Apo-9′-Fucoxanthinone,Isolated from Sargassum muticum,Inhibits CpG-Induced Inflammatory Response by Attenuating the Mitogen-Activated Protein Kinase Pathway

Sargassum muticum (S. muticum) is a brown edible alga and widely distributed in Korea. This report was designed to evaluate the anti-inflammatory properties of apo-9′-fucoxanthinone (APO-9′) isolated from S. muticum on pro-inflammatory cytokine production. S. muticum extract (SME) exhibited significant inhibitory effects on pro-inflammatory cytokine production in bone marrow-derived macrophages (BMDMs) and dendritic cells (BMDCs). APO-9′ pre-treatment in the CpG DNA-stimulated BMDMs and BMDCs showed a strong dose-dependent inhibitory effect on interleukin (IL)-12 p40, IL-6 and tumor necrosis factor (TNF)-α production with IC₅₀ values ranging from 5.31 to 13.79. It exhibited a strong inhibitory effect on the phosphorylation of ERK1/2 and on activator protein (AP)-1 reporter activity. APO-9′ pre-treatment exhibited significant inhibition of CpG DNA-induced production of inducible nitric oxide synthase. Taken together, these data suggest that SME and APO-9′ have a significant anti-inflammatory property and warrant further studies concerning the potentials of SME and APO-9′ for medicinal use.     

Lithothamnion muelleri Controls Inflammatory Responses,Target Organ Injury and Lethality Associated with Graft-versus-Host Disease in Mice

Lithothamnion muelleri (Hapalidiaceae) is a marine red alga, which is a member of a group of algae with anti-inflammatory, antitumor, and immunomodulatory properties. The present study evaluated the effects of treatment with Lithothamnion muelleri extract (LM) in a model of acute graft-versus-host disease (GVHD), using a model of adoptive splenocyte transfer from C57BL/6 donors into B6D2F1 recipient mice. Mice treated with LM showed reduced clinical signs of disease and mortality when compared with untreated mice. LM-treated mice had reduced tissue injury, less bacterial translocation, and decreased levels of proinflammatory cytokines and chemokines (interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-C motif) ligand 3 (CCL3) and chemokine (C-C motif) ligand 5 (CCL5)). The polysaccharide-rich fraction derived from LM could inhibit leukocyte rolling and adhesion in intestinal venules, as assessed by intravital microscopy. LM treatment did not impair the beneficial effects of graft-versus-leukaemia (GVL). Altogether, our studies suggest that treatment with Lithothamnion muelleri has a potential therapeutic application in GVHD treatment.     

乙酰乙酸抑制脂多糖诱导的奶牛中性粒细胞炎症信号通路的激活

为研究乙酰乙酸(Acetoacetic acid,AcAc)对奶牛中性粒细胞炎症信号通路的影响,以脂多糖(Lipopolysaccharide,LPS)诱导的奶牛中性粒细胞炎症模型为研究对象,利用qRT-PCR、生化和酶联免疫吸附法(ELISA)测定IL-1β、IL-6、TNF-α和IKKβ激酶活性。结果表明:1)qRT-PCR结果显示,与对照组相比较,LPS处理组IL-1β、IL-6和TNF-αmRNA的表达显著增强(P0.01)。与LPS处理组比较,LPS+AcAc混合处理组,其表达量显著下调(P0.05);2)生化检测结果显示,与对照组相比较,LPS处理组中性粒细胞IKKβ激酶活性显著增强(P0.01)。与LPS处理组比较,LPS+AcAc混合处理组IKKβ激酶活性则显著降低(P0.05);3)ELISA结果显示,与对照组相比较,LPS增加促炎因子TNF-α、IL-6和IL-1β的释放。相对于LPS处理组,LPS+AcAc混合处理组促炎因子的释放则显著降低(P0.01)。综上,AcAc可以抑制LPS诱导的奶牛中性粒细胞炎症信号通路的激活,具有一定的抗炎功能。     

牛骨胶原蛋白肽的表征及其对Balb/c小鼠的抗疲劳作用

为了开发牛骨胶原蛋白肽(BBP)的抗疲劳功能,对BBP的氨基酸组成和肽段序列进行表征;选取16只7周龄、SPF级的Balb/c小鼠并随机分为2组,包括对照组(生理盐水)和肽干预组(w(BBP)=200 mg/kg)),每日定时灌胃。BBP干预4周后,测定小鼠的负重游泳时间和运动后血清代谢积累物含量。BBP干预18周后,测定血清氧化因子、炎症因子含量和肠道菌群组成。结果表明：1)BBP疏水性氨基酸比例为61.37%,大部分肽段来源于蛋白P02453(I型胶原蛋白的α1链)。2)BBP干预后小鼠负重游泳时间显著提高,且运动后血氨浓度显著降低、谷胱甘肽浓度显著升高(P<0.05),表明了BBP潜在的抗疲劳能力。3)BBP干预后,在非运动状态下小鼠血清SOD和GSH-Px显著升高,MDA浓度显著降低(P<0.05),表明了BBP潜在的抗氧化能力;在免疫方面,BBP干预后小鼠血清抗炎因子IL-10和促炎因子IL-6、TNF-α浓度均显著下降(P<0.05),主要的免疫器官胸腺指数显著下降(P<0.01),脾指数显著上升(P<0.05);在粪便中,潜在的有益菌Akke...     

TFDG对IL-1β体外诱导大鼠软骨细胞炎性损伤的保护作用研究

体外分离培养SD雄性大鼠膝关节软骨细胞,经甲苯胺蓝及Ⅱ型胶原(Col Ⅱ)免疫荧光染色鉴定后,加入白介素-1β(IL-1β)诱导建立骨关节炎(OA)细胞模型,探讨茶黄素双没食子酸酯(TFDG)对OA软骨细胞的保护作用。细胞形态观察发现TFDG能明显改善OA软骨细胞形态。实时荧光定量PCR(Real-time PCR)结果显示,TFDG不仅可以上调软骨细胞分子标志物Col Ⅱ mRNA的表达,还可以下调炎症因子IL-1β、IL-6mRNA的表达。酶联免疫吸附实验(ELISA)检测结果进一步表明TFDG可明显降低炎症因子的分泌。免疫印迹(Western blot)检测结果证明,TFDG预干扰可降低炎症诱导酶环氧化酶COX-2蛋白表达量。这些结果说明TFDG通过减弱炎症反应,从而对IL-1β体外诱导大鼠软骨细胞炎性损伤起到保护作用。     

Up-regulation of miR-181a attenuates releases of CSE-induced pro-inflammatory factors and expression of collagen IV,fibronectin and α-SMA in human bronchial epithelial cells

AIM: To investigate the effect and potential mechanism of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced the productions of pro-inflammatory factors and the expression of collagen IV, fibronectin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (HBECs). METHODS: CSE-induced miR-181a expression was detected by RT-qPCR in the HBECs. After tansfected with miR-181a mimic, the releases of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and transforming growth factor-β1 (TGF-β1) were measured by ELISA, the protein expression of collagen IV, fibronectin and α-SMA was determined by Western blot. The activation of NF-κB/TGF-β1/Smad3 pathway was also evaluated by Western blot. RESULTS: CSE increased the levels of TNF-α, IL-1β, IL-6 and TGF-β1 and the expression of collagen IV, fibronectin and α-SMA, and decreased the expression of miR-181a in the HBECs (P<0.05). However, transfected with miR-181a mimic partially prevented the releases of TNF-α, IL-1β, IL-6 and TGF-β1, and inhibited the expression of collagen IV, fibronectin and α-SMA (P<0.05). Additionally, the activation of NF-κB/TGF-β1/Smad3 evoked by CSE was attenuated after transfected with miR-181a mimic. CONCLUSION: Up-regulation of miR-181a prevents the releases of CSE-induced pro-inflammatory factors and expression of collagen IV, fibronectin and α-SMA in the HBECs, and its mechanism may be related to the inhibition of NF-κB/TGF-β1/Smad3 pathway.     

植物多酚对氧化应激与炎症信号通路的调控机制

炎症及氧化应激是造成动物机体组织和器官损伤的主要原因之一,肠道炎症可造成肠黏膜损伤,进而影响其屏障功能,减弱动物对外界刺激的防御能力。植物多酚具有抗氧化、抗炎、调节肠道菌群等多种潜在功效,且具有低毒、无耐药性等特点,因此,在新型饲料添加剂的开发中具有广阔的应用前景。但目前大部分植物多酚在动物体内的代谢及调控机制尚不明确,这极大阻碍了其合理有效利用。本文基于近期研究就植物多酚对氧化应激与炎症信号通路的调控机制进行综述,为其在新型饲料添加剂中的应用提供理论依据。     

外源添加短链脂肪酸调控断奶前犊牛胃肠道健康发育潜在功能和机制

胃肠道健康发育是影响犊牛生长及其潜在生产性能发挥的关键。研究报道,短链脂肪酸(SCFA)和胃肠道微生物可促进幼龄动物胃肠道健康发育,但具体机制还不明确。新生犊牛胃肠道发育不健全,胃肠道内微生物种类及丰度均较低,内源性产生的代谢产物SCFA较少。现有文献表明,SCFA具有通过影响断奶前犊牛胃肠道微生物的定植、维持肠道黏膜屏障的完整性及提高肠道抗炎能力,进而促进犊牛胃肠道健康发育的功能。本文拟从胃肠道上皮和微生物2个层次来探究并综述外源添加SCFA促进断奶前犊牛胃肠道发育的分子机制,及其对断奶前犊牛胃肠道微生物定植的影响及机理,为犊牛健康培育与科学饲养提供理论基础。