Jing-Yuan Wan

Chongqing Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (16)23.94 Total impact

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    ABSTRACT: Recently, increasing evidences have indicated that abnormal behavior and white matter changes had appeared before senile plaques were formed in Alzheimer's disease (AD). However, the exact nature of these changes in behavior and white matter structure in early AD are unclear. This study used the Morris water maze, an ELISA assay, a transmission electron microscopic technique and new stereological methods to investigate the behavior, Aβ protein expression and white matter structure of Tg2576 transgenic mice at four ages. Only 10 months of age, the time latency in the Morris water maze tasks for Tg2576 transgenic mice were significantly longer than that of wild-type mice. The concentration of Aβ40 protein in the white matter of the Tg2576 transgenic mice was significantly increased in four ages mice, but the Aβ42 protein was significantly increased only in the 6-month-old mice. In 10-month-old mice, the axon volume in the white matter of the Tg2576 transgenic mice was significantly decreased when compared to the wild-type mice. These results suggest that the deposition of Aβ in the white matter of Tg2576 transgenic mice appeared before the spatial memory decline. The early detection of the Aβ content in the white matter of AD might help diagnose suspected AD. In addition, the axon changes in the white matter of AD might be one of the morphological causes of the behavioral deficits observed in 10-month-old transgenic mouse models of AD, and protecting the axons in the white matter might be an important method for delaying the progression of AD.
    Neuroscience Letters 09/2013; · 2.03 Impact Factor
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    ABSTRACT: The prognosis for fulminant hepatic failure (FHF) still remains extremely poor with a high mortality and, therefore, better treatments are urgently needed. Syringin, a main active substance isolated from Eleutherococcus senticosus, has been reported to exhibit immunomodulatory and anti-inflammatory properties. In this study, we investigated the effects and underlying mechanisms of syringin on lipopolysaccharide (LPS) and D-galactosamine (D-GalN)-induced FHF in mice. Mice were administered syringin (10, 30 and 100 mg kg(-1) , respectively) intraperitoneally (i.p) 30 min before LPS/D-GalN then mortality and liver injury were evaluated subsequently. We found that syringin dose-dependently attenuated LPS/D-GalN-induced FHF, as indicated by reduced mortality, inhibited aminotransferase and malondialdehyde (MDA) content, an increased glutathione (GSH) concentration and alleviated pathological liver injury. In addition, syringin inhibited LPS/D-GalN-induced hepatic caspase-3 activation and hepatocellular apoptosis, myeloperoxidase (MPO) activity and intercellular adhesion molecule-1 (ICAM-1) expression, as well as hepatic tissues tumor necrosis factor-alpha (TNF-α) production and NF-κB activation in a dose-dependent manner. These experimental data indicate that syringin might alleviate the FHF induced by LPS/D-GalN through inhibiting NF-κB activation to reduce TNF-α production. Copyright © 2013 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 04/2013; · 2.60 Impact Factor
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    ABSTRACT: To investigate the protective effects of polydatin on sepsis-induced acute liver injury (ALI) in mice, and to preliminarily study its mechanisms. The sepsis model was established using cecal ligation and puncture (CLP).A sham-operation control group was also set up. Polydatin (50, 100, and 300 mg/kg, respectively) was administrated to mice 1 h before CLP. The survival and liver injury were evaluated subsequently per 6 h after CLP. The survived mice were scarified 24 h later. The serum and the liver tissue sample were collected. The serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by colorimetric method. The content of tumor necrosis factor-alpha (TNF-alpha) was assayed by ELISA. The cyclooxygenase-2 (COX-2) expression in the liver tissue was detected by Western blot. The pathological changes of the hepatic tissue were analyzed by hematoxylin and eosin stain. The mortality of mice reached as high as 50% at 24 h after CLP. The biochemical indices and the pathological changes of the liver tissue showed obvious lesion. The success rate of modeling was 90%. Compared with the sham-operation control group, the serum ALT,AST activity, the TNF-alpha content, and the hepatic COX-2 protein expression markedly increased in the CLP group (P < 0.01). Polydatin improved the sepsis-induced mortality dose-dependently, inhibited increased ALT, AST activity and TNF-alpha, decreased the hepatic COX-2 protein expression, and attenuated the pathological injury of the liver (P < 0.05). Polydatin could effectively protect sepsis-induced ALI, which might be achieved possibly through inhibiting serum TNF-alpha production and hepatic COX-2 expression.
    Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban 02/2013; 33(2):225-8.
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    ABSTRACT: The present study was carried out to investigate the effects and mechanisms of polydatin (PD) in septic mice. The model of cecal ligation and puncture (CLP-)induced sepsis was employed. Pretreatment of mice with PD (15, 45, and 100 mg/kg) dose-dependently reduced sepsis-induced mortality and lung injury, as indicated by alleviated lung pathological changes and infiltration of proteins and leukocytes. In addition, PD inhibited CLP-induced serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production, lung cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase isoform (iNOS) protein expressions and NF-κB activation. Notably, PD upregulated the expression and activity of heme oxygenase (HO-)1 in lung tissue of septic mice. Further, the protective effects of PD on sepsis were abrogated by ZnPP IX, a specific HO-1 inhibitor. These findings indicated that PD might be an effective antisepsis drug.
    Mediators of Inflammation 01/2013; 2013:354087. · 3.88 Impact Factor
  • Bin Wang, Jing-Yuan Wan, Li Zhang, Su Min
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    ABSTRACT: Pulmonary inflammation is the key pathological presentation of mechanical ventilation-induced lung injury (VILI), and synthetic RGDS peptide has been suggested to attenuate pulmonary inflammation. The present study aimed to determine whether RGDS peptide has protective effects on VILI. Rats received 4 hours of high tidal volume mechanical ventilation with or without pretreatment with RGDS. Rats that were kept on spontaneous respiration served as controls. At the end of 4 hours, rats that received 4 hours of mechanical ventilation exhibited serious pulmonary pathological changes, more polymorphonulear and mononuclear leukocyte recruitment, more tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) production, higher total protein contents in the bronchoalveolar lavage fluids (BALFs) and more lung phosphorylation of integrin β3 and nuclear factor-κB inhibitor (I-κB), and increased NF-κB p65 binding activity than did the control group. Administration of RGDS peptide tended to significantly inhibit all these changes induced by mechanical ventilation. These results suggested that RGDS pretreatment might improve VILI in rats by attenuating inflammatory cascade related to integrin αVβ3 and NF-κB.
    Experimental Lung Research 03/2012; 38(4):204-10. · 1.47 Impact Factor
  • Ya-feng Chen, Hong Jiang, Xia Gong, Jing-yuan Wan
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    ABSTRACT: To investigate whether Resolvin E1 (RvE1) could protect against ox-LDL-induced injury on human vein vascular endothelial cells and reveal related molecular mechanisms. Human vein vascular endothelial cells were randomly assigned to six groups, which were treated with saline, RvE1, wortmanin, ox-LDL, ox-LDL and RvE1, ox-LDL and RvE1 and wortmanin, respectively. After 48 h, survival rates were determined by MTT, apoptosis rate of cells were determined by flow cytometry, TNF-α contents were assayed by ELISA, caspase 3 and 9 activities were measured by microplate reader, and the expression of p-AKT and LOX-1 were determined by Western blot. Compared with normal saline group, survival rate was markedly decreased and apoptosis rate, TNF-α content, caspase 3 and 9 activities, and the expression of LOX-1 were significantly increased in ox-LDL group (P < 0.01). Survival rate was significantly increased and apoptosis rate, TNF-α content, caspase 3 and 9 activities, and the expression of LOX-1 were significantly decreased in ox-LDL + RvE1 group compared to ox-LDL group (P < 0.01), these beneficial effects of RvE1 could be blocked by PI3K inhibitor wortmanin (P < 0.05). The present data showed that RvE1 could effectively protect against ox-LDL-induced endothelial cell injury, which might be mediated by PI3K-AKT signaling pathway.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 11/2011; 39(11):1039-43.
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    ABSTRACT: Asiaticoside (AS), a major triterpenoid saponin component isolated from Centella asiatica, has been described to exhibit antioxidant and anti-inflammatory activities. The present study aimed to determine the protective effects and the underlying mechanisms of AS on septic lung injury induced by cecal ligation and puncture (CLP). Mice were pretreated with the AS (45 mg/kg) or AS as well as GW9662 at 1h before CLP, the survival, lung injury, inflammatory mediators and signaling molecules, and Peroxisome proliferator-activated receptor-γ (PPAR-γ) were determined 24 h after CLP. The results showed that AS significantly decreased CLP-induced the mortality, lung pathological damage, the infiltration of mononuclear, polymorphonuclear (PMN) leucocytes and total proteins. Moreover, AS inhibited CLP-induced the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB), the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein in lung tissues, and the production of serum tumor necrosis factor (TNF-α) and interleukin-6 (IL-6). Interestingly, the expression of PPAR-γ protein in lung tissue was up-regulated by AS. Furthermore, GW9662 (the inhibitor of PPAR-γ) significantly reversed these beneficial effects of AS in septic mice. These findings suggest that AS could effectively protect from septic lung injury induced by CLP and the underlying mechanisms might be related to up-regulation of PPAR-γ expression to some extent, which inhibits MAPKs and NF-κB pathway.
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 09/2011; 63(6):519-25. · 1.43 Impact Factor
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    ABSTRACT: Resolvin D1 (RvD1), an endogenous lipid molecule derived from docosahexaenoic acid (DHA), has been described to promote inflammatory resolution. The present study aimed to determine the protective effects and the underlying mechanisms of RvD1 on lipopolysaccharide (LPS)-induced acute lung injury (ALI). Pretreatment RvD1 to mice 30 min before inducing ALI by LPS decreased the mortality and improved lung pathological changes, inhibited LPS-induced increases in polymorphonulear and mononuclear leukocytes recruitment, total proteins content, tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) production in the bronchoalveolar lavage fluids (BALFs). In addition, RvD1 markedly reduced LPS-induced the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and adhesion molecules, as well as myeloperoxidase (MPO) activity. Moreover, RvD1 markedly inhibited LPS-induced the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). Furthermore, pretreatment with Boc, a lipoxin A4 receptor (ALX) antagonist, significantly reversed these beneficial effects of RvD1 on LPS-induced acute lung injury in mice. Taken together, our study showed that RvD1 improved survival rate and attenuated ALI in mice induced by LPS, and the protective mechanisms might be related to selective reaction with ALX, which inhibits MAPKs and NF-κB pathway.
    Pulmonary Pharmacology &amp Therapeutics 08/2011; 24(4):434-41. · 2.54 Impact Factor
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    ABSTRACT: Myeloid differentiation protein-2 (MD-2), a secreted glycoprotein that binds to both lipopolysaccharide (LPS) and toll like receptor 4 (TLR4), contributes to the fine ligand recognition and signaling activation on LPS-induced inflammation. Here we synthesized a novel MD-2 mimetic peptide (MDMP), derived from the putative LPS-binding domain and TLR4-binding domain of MD-2, and found that MDMP dose-dependently bound to LPS and inhibited LPS-activated Limulus amebocyte lysate (LAL). Pretreatment with MDMP dampened LPS-induced inflammatory responses in RAW264.7 cells, including down-regulation of TLR4-MD-2 complex on the cell surface, suppression of LPS binding to the cells, inhibition of mitogen-activated protein kinase (MAPKs) and nuclear factor kappa B (NF-kappaB) activation, reduction of tumor necrosis factor-alpha (TNF-alpha) production. Further, in vivo pretreatment with MDMP markedly protected against LPS-induced acute lung injury and liver injury, as indicated by the notable reduction of lethality, inflammatory responses and TNF-alpha production. These results demonstrate that MDMP attenuates LPS-induced inflammatory responses in vivo and in vitro, and suggests that MDMP may be useful in the treatment of inflammation associated with LPS.
    International immunopharmacology 09/2010; 10(9):1091-100. · 2.21 Impact Factor
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    ABSTRACT: Fulminant hepatic failure (FHF) remains an extremely poor prognosis and high mortality; better treatments are urgently needed. Tetrandrine (TET), a traditional anti-inflammatory drug, has been reported to exhibit hepatoprotective activities in several liver injury models. We now investigated the effects and underlying mechanisms of TET on lipopolysaccharide (LPS) and D-galactosamine (D-GalN)-induced FHF in mice. TET (50, 100, and 200 mg/kg) was given intraperitoneally 1h before LPS/D-GalN injection in mice. The mortality and liver injury was evaluated subsequently. The results showed that administering TET to mice reduced mortality and improved liver injury induced by LPS/D-GalN in a dose-dependent manner. In addition, TET dose-dependently inhibited LPS/D-GalN-induced NF-kappaB activation, serum and hepatic tissues tumor necrosis factor-alpha (TNF-alpha) production, caspase-3 activation and hepatocellular apoptosis, myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 (ICAM-1) and endothelial cell adhesion molecule-1 (ECAM-1) expression. Our experimental data indicated that TET might alleviate the FHF induced by LPS/D-GalN through inhibiting NF-kappaB activation to reduce TNF-alpha production.
    International immunopharmacology 03/2010; 10(3):357-63. · 2.21 Impact Factor
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    ABSTRACT: Asiaticoside (AS), a triterpenoid product isolated from Centella asiatica, has been described to exhibit anti-in fl ammatory activities in several inflammatory models. However, the effects of AS on liver injury are poorly understood. The present study was undertaken to investigate whether AS is efficacious against Lipopolysaccharide (LPS) /D-galactosamine (D-GalN)-induced acute liver injury in mice and its potential mechanisms. AS (5, 10 and 20 mg/kg/d) was pretreated orally once daily for 3 days before LPS/D-GalN injected in mice. The mortality, hepatic tissue histology, plasma levels of Tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) and aspartate aminotransferase (AST), hepatic tissue TNF-alpha and caspase-3 activity were measured. Besides, western blotting analysis of phospho-p38 mitogen-activated protein kinase (phospho-p38 MAPK), phospho-c-jun N-terminal kinase (phospho-JNK) and phospho-extracellular signal regulated kinase (phospho-ERK) were determined. As a result, AS showed significant protection as evidenced by the decrease of elevated aminotransferases, hepatocytes apoptosis and caspase-3, alleviation of mortality and improvement of liver pathological injury in a dose-dependent manner. Further, we found that AS dose-dependently reduced the elevation of phospho-p38 MAPK, phospho-JNK, phospho-ERK protein and TNF-alpha mRNA expression in liver tissues and plasma TNF-alpha. These results suggest that AS has remarkable hepatoprotective effects on LPS/D-GalN-induced liver injury and the possible mechanism is related to inhibition of TNF-alpha and MAPKs.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 02/2010; 17(10):811-9. · 2.97 Impact Factor
  • Meng-Jiao Wu, Jing-Yuan Wan
    Sheng li ke xue jin zhan [Progress in physiology] 02/2010; 41(1):40-2.
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    ABSTRACT: Baicalin, a traditional anti-inflammatory drug, has been found to protect against liver injury in several experimental animal hepatitis models; however, the mechanisms underlying the hepatoprotective properties of baicalin are poorly understood. In the present study,we investigated the effects of baicalin on the acute liver injury in mice induced by Lipopolysaccharide/D-galactosamine (LPS/D-GalN). Baicalin (50, 150, and 300 mg/kg) was pretreated intraperitoneally (i.p.) at 2, 24, and 48 h respectively before LPS/D-GalN injected in mice. The mortality, hepatic tissue histology, hepatic tissue Tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase (MPO), plasma levels of TNF-alpha and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed. Besides, western blotting analyses of nuclear factor kappa B (NF-kappaB) translocation and Heme oxygenase-1(HO-1) protein expression, as well as HO-1 activity were determined. The results showed that baicalin protected against LPS/D-GalN-induced liver injury, including dose-dependent alleviation of mortality and hepatic pathological damage, decrease of ALT/AST release and the rise of MPO. Baicalin reduced nuclear translocation of NF-kappa B, TNF-alpha mRNA and protein levels in hepatic tissues and plasma levels of TNF-alpha induced by LPS/D-GalN. Moreover, baicalin dose-dependently increased HO-1 protein expression and activity. Further, inhibition of HO-1 activity significantly reversed the protective effect of baicalin against LPS/D-GalN-induced liver injury. These results suggest that baicalin can effectively prevent LPS/D-GalN-induced liver injury by inhibition of NF-kappa B activity to reduce TNF-alpha production and the underlying mechanism may be related to up-regulation of HO-1 protein and activity.
    European Journal of Pharmacology 07/2008; 587(1-3):302-8. · 2.59 Impact Factor
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    ABSTRACT: To observe the effect of asiaticoside (AS) on IL-6,TNF-alpha, IL-10 of bronchoaliveolar lavage fluid (BALF) of acute lung injury (ALI) induced by lipopolysaccharides (LPS). 56 Balb/c mice were randomly divided into control, model, sham operation,vehicle, model + asiaticoside 5, 15, 45 mg/kg groups. Model of ALI were established by intratracheal instillation of LPS 20 microl ( 2.5 mg/kg), mice were killed 24 hours later, the content of IL-6 ,TNF-alpha, IL-10 of BALF was detected by enzyme-linked immunosorbentassay (ELISA). AS could reduce the content of IL-6, TNF-alpha and increase IL-10 of BALF in dose-dependent manner. The protective effects against ALL induced by LPS on AS are related to reducing the content of IL-6, TNF-alpha, increasing secretion IL-10 and keeping the balance between inflammatory factors and anti-inflammatory factors.
    Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials 04/2008; 31(4):547-9.
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    ABSTRACT: The study is to investigate the effect of asiaticoside on collagen-induced arthritis (CIA). The model of CIA mice was prepared and the change of secondary paw swelling and the arthritis scores were observed. In vitro proliferation of spleen cells was examined using MTT assay. The cell-free protein extracts from the arthritic joints and nonarthritic joints were used for the analysis of protein expression of cyclooxygenase-2 (COX-2). And the level of PGE2 in joints was assayed using PGE2 express EIA kit. The tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels in the serum were measured by ELISA. Histopathological examination was performed by hematoxylin-eosin (HE) stain method. Asiaticoside (10, 20 and 40 mg x kg(-1) x d(-1), 22 d, ig) significantly reduced paw swelling, and decreased the arthritis scores. There was a significant reduction in proliferation of spleen cells of CIA mice treated with asiaticoside as compared with that of untreated CIA mice. COX-2, PGE2, TNF-alpha and IL-6 production in CIA mice were inhibited by asiaticoside. Meanwhile, the pathological examination showed that articular cartilage degeneration with synovial hyperplasia and inflammatory cells infiltration in CIA mice was suppressed by asiaticoside. Its active mechanism may be related to inhibiting proliferation of lymphocyte and reduction of expression of COX-2 and inflammatory cytokines.
    Yao xue xue bao = Acta pharmaceutica Sinica 08/2007; 42(7):698-703.
  • Fu-Ling Luo, Jing-Yuan Wan, Qi-Xin Zhou
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    ABSTRACT: Endotoxin tolerance has been attacted for more than 50 years, but so far its molecular mechanisms remain to be resolved. TLR4, the major receptor for LPS, was found to be involved in LPS signaling transduction and to have a close relationship with endotoxin tolerance. Quantitative, structural and functional changes of receptors, adaptor proteins and transcription factors in TLR4 signaling pathways might have effects on the decrease in proinflammatory cytokines, increase in anti-inflammatory cytokines and activation of special signaling pathways (such as PI3K pathways) as well as some negative regulation factors (SHIP1,SOCS, FLN29, et al) during the development of endotoxin tolerance. Furthermore, TLR2, Gi protein, PKC and several selective splicing isoforms are involved in endotoxin tolerance. So endotoxin tolerance is a complicated pathophysiological process caused by diverse reasons and involved in many biological substances. It is also an important protective mechanism of human body infected with G- bacteria. Exploring the mechanism of endotoxin tolerance, seeking endogenous protective mechanism of human body would provide new theory and new ways to overcome series of fatal infective diseases including sepsis.
    Sheng li ke xue jin zhan [Progress in physiology] 11/2006; 37(4):319-24.