目的 探讨牙髓卟啉单胞菌(Porphyromonas endodontalis,Pe)脂多糖对成骨细胞产生巨噬细胞集落刺激因子(macrophage colony stimulating factor,M-CSF) mRNA和蛋白表达的影响及是否有核因子κB信号通路的参与.方法 以不同质量浓度的Pe-脂多糖(0～50 mg/L)刺激MC3T3-E1细胞和以10 mg/L Pe-脂多糖作用于细胞不同时间(0～ 24 h)后,采用反转录-PCR和酶联免疫吸附试验(enzyme-linked immunoadsordent assay,ELISA)检测M-CSF mRNA和蛋白的表达,其中未加Pe-脂多糖刺激组为空白对照组.采用核因子κB信号通路特异性抑制剂BAY 11-7082预处理1h,检测其对Pe-脂多糖刺激MC3T3-E1细胞后M-CSF mRNA和蛋白表达的影响,实验分组如下:空白对照组、BAY组(10 μmol/L BAY 11-7082单独作用MC3T3-E1细胞)、Pe-脂多糖组(10 mg/L的Pe-脂多糖刺激MC3T3-E1细胞6h)、BAY+Pe-脂多糖组(10 μmol/L BAY 11-7082预处理细胞1h,10 mg/L的Pe-脂多糖刺激MC3T3-E1细胞6h).结果 不同质量浓度Pe-脂多糖(0～50 mg/L)刺激MC3T3-E1细胞后,M-CSFmRNA和蛋白的表达具有剂量依赖性,蛋白表达量从(35±2) ng/L(空白对照组)增加到(170±8) ng/L(50 mg/L组).当10 mg/L Pe-脂多糖作用于MC3T3-E1细胞6h时,M-CSF mRNA的表达量

Objective To investigate the effects of lipopolysaccharides(LPS) extracted from Porphyromonas endodontalis(Pe) on the expression of macrophage colony stimulating factor(M-CSF) mRNA and protein in MC3T3-E1 cells and the role of nucler factor-κB(NF-κB) in the process.Methods MC3T3-E1 cells were treated with different concentrations of Pe-LPS(0-50 mg/L) and 10 mg/L Pe-LPS for different hours (0-24 h).The expression of M-CSF mRNA and protein was detected by reverse transcription polymerase chain reaction(RT-PCR) and enzyme-linked immunoadsordent assay(ELISA).The cells untreated by Pe-LPS served as control.The expression of M-CSF mRNA and protein was also detected in 10 mg/L Pe-LPS treated MC3T3-E1 cells after pretreated with BAY 11-7082 for 1 h,a special NF-κB inhibitor.The groups were divided as follows,control group,BAY group(10 μmol/L BAY 11-7082 treated alone MC3T3-E1 cells),Pe-LPS group(10 mg/L Pe-LPS stimulated MC3T3-E1 cells for 6 h),BAY combine with Pe-LPS group (10

观察海藻多糖胶囊对高脂血症大鼠血脂的影响。实验采用灌服高脂乳剂形成高脂血症模型;2次给大鼠灌胃海藻多糖胶囊15d及30d测定血清总胆固醇(TCHO)、甘油三酯(TG)及低密度脂蛋白胆固醇(LDL-C)等;与模型组比较,海藻多糖胶囊可明显降低血清TCHO、TG和LDL-C等。海藻多糖胶囊降血脂作用显著。

To investigate the effects of Algae Polysaccharides capsules on blood lipids in experimental hyperlipidemic rats .The experimental hy-perlipidmic rat model was established by ig high cholesterol emulsion .Two times fed to rats by gastric algae polysaccharides capsules 15 and 30 days .The determination of serum total cholesterol ,triglyceride and low density lipoprotein cholesterol ,etc .Compared with model group ,the serum levels of total cholesterol ,Triglycerine and low density lipoprotein cholesterol decreased obviously .The experimental results showed that algae polysaccharides capsules fall hematic fat action of hyperlipidemia rats obviously .

目的探讨脂多糖预处理时糖原合成酶激酶3(glycogen synthase kinase-3,GSK-3)功能活性的变化及其对肝组织糖原代谢的影响和机制。方法雄性SD大鼠随机分为正常对照、脂多糖预处理和GSK-3抑制剂氯化锂预处理组,分别进行相应处理后再接受大剂量脂多糖(10 mg/kg)攻击以建立脂多糖诱导的急性肝损伤模型;采用PAS染色法观察肝组织糖原聚集,用试剂盒法定量检测肝组织糖原含量,以Western Blot法半定量分析GSK-3的蛋白表达和抑制性磷酸化水平,采用考马斯亮兰比色法测定肝组织钙依赖蛋白酶的活性。结果尽管大剂量脂多糖攻击后各组动物肝组织糖原含量组间比较均无显著差异(P0.05),但均较攻击前有显著降低(P0.05),且脂多糖和氯化锂预处理均可导致肝组织糖原含量增加(P0.05);尽管诱导脂多糖预处理并未改变GSK-3的蛋白表达水平(P0.05),但导致GSK-3β抑制性磷酸化(P0.05)和GSK-3α不完全裂解;大剂量脂多糖攻击后肝组织钙依赖蛋白酶活性较前显著升高(P0.05),但组间比较无显著差异(P0.05)。结论脂多糖预处理导致GSK-3β抑制性磷酸化和GSK-3α不完全裂解,促进肝组织糖原合成和聚集,但不影响钙依赖蛋白酶活性,有利于增加肝组织糖原储备并可能在遭受大剂量脂多糖攻击时提供能量需求。

Objective To investigate the changes in the functional activity of glycogen synthase kinase-3 (GSK-3) in the hepatic tissue after endotoxin (lipopolysaccharide, LPS) tolerance and explore the effects of LPS-induced GSK-3 inhibition on glycogen metabolism in the liver. Methods Male SD rats were randomly divided into normal control, endotoxin pretreatment and GSK-3 inhibitor (lithium chloride) groups with corresponding pretreatments prior to a large dose of LPS challenge (10 mg/kg) to induce liver injury. Glycogen deposition and content in the hepatic tissue was detected using periodic acid-Schiff (PAS) staining and a glycogen quantification kit, respectively. Western blotting was performed for semi-quantitative analysis of protein level and inhibitory phosphorylation of GSK-3, and a Coomassie brilliant blue G-250-based colorimetric assay was used to detect calpain activity in the liver. Results Glycogen content in the liver decreased significantly after LPS challenge in all the 3 groups

本文通过大量的国内外研究资料对近年来魔芋多糖的研究进行梳理。目前大量关于魔芋多糖生物学功能的研究集中在人体和动物实验，未见细胞培养实验。魔芋多糖的主要生物学功能包括降脂、降糖、促进免疫功能、防止细胞脂质过氧化、对抗皮肤炎症因子等多重功效。本文根据大量的文献和实验研究，并结合其功能和机制，展望魔芋多糖在运动医学领域中的应用。

In this paper, a large number of domestic and foreign research data for researches in recent years are col-lected to sort out konjac polysaccharide. At present, most researches on the biological function are on the concentration of human and animal experiments, without cell experiments. The main biological functions of konjac polysaccharide in-clude: lipid-lowering, hypoglycemic, promote immune function and prevent cell lipid peroxidation, against skin inflam-matory cytokines such as multiple effects. According to a lot of data and experimental researches, combined with its functionality, this paper looks forward to the application of konjac polysaccharide in the sports medical field.

背景：对于肠上皮细胞遭受高热和肠道细菌以及由细菌产生的内毒素等多重打击后经历了怎样的分子生物学变化，一直缺乏切实、可靠实验依据。 目的：观察脂多糖联合热打击对人肠上皮细胞损伤及炎症因子白细胞介素6、肿瘤坏死因子肿瘤坏死因子a 释放的影响。 方法：体外培养人肠上皮细胞株(SW 480)，将3×105细胞种入实验用培养皿。实验分组为：对照组(37℃)，热打击组(43℃2 h)，脂多糖刺激组(1 mg /L脂多糖6 h)，热打击联合脂多糖刺激组(43℃+脂多糖)。采用WST-1法观察细胞毒效应和细胞存活率；同时采用ELISA法观察各组炎症因子白细胞介素6和肿瘤坏死因子a水平。 结果与结论：与对照组相比，热打击组具有细胞毒效应，其细胞活率明显下降，细胞炎症因子白细胞介素6和肿瘤坏死因子 a 水平也有所增高。脂多糖组单独作用也具有细胞毒效应，细胞活力、细胞增殖率也明显下降，同时白细胞介素6和肿瘤坏死因子a水平明显升高。而热打击和脂多糖联合打击后，可观察到两者的协同作用。结果说明，热打击和脂多糖单独作用均可引起细胞损伤，增加炎症因子白细胞介素6和肿瘤坏死因子 a 表达，并且二者之间存在协同效应。实验结果为理解重症中暑病理过程中，肠道功能障碍、肠道细菌和内

BACKGROUND:There is no practical and reliable experimental evidence for changes in molecular biology of intestinal epithelial cels suffering from heat stress, intestinal bacteria and endotoxin produced by bacteria. OBJECTIVE:To observe the effect of lipopolysaccharide stimulation combined with heat stress on human intestinal epithelial cel injury and release of interleukin-6 and tumor necrosis factor-alpha. METHODS: Human intestinal epithelial cel lines (SW 480) culturedin vitro was seeded into culture dishes at a density of 3×105, and then divided randomly into four groups: control group was cultured in an incubator of 37℃; heat stress group was cultured in the incubator of 43℃ for 2 hours; lipopolysaccharide group was stimulatedby 1 mg/L lipopolysaccharide for 6 hours; lipopolysaccharide+heat stress group (combination group) was subjected to heat stress for 2 hours folowed by lipopolysaccharide stimulation for 6 hours. WST-1 method was used to investigate the cytotoxic e