Ling-Hong Yu

Peking Union Medical College Hospital, Peping, Beijing, China

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Publications (5)4.74 Total impact

  • Ling-Hong Yu · Huai-Ling Wei · Xiu-Qi Bao · Dan Zhang · Hua Sun
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    ABSTRACT: The aim of this study is to investigate the protective effect of N-[2-(4-hydroxyphenyl)ethyl]-2-(2, 5-dimethoxyphenyl)-3-(3-methoxy-4-hydroxyphenyl)acrylamide (FLZ), a novel synthetic squamosamide cyclic derivative, against Parkinson's disease (PD) model mice induced by the inflammatory bacterial endotoxin, lipopolysaccharides (LPS) and the neurotoxin 1-methy-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). C57/BL mice were ip injected LPS (5 mg x kg(-1)) once. One week following the LPS injection, mice received a subcutaneous injection of MPTP (25 mg x kg(-1)) once daily for 2 days. Eight weeks later, FLZ (25, 50 and 75 mg x kg(-1)) was orally administered to mice once daily for 60 days. The motor ability of the mice was evaluated by rod climbing test and footprint test. The dopamine (DA) levels in mouse striatum were determined by high performance liquid chromatography system. The tyrosine hydroxylase (TH)-positive cells were showed by immunohistochemical analysis. FLZ treatment significantly improved motor dysfunction of mice challenged by LPS plus MPTP. The increase of TH-positive cell numbers and elevation of DA levels may be contributed to the beneficial effects of FLZ on motor behavior. This study showed FLZ has significant therapeutic effect on LPS plus MPTP induced chronic PD model, which indicates its potential as a new candidate drug to treat PD.
    No preview · Article · Oct 2013 · Yao xue xue bao = Acta pharmaceutica Sinica
  • Zheng-Huai Tan · Ling-Hong Yu · Huai-Ling Wei · Geng-Tao Liu
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    ABSTRACT: This paper investigates the effect of natural scutellarin on acute lung injury (ALI) induced by Escherichia coli endotoxin lipopolysaccharide (LPS) in mice and its mechanism of action. Mouse ALI was induced by the injection of LPS (15 mg/kg) via the tail vein, and mice were intraperitoneally injected with 50 and 25 mg/kg of scutellarin before the LPS injection. The lung index, serum NO2(-)/NO3(-), and tumor necrosis factor-alpha (TNF-alpha) levels were determined using kits. The lung lesions were examined by light microscope. The mRNA levels of TNF-alpha, inducible nitric oxide synthase (iNOS), and FasL in pulmonary tissues were detected by RT-PCR. c-Fos, c-Jun, IkappaB, and iNOS proteins were detected by the western blotting method. Pretreatment with 25 and 50 mg/kg of scutellarin significantly reduced lung injury induced by LPS, which expressed in the decrease in lung morphological lesions, serum NO2(-)/NO3(-), TNF-alpha levels, lactate dehydrogenase release, and total protein in the lavage fluid of bronchoalveolar of the lung. The mRNA level of TNF-alpha, iNOS, the protein content of c-Fos, iNOS, and the activation of NF-kappaB in pulmonary tissues were all inhibited, while the lung glutathione level increased. In conclusion, scutellarin has protective action against LPS-induced lung damage in mice, and its underlying mechanism might be the inhibition of IkappaB alpha degradation and the expression of TNF-alpha mRNA.
    No preview · Article · Mar 2010 · Journal of Asian natural products research
  • Ling-Hong Yu · Geng-Tao Liu
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    ABSTRACT: The aim of this paper was to investigate the protective effect of schisanhenol (Sal) isolated from Schisandra rubriflora Rhed, on human ox-LDL-induced bovine aorta endothelial cells (BAECs) apoptosis and intracellular reactive oxygen species (ROS) production in vitro. The BAECs were cultured with ox-LDL (200 microg/ml) in the presence and absence of Sal (10 and 50 micromol L(- 1)) for 24 h. The cytotoxicity of ox-LDL was evaluated by LDH leakage, cell viability and morphological change. Cell apoptosis was estimated by DNA ladder, chromatin condensation, and flow cytometry assay. The intracellular ROS production was detected by using DCF, a ROS probe, with laser confocal microscopy and flow cytometry. Sal was shown to reduce LDH leakage and increase cell viability. Sal also attenuated ox-LDL-induced BAECs apoptosis as indicated in typical internucleosomal DNA degradation (DNA ladder), condensed chromatin, and the sub-G1 peak appearance in flow cytometry assay. Furthermore, Sal was shown to inhibit ROS generation in BAECs with stimulation of ox-LDL. The results indicated that the anti-apoptosis effect of Sal on BACSs might be related to its inhibition of ROS generation.
    No preview · Article · Sep 2008 · Journal of Asian Natural Products Research
  • Zheng-huai Tan · Ling-hong Yu · Huai-ling Wei · Geng-tao Liu
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    ABSTRACT: To study the protective action of ulinastatin against lipopolysaccharide (LPS)-induced acute lung injury in mice and the mechanism of its action. Mice were intraperitoneally injected with ulinastatin (50 and 100 ku x kg(-1)) or saline at a period of 12 h, separately, 30 min after the last injection of ulinastatin, except normal control, all mice of other groups were injected a dose of LPS 15 mg x kg(-1) via tail vein. The levels of TNFalpha in serum and lung were measured by ELISA. The expression of TNFalpha mRNA and iNOS mRNA in lung was assayed by RT-PCR. The expression of c-Fos and c-Jun protein in lung was measured by Western blotting method. And the NO2- / NO3- level in serum and MDA in lung were measured with kits. The levels of NO2- / NO3- and TNFalpha in serum, MDA and TNFa in lung all increased after iv injection of LPS. The expressions of TNFa mRNA, iNOS mRNA, c-Fos and c-Jun in lung of LPS-injected mice were enhanced. Pretreatment with ulinastatin 100 ku x kg(-1) decreased the levels of NO2- / NO3- in serum and lung, reduced the index of lung, and inhibited the expressions of iNOS mRNA and c-Jun in lung induced by LPS in mice, while ulinastatin showed no effect on TNFa level in serum and lung. Ulinastatin protected mice from acute lung injury induced by lipopolysaccharides via inhibiting the activation of c-Jun and iNOS mRNA expression.
    No preview · Article · Aug 2006 · Yao xue xue bao = Acta pharmaceutica Sinica
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    Ling-Hong Yu · Geng-Tao Liu · You-Min Sun · Hong-Yu Zhang
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    ABSTRACT: To investigate the effect of schisanhenol (Sal) on copper ion-induced oxidative modulation of human low density lipoprotein (LDL). The antioxidative activity of eight schisandrins (DCL) on microsome lipid peroxidation induced by Vit C/NADPH system was first observed, and then, the effect of Sal on Cu2+-induced human LDL oxidation was studied. The generation of malondialdehyde (MDA), lipofuscin, reactive oxygen species (ROS), consumption of a-tocopherol as well as electrophoretic mobility of LDL were determined as criteria of LDL oxidation. Finally, the quantum chemical method was used to calculate the theoretical parameters of eight DCL for elucidating the difference of their antioxidant ability. Sal was shown to be the most active one among eight schizandrins in inhibiting microsome lipid oxidation induced by Vit C/NADPH. Sal 100, 50, and 10 micromol/L inhibited production of MDA, lipofuscin and ROS as well as the consumption of a-tocopherol in Cu2+-induced oxidation of human LDL in a dose-dependent manner. Sal also reduced electrophoretic mobility of the oxidized human LDL. Further study of quantum chemistry found that Sal was the strongest one among eight DCL to scavenge O2, R, RO and ROO radicals. Sal has antioxidative effect on human LDL oxidation. The mechanism of Sal against LDL oxidation may be through scavenging free radicals.
    Preview · Article · Sep 2004 · Acta Pharmacologica Sinica