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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Shan HU,Qi-Liang MAO-YING,Yan-Qing WANG~* Department of Integrative Medicine and Neurobiology,Shanghai Medical College,Institute of Acupuncture Research, Institutes of Brain Science,State Key Laboratory of Medical Neurobiology,Fudan University,Shanghai 200032,China

＜正＞Objective lipoxins represent a unique class of lipid mediators that can function as "braking signals" in *** A4（LXA4） and LXB4 are positional *** addition,a synthetic analogue of ATL（aspirintriggered lipoxin） has the same anti-inflammatory activities as the endogenous lipoxins and is more resistant to metabolic *** has been reported that both lipoxins and aspirin-triggered lipoxins can inhibit inflammation *** bone cancer pain,many researches have indicated that the neuroinflammation involved in the pain processing. In this article,we performed a series of studies on the role of ATL in bone cancer *** Female SD rats （160-180 g） were used to establish the model of bone cancer pain by percutaneous direct puncture technique and inoculating the Walker256 mammary gland carcinoma cells into right tibial medullary cavity *** mechanic allodynia of rats were evaluated by von Frey hair and we gave the drugs by intrathecal ***（1） Compared to the vehicle-treated animals,intrathecal LXA4,LXB4 and ATL can up-regulate mechanical threshold;（2） ATL has a longer anti-allodynic effect than the other lipoxin *** Both lipoxins and the analogy of lipoxins have anti-allodynic effects in tibial bone cancer ***,the molecular mechanism of lipoxins in bone cancer pain is still unclear and need to be further studied.

关键词： lipoxins aspirin-triggered lipoxin allodynia bone cancer pain

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Lipoxin A_4 negatively regulates lipopolysaccharide-induced differentiation of RAW264.7 murine macrophages into dendritic-like cells

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Chinese Medical Journal 2007年第11期120卷 981-987页

作者： ZHANG Li WU Ping JIN Sheng-wei YUAN Ping WAN Jing-yuan ZHOU Xiao-yan XIONG Wei FANG Feng YE Du-yun Department of Pathophysiology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Anesthesiology Wuhan Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Department of Pharmacology Chongqing Medical University Chongqing 400016 China Department of Pediatrics Wuhan Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

Background lipoxins （LXs）, endogenous anti-inflammatory and pro-resolving eicosanoids generated during various inflammatory conditions, have novel immunomodulatory properties. Because dendritic cells （DCs） play crucial roles in the initiation and maintenance of immune response, we determined whether LXs could modulate the maturation process of DCs and investigated the effects of lipoxin A4 （LXA4） on lipopolysaccharide （LPS）-induced differentiation of RAW264.7 cells into dendritic-like cells. Methods RAW264.7 cells were cultured in vitro with 1 pg/ml LPS in the absence or presence of LXA4 for 24 hours, and cellular surface markers （MHC-II, CD80 （B7-1）, CD86（B7-2）） were measured by flow cytometry （FCM）. Mixed lymphocyte reaction was performed to evaluate the allostimulatory activity. Cytoplastic IKB degradation and nuclear factor kappa B （NF-KB） translocation were detected by Western blotting. Luciferase reporter plasmid was transiently transfected into RAW264.7 cells, and luciferase activity was determined to measure the transcriptional activity of NF-KB. Results LXA4 reduced the ratio of LPS-treated RAW264.7 cells to DCs with morphological characteristics and inhibited the expression of MHC I1. LPS-induced up-regulation of CD86 was moderately suppressed by LXA4 but no obvious change of CD80 was observed. Moreover, LXA4 weakened the aUostimulatory activity of LPS-treated RAW264.7 cells. These alterations of LPS＋LXA4-treated cells were associated with a marked inhibition of IKB degradation, NF-KB translocation and then the transcriptional activity of NF-KB. Conclusions LXA4 negatively regulates LPS-induced differentiation of RAW264.7 cells into dendritic-like *** activity reveals an undescribed mechanism of LXA4 to prevent excessive and sustained immune reaction by regulating maturation of DCs.

关键词： lipoxins dendritic cells lipopolysaccharides nuclear factor kappa B

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BML-111 protected carbon tetrachloride-induced hepatic fibrosis in rats and the possible mechanisms

BML-111 protected carbon tetrachloride-induced hepatic fibro...

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第九届全国免疫学学术大会

作者： Zhou XY Yu ZJ Yan D Wang HM Xu FY Huang YH Min WP Medical College of Nanchang University Institute of Immunotherapy Nanchang University Jiangxi Academy of Medical sciences

Objective:LXs are a class of newly found arachidonic acid metabolites,possess potent anti-inflammatory and proresolution *** had previously confirmed the LXs agonists BML-111 had possessed the protection effects for ***,this study we investigated the protection effects of BML-111 on hepatic fibrosis and the possible ***:Forty Sprague-Dawley(SD)rats were used,CCL,was subcutaneous injected to build experimental hepatic fibrosis,and BML-111(1mg/kg)was injected to prevent or treat *** degree of liver injury and inflammatory cell infiltration were observed by HE *** and ALT activity in serum were tested to evaluate the liver *** level of hepatic fibrosis was conjunctively confirmed through general feature of liver,VG stain and Masson stain of liver biopsy,and content of hydroxyproline(Hyp).Western-blot and immunohistochemistry were used to examine the expressions of *** expression levels of TGF-β1 and PDGF were detected by ELISA and ***-blot was used to observe the expression levels of MMP-2,MMP-3,MMP-7,MMP-9,and *** content of MDA,the activity of SOD,GSH-Px and CAT,and the T-AOC were detected by reagent *** NF-κBp65 nuclear translocation was observed by ***:The data suggested:(1)Histopathologal examination via VG and Masson staining demonstrated the model of hepatic fibrosis in rat was well.(2)BML-111 inhibited liver injury and inflammatory cell infiltration in prevention group and treatment group.(3)The results of histopathologal and Hyp examination suggested BML-111 improved the degree of hepatic fibrosis.(4)Relative to the CCL,group,BML-111 repressed the expression ofα-SMA(P<0.01in prevention group,and P<0.05 in treatment group,n=6),the mark of hepatic stellate cell activation.(5)Compare to the model,BML-111 reduced the expression levels of TGF-pi(P<0.01 in prevention group,and P<0.05 in treatment group,n=4)and PDGF(P<0.01 in prevention group,and P<0.0

关键词： lipoxins hepatic fibrosis Hepatic stellate cell inflammation

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<i>In Vitro</i>and <i>in Vivo</i>Anti-Inflammatory Effect of a Biotechnologically Modified Borage Seed Extract: Evidence for Lipid Pro-Resolving Mediators’ Implication in the Enhancement of Psoriatic and Atopic Dermatitis Lesions

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Journal of Cosmetics, Dermatological Sciences and Applications 2015年第2期5卷 151-160页

作者： Gérald Chene Vincent Baillif Emeline Van Goethem Jean-Eric Branka Toni Ionescu Géraldine Robert Luc Lefeuvre Ambiotis SAS Cana Biotech 2 Toulouse France EPHYSCIENCE Nantes France Laboratoires Dermatologiques d’Uriage Siège Social Courbevoie France

Aim: Resolvins, maresins and lipoxins are lipid mediators issued from essential polyunsaturated fatty acids which are the first anti-inflammatory and pro-resolving signals identified during the resolution phase of inflammation. As borage oil and/or borage seed extracts have shown beneficial action in treatment of atopic dermatitis or eczema in human and canine, we have modified a borage oil component by using biotechnology in order to get a compound structurally related to a polyunsaturated fatty acid, and we have studied its ability to reduce inflammation mediators production through the generation of resolvins, maresins and/or lipoxins. Additionally, we have demonstrated the potent anti-inflammatory effect of this new compound which consists in borage seed oil aminopropanediol amides, through an in vivo study concerning subjects suffering from psoriasis or atopic dermatitis. Study Design/Methods: For the in vitro study, inflammation was induced in co-cultures of human dendritic cells and normal keratinocytes by the addition of PMA and the calcium ionophore A23187. Ability of our borage seed oil aminopropanediol amides to increase resolvin D2, maresin 1 and lipoxins A4 and B4 synthesis was then measured. Pro-inflammatory cytokines (IL-1β, IL-6, IL-8) and PGE2 productions were also quantified. For the in vivo study, 36 subjects suffering from psoriasis or atopic dermatitis have used twice a day during 30 days, a formulation containing borage seed oil aminopropanediol amides. Before the beginning of the study and after 30 days’ treatment, the severity of psoriasis and of atopic dermatitis was evaluated by using the PGA and the SCORAD scoring scales, respectively. Results: Borage seed oil aminopropanediol amides were able to significantly increase the resolvin D2, maresin 1 and lipoxins A4 and B4 synthesis. Concomitantly, they were also able to significantly inhibit the production of IL-1β, IL-6, IL-8 and PGE2 induced by the PMA and the calcium ionophore A23187 in the

关键词： Human Skin Biotechnologically Modified Borage Extract Interleukins Inflammation Psoriasis Atopic Dermatitis Resolvins Maresins lipoxins

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The lipoxin receptor agonist BML-111 protects against LPS/D-GalN-induced acute liver injury in rats

The lipoxin receptor agonist BML-111 protects against LPS/D-...

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第九届全国免疫学学术大会

作者： Zhou XY Yan D Yu ZJ Wang HM Xu FY Huang YH Min WP Medical College of Nanchang University Institute of Immunotherapy Nanchang University Jiangxi Academy of Medical sciences

Objective:lipoxins(LXs),a class of arachidonic acid metabolites,display unique anti-inflammatory and pro-resolving actions in a variety of inflammatory *** present study was undertaken to investigate the effects of BML-111(the lipoxin A receptor agonist)in a model of acute liver injury,and to explore the ***:Acute liver injury was induced by intraperitoneal injection of LPS and D-Galactosamine(D-GalN).Forty SD rats were randomly divided into three groups,namely control group,model group and prevention *** carried out histopathological analysis to quantify hepatic neutrophil *** antioxidant capacity of BML-111 was analyzed using biochemical *** levels of TNF-αand IL-1βwere measured using ELISA,and the hepatic expression levels of TGF-β1 and AngII were examined using ***:The data demonstrated:(1)Administration of LPS and D-GalN caused severe damage in liver,the model of acute liver injury in rat was well.(2)Histopathologal examination demonstrated that the rats treated with LPS and D-GalN had marked necrosis,neutrophil infiltration and hyperemia.(3)LPS/D-GalN decreased the hepatic levels of CAT(43.6%,P<0.05),SOD(51.8%,P<0.05),T-AOC(28.1%,P<0.05)and hydroxyl radical-scavenging potential(30.1%,P<0.05),accompanied by a significant increase of MDA content in liver(88.5%,P<0.01).(4)LPS/D-GalN increased the expression levels of TNF-α(about five times,P<0.01)and Angll(65.8%,P<0.01),while inhibiting the expression of hepatic TGF-β1(75.5%,P<0.01).(5)As to the model,BML-111 prevented LPS/D-GalN-induced pathological changes.(6)As to the model,BML-111 increased the activities of SOD(149.9%,P<0.01),CAT(120%,P<0.01),TAOC(173.4%,P<0.01),stimulated hydroxyl radical-scavenging potential(89.3%,P<0.01),and decreased MDA levels(58.2%,P<0.05).(7)As to the model,BML-111 reduced TNF-a level(67.3%,P<0.01)and Angll expression(65.9%,P<0.05),and increased the expression of TGF-01(about 12.3 times,P<0.01).Conclusion:BML-11

关键词： lipoxins liver injury antioxdation inflammation

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A defect in the activities of △~6 and △~5 desaturases and pro-resolution bioactive lipids in the pathobiology of non-alcoholic fatty liver disease

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World Journal of Diabetes 2011年第11期2卷 176-188页

作者： Undurti N Das UND Life Sciences School of Biotechnology Jawaharlal Nehru Technological University Bio-Science Research Centre Gayatri Vidya Parishad College of Engineering Visakhapatnam-530 048

Non-alcoholic fatty liver disease (NAFLD) is a low-grade systemic inflammatory condition, since liver and adipose tissue tumor necrosis factor-α (TNF-α) and TNF receptor 1 transcripts and serum TNF-α levels are increased and IL-6-/-mice are less prone to NAFLD. Fatty liver damage caused by high-fat diets is associated with the generation of pro-inflammatory prostaglandin E2 (PGE2). A decrease in the levels of arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and the usefulness of EPA and DHA both in the prevention and management of NAFLD has been reported. AA, EPA and DHA and their anti-inflammatory products lipoxins (LXs), resolvins and protectins suppress IL-6 and TNF-α and PGE2 production. These results suggest that the activities of △6 and △5 desaturases are reduced in NAFLD and hence, the dietary essential fatty acids, linoleic acid (LA) and α-linolenic acid (ALA) are not metabolized to their long-chain products AA, EPA and DHA, the precursors of anti-inflammatory molecules, LXs, resolvins and protectins that could prevent NAFLD. This suggests that an imbalance between proand anti-inflammatory bioactive lipids contribute to NAFLD. Hence, it is proposed that plasma and tissue levels of AA, EPA, DHA and LXs, resolvins and protectins could be used as predictors and prognostic biomarkers of NAFLD. It is suggested that the synthesis and use of more stable analogues of LXs, resolvins and protectins need to be explored in the prevention and management of NAFLD.

关键词： Prostaglandins Lipids Arachidonic acid Eicosapentaenoic acid Non-alcoholic fatty liver disease Docosahexaenoic acid lipoxins Resolvins Protectins Cytokines Free radicals Hyperlipidemia

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