreatment with the K<sup>+</sup>channel antagonists tetraethylammonium and glibenclamide in endothelium-denuded aorta. We conclude that biochanin A induces an endothelium-independent relaxation in rat aortic rings. The underlying mechanism may involve the blockage of Ca<sup>2+</sup>entry through both voltage-dependent and receptor-operated Ca<sup>2+</sup>channels, the inhibition of intracellular Ca<sup>2+</sup>release, and the activation of large-conductance Ca<sup>2+</sup>-activated K<sup>+</sup>channels and ATP-sensitive K<sup>+</sup>channels.
    Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 01/2005; 3:2244-7.