The Key Laboratory of Basic Pharmacology of Guizhou Province

Zunyi, China

The Key Laboratory of Basic Pharmacology of Guizhou Province

Zunyi, China
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Nie J.,Zunyi Medical College | Nie J.,The Key Laboratory of Basic Pharmacology of Guizhou Province | Luo Y.,Guizhou Aerospace Hospital | Huang X.-N.,Zunyi Medical College | And 6 more authors.
European Journal of Pharmacology | Year: 2010

The present study was undertaken to investigate the protective effects of icariin on the learning and memory abilities in Alzheimer's disease model rats and explore its protection mechanisms. Beta-amyloid peptide (Aβ) is a key etiology in Alzheimer's disease and targeting on Aβ production and assembly is a new therapeutic strategy. Six-month (400-600 g) Wistar rats were unilaterally injected with amyloid β-protein fragment 25-35 (Aβ 25-35) 10 μg (5 g/l, 2 μl) into the right hippocampus. The day following Aβ injection, icariin 30, 60 or 120 mg/kg was administered by gavage for 14 days. The ability of spatial learning and memory of the animals was tested by the Morris water maze. In place navigation test, icariin significantly decreased the mean escape latency and searching distance. In the space probing test, icariin increased remarkably the searching time and searching distance in the quadrant where the platform was originally located. All tests indicated icariin improved the ability of spatial learning and memory in Alzheimer's disease model rats. Furthermore, immunohistochemistry and real time RT-PCR analysis showed that icariin significantly reduced the contents of Aβ 1-40 and the mRNA levels of β-secretase in the hippocampus and increased the mRNA level of superoxide dismutase-2, but it had no apparent effects on the immunostain and mRNA level of amyloid protein precursor. These results demonstrate that icariin can improve the learning and memory abilities in Aβ 25-35-induced Alzheimer's disease rats. The mechanisms appear to be due to the decreased production of insoluble fragments of Aβ through suppression of β-secretase expression. © 2009 Elsevier B.V. All rights reserved.


Jin H.,Zunyi Medical College | Jin F.,The Key Laboratory of Basic Pharmacology of Guizhou Province | Jin J.-X.,Institute of Traditional Medicine at Qian Xi Nan | Xu J.,Zunyi Medical College | And 3 more authors.
Food and Chemical Toxicology | Year: 2013

The medicinal fungus Ganoderma lucidum has been shown to have hepatoprotective effects. G. lucidum contains triterpenes and polysaccharides, and the Sporoderm-broken G. lucidum powder is particular beneficial. This study utilized G. lucidum spore to examine its effect on [Cd(II)]-induced hepatotoxicity in mice and the mechanism of the protection. Mice were pretreated with G. lucidum spore (0.1, 0.5, and 1.0. g/kg, po, for 7. days), and subsequently challenged with a hepatotoxic dose of Cd(II) (3.7. mg/kg, ip). Liver injury was evaluated 8. h later. G. lucidum spore protected against Cd(II)-induced liver injury in a dose-dependent manner, as evidenced by serum alanine aminotransferase, aspartate aminotransferase and histopathology. To examine the mechanism of protection, subcellular distribution of Cd(II) was determined. G. lucidum spore decreased Cd(II) accumulation in hepatic nuclei, mitochondria, and microsomes, but increased Cd(II) distribution to the cytosol, where Cd(II) is sequestered by metallothionein, a protein against Cd(II) toxicity. Indeed, G. lucidum spore induced hepatic metallothionein-1 mRNA 8-fold, and also increased metallothionein protein as determined by the Cd(II)/hemoglobin assay. Cd(II)-induced oxidative stress was also decreased by G. lucidum spore, as evidenced by decreased formation of malondialdehyde. In summary, G. lucidum spore is effective in protection against Cd(II)-induced hepatotoxicity, and this effect is due, at least in part, to the induction of hepatic metallothionein to achieve beneficial effects. © 2012.


Li F.,Zunyi Medical College | Gong Q.-H.,Zunyi Medical College | Wu Q.,The Key Laboratory of Basic Pharmacology of Guizhou Province | Lu Y.-F.,Zunyi Medical College | And 2 more authors.
Pharmacology Biochemistry and Behavior | Year: 2010

The effects of icariin (ICA), a major constituent of flavonoids from the Chinese medical herb Epimedium brevicornum Maxim, on spatial memory performances and expressions of hippocampus brain-derived neurotrophic factor (BDNF) and tyrosine kinase TrkB (tropomyosin receptor kinase B) were investigated in d-galactose (d-gal)-treated rats. Subcutaneous injection of d-gal (500. mg/kg/d) for four months caused memory loss as detected by the Morris water maze, morphologic abnormalities of neurons in hippocampus region and the reduced expression of BDNF and TrkB were observed. ICA (60. mg/kg/d) given orally 1. h after subcutaneous injection of d-gal daily for 4. months markedly attenuated d-gal-induced rats behavioral dysfunction and neurodegeneration, as evidenced by shortened escape latency and searching distance and rescued morphologic abnormalities, and also elevated the mRNA levels and the protein expressions of BDNF and TrkB in hippocampus, as evidenced by quantitative real-time RT-PCR and Western blotting analysis. But ICA had no significant influence on normal rats which were not injected d-gal. These results clearly demonstrated that d-gal produced learning and memory deficits after chronic administration, and ICA can protect neuron from d-gal insults and improve the memory loss. © 2010 Elsevier Inc.


Yu X.-F.,Zunyi Medical College | Yu X.-F.,The Key Laboratory of Basic Pharmacology of Guizhou Province | Deng J.,Zunyi Medical College | Yang D.-L.,Zunyi Medical College | And 6 more authors.
Vascular Pharmacology | Year: 2011

Ginsenosides, the active components found in Panax ginseng, have been reported to inhibit the cardiac hypertrophy in rats. This study aims to observe the potential effect of total ginsenosides (TG) on the hypertrophic vascular diseases. The model of vascular neointimal hyperplasia was established by rubbing the endothelia of the common carotid artery with a balloon in male Sprague Dawley rats. TG (15. mg/kg/day, 45. mg/kg/day), L-arginine (L-arg) 200. mg/kg/day, and NG-nitro-L-arginine-methyl ester (L-NAME) 100. mg/kg/day used with the same dose of L-arg or TG 45. mg/kg/day were given for 7 and 14 consecutive days after surgery. TG and L-arg administrations significantly ameliorated the histopathology of injured carotid artery, which was abolished or blunted by L-NAME, an NOS inhibitor; TG and L-arg could also remarkably reduce the expression of proliferating cell nuclear antigen (PCNA), a proliferation marker of vascular smooth muscle cells(VSMCs), in neointima of the injured artery wall. Further study indicated that balloon injury caused a decreased superoxide dismutase (SOD) activity and an elevated malondialdehyde (MDA) content in plasma, and reduced the cGMP level in the artery wall, which were reversed by TG. It was concluded that TG suppress the rat carotid artery neointimal hyperplasia induced by balloon injury, which may be involved in its anti-oxidative action and enhancing the inhibition effects of NO/cGMP on VSMC proliferation. © 2010 Elsevier Inc.

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