Guilan Li

shanxi agricultural university, Shanxi, Liaoning, China

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Publications (7)15.24 Total impact

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    ABSTRACT: Taraxerol, a triterpenoid compound, has potent anti-inflammatory effects. However, the molecular mechanisms are not clear. In the study, taraxerol concentration dependently inhibited nitric-oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels and these inhibitions decreased the production of nitric oxide (NO), prostaglandin 2 (PGE(2)), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β induced by LPS. Furthermore, we found that taraxerol suppressed translocation of nuclear factor-κB (NF-κB), phosphorylation of IκBα, blocked the IκBα degradation as well as IKK and mitogen-activated protein kinase (MAPK) activation by inactivation of TGF-β-activated kinase-1 (TAK1) and Akt. In addition, taraxerol significantly inhibited the formation of TAK1/TAK-binding protein1 (TAB1), which was accompanied by inducing degradation of TAK1, decreasing LPS-induced polyubiquitination of TAK1 as well as TAK1 phosphorylation. Taken together, our data suggest that taraxerol downregulates the expression of proinflammatory mediators in macrophages by interfering with the activation of TAK1 and Akt, thus preventing NF-κB activation.
    International immunopharmacology 01/2013; · 2.21 Impact Factor
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    ABSTRACT: Ganoderic acid A is a lanostane triterpene isolated from Ganoderma lucidum. It has been reported to exhibit antitumor activity, which is mainly mediated through its inhibitory effect on nuclear transcription factor-kappaB and activator protein-1. But the role of ganoderic acid A in JAK-STAT3 signaling pathways is still unclear. In the present study, we investigated the effect of ganoderic acid A on the signal transducer and activator of the transcription 3 pathway and evaluated whether suppression of the signal transducer and activator of transcription 3 activity by ganoderic acid A could sensitize HepG2 cells to cisplatin. Our results show that ganoderic acid A significantly suppressed both the constitutively activated and IL-6-induced signal transducer and activator of transcription 3 phosphorylation in HepG2 cells. Inhibition of the signal transducer and activator of transcription 3 tyrosine phosphorylation was found to be achieved through suppression of JAK1 and JAK2. Furthermore, ganoderic acid A promoted cisplatin-induced cell death by enhancing the sensitivity of HepG2 cells to cisplatin mainly via the signal transducer and activator of transcription 3 suppression. These observations suggest a potential therapeutic strategy of using ganoderic acid A in combination with chemotherapeutic agents for cancer treatment.
    Planta Medica 09/2012; · 2.35 Impact Factor
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    ABSTRACT: Arctigenin, a natural dibenzylbutyrolactone lignan compound, has been reported to possess anti-inflammatory properties. Previous works showed that arctigenin decreased lipopolysaccharide (LPS)-induced iNOS at transcription level. However, whether arctigenin could regulate iNOS at the post-translational level is still unclear. In the present study, we demonstrated that arctigenin promoted the degradation of iNOS which is expressed under LPS stimulation in murine macrophage-like RAW 264.7 cells. Such degradation of iNOS protein is due to CHIP-associated ubiquitination and proteasome-dependency. Furthermore, arctigenin decreased iNOS phosphorylation through inhibiting ERK and Src activation, subsequently suppressed iNOS enzyme activity. In conclusion, our research displays a new finding that arctigenin can promote the ubiqitination and degradation of iNOS after LPS stimulation. iNOS activity regulated by arctigenin is likely to involve a multitude of crosstalking mechanisms.
    International immunopharmacology 07/2012; 14(2):138-44. · 2.21 Impact Factor
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    ABSTRACT: l-Theanine is a unique amino acid in green tea. We here evaluated the protective effects of l-theanine on ethanol-induced liver injury in vitro and in vivo. Our results revealed that l-theanine significantly protected hepatocytes against ethanol-induced cell cytotoxicity which displayed by decrease of viability and increase of LDH and AST. Furthermore, the experiments of DAPI staining, pro-caspase3 level and PARP cleavage determination indicated that l-theanine inhibited ethanol-induced L02 cell apoptosis. Mechanically, l-theanine inhibited loss of mitochondrial membrane potential and prevented cytochrome c release from mitochondria in ethanol-treated L02 cells. l-Theanine also prevented ethanol-triggered ROS and MDA generation in L02 cells. l-Theanine restored the antioxidant capability of hepatocytes including GSH content and SOD activity which were reduced by ethanol. In vivo experiments showed that l-theanine significantly inhibited ethanol-stimulated the increase of ALT, AST, TG and MDA in mice. Histopathological examination demonstrated that l-theanine pretreated to mice apparently diminished ethanol-induced fat droplets. In accordance with the in vitro study, l-theanine significantly inhibited ethanol-induced reduction of mouse antioxidant capability which included the activities of SOD, CAT and GR, and level of GSH. These results indicated that l-theanine prevented ethanol-induced liver injury through enhancing hepatocyte antioxidant abilities.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 02/2012; 50(2):363-72. · 2.99 Impact Factor
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    ABSTRACT: As a natural alkaloid extracted from Amaryllidaceae, lycorine shows various biological effects on tumor cells. Here we show that lycorine dose-dependently inhibited the LPS-induced up-regulation of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein level in RAW264.7 cells. Besides, it also inhibited NO, PGE(2), TNF-α and IL-6 release from LPS-treated RAW264.7 cells. RT-PCR experiments showed that lycorine suppressed LPS-induced iNOS but not COX-2 gene expression. Moreover, lycorine decreased LPS-induced mortality in mice. Mechanistically, LPS-induced activation of P38 and STATs pathways was suppressed significantly by lycorine. In addition, lycorine did not interfere with the phosphorylation of ERK1/2, JNK1/2 and NF-κB pathways. In conclusion, lycorine inhibits LPS-induced production of pro-inflammatory mediators and increases the survival rate of mice after LPS challenge, suggesting that lycorine could play an anti-inflammatory role in response to LPS.
    International immunopharmacology 12/2011; 12(1):249-56. · 2.21 Impact Factor
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    ABSTRACT: L-theanine is a natural amino acid in green tea and it has been well known for its activities of relieving depression and neuroprotection. However, cytoprotective effect and its mechanism of L-theanine on hepatocytes have not been reported. The objective of this work was to investigate the hepatoprotective effect of L-theanine as well as its mechanism by using the human hepatic L02 cells injured by hydrogen peroxide (H2O2). Results showed that L-theanine dose dependently decreased H2O2-induced cell viability loss and lactate dehydrogenase (LDH) release. L-theanine pretreatment improved nuclear morphology of the cells injured by H2O2. By using flow cytometric analysis, we found that L-theanine significantly inhibited H2O2-induced cell apoptosis. Further, L-theanine attenuated H2O2-induced reduction in pro-caspase3 and cleavage of poly (adenosine diphosphate-ribose) polymerase (PARP). H2O2-activated p38 mitogen-activated protein kinase (MAPK) was also inhibited by L-theanine. These data suggest that L-theanine could protect L02 cells against H2O2-induced apoptosis via suppression of p38 MAPK. L-theanine might potentially be useful in the prevention and treatment of liver diseases. KeywordsL-theanine–L02 cells–Hydrogen peroxide–Apoptosis
    European Food Research and Technology 01/2011; 233(3):427-435. · 1.39 Impact Factor
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    ABSTRACT: HSP27 is a member of the small HSP family which has been linked to different signaling pathways regulating critical cellular functions. But the role of HSP27 in LPS-induced inflammatory signaling pathways is still unclear. In the present study, both overexpression and RNA interference experiments indicated that HSP27 increased LPS-induced expression of iNOS and COX-2 and release of NO/PGE2 through enhancing NF-kappaB but not MAPK activation. The effects of HSP27 on LPS-induced iNOS/COX-2 expression and relative signaling cascade were closely related with the phosphorylation of HSP27. Further studies have shown that HSP27-regulated LPS-induced activation of NF-kappaB by interacting with TRAF6 and increasing the association of TRAF6-IKKgamma. This could be a probable mechanism by which HSP27 modulates LPS-induce inflammatory signaling pathways. Thus, HSP27 may play a potential role in regulating inflammatory responses in immunologic system.
    Cellular Immunology 01/2010; 264(2):127-34. · 1.87 Impact Factor

Publication Stats

25 Citations
15.24 Total Impact Points


  • 2013
    • shanxi agricultural university
      Shanxi, Liaoning, China
  • 2012
    • Bengbu Medical College
      Pang-pu, Anhui Sheng, China
  • 2010–2012
    • Nanjing Normal University
      • College of Life Sciences
      Nanjing, Jiangsu Sheng, China