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lps相关的网络例句
与 lps 相关的网络例句 [注:此内容来源于网络,仅供参考]

Rats were anesthetizedwith pentobarbital and then randomized into four groups: control,ISO-control (pretreatment with 30 min of 1.4% ISO), lipopolysaccharide(LPS; 10 mg/kg IV), and ISO-LPS.The mesentery was prepared for intravital videomicroscopy.

大鼠戊巴比妥麻醉后随机分为四组:对照组、异氟醚组(吸入1.4%的异氟醚30分钟)、脂多糖组( LPS ;10mg/kg IV )、 ISO-LPS 组(先吸入异氟醚后使用 LPS )。

The direct effect of EGCG on LPS in vitro:We investigated the direct effect of EGCG on LPS through the transmission electron microscopy and limulus test for the first time. The results showed that EGCG had no significant effect on the structure and quantity of LPS.

体外EGCG对LPS的直接作用:本研究首次应用透射电镜观察及内毒素鲎实验检测法研究EGCG对LPS的直接作用,结果表明EGCG对INS的结构和量无显著影响,提示EGCG对LPS无直接作用。

A549 cell line was stimulated with LPS (10 μg/mL) and then treated with Rs504393 (10 μg/mL) for 6 hours. ALI model was established with intranasal administration of LPS (5 mg/kg) in C57BL/6J mice. RS504393 (5 mg/kg) was administered 30 min before LPS dripped nasally. IL-8, IL-1β, plasminogen activator inhibitor-1, monocyte chemoattractant protein-2, and the expressions of CCR1 and CCR2b were studied by using Realtime-RT-PCR, ELISA and cyto-flowmetry.

体外实验选用A549细胞系,应用LPS(10μg/mL)刺激合并RS504393(10μg/mL)治疗6 h后,流式细胞仪技术检测CCR1和CCR2的表达,ELISA法检测细胞培养上清液内白介素-8的浓度;体内实验选用C57BL/6J小鼠,腹腔注射RS504393(5 mg/kg)预处理30 min后经鼻滴入JPS(5 mg/kg),LPS刺激4 h后收集BALF和肺脏标本,计数BALF内细胞总数,应用BCA法检测BALF内蛋白浓度,Realtime-RT PCR和ELISA法检测BALF和肺脏IL-1β、凝血酶原激活物抑制物-1和单核细胞趋化蛋白-2的表达。

To evaluate the influence of Chinese nutgall water extract on the toxic effect of LPS to HDPCs, MTT method was used to examine the influence of Chinese nutgall extract on the inhibitory effect of LPS to HDPCs'proliferation, TEM was used to examine the effect of Chinese nutgall extract on the damage of HDPCs'ultrastructure by LPS, a modified enzyme dynamical method was used to examine the influence of Chinese nutgall extract on the inhibitory effect of LPS to HDPCs'ALP activity, radioimmunoussary was used to examine the effect of Chinese nutgall extract on the production of IL-6 from HDPCs stimulated by LPS.

本研究通过细胞培养技术、MTT实验、放射免疫检测法及透射电镜观察等方法观察五倍子水提取物对LPS抑制HDPCs增殖和HDPCs的ALP活性,LPS损伤HDPCs超微结构,LPS诱导HDPCs分泌IL-6的影响,探讨五倍子水提取物拮抗LPS对HDPCs的毒性作用。

GdCl3(10mg/kg) or the same volume of NS was continually injected of vein at 48h and 24h before LPS(5mg/kg) was injected in the male kunming species mouse. Then took out of liver or isolated KCs 30 minute after LPS was injected and assay the protein expression and phosphorylation level of ERK1/2 and p38MAPK of liver or KCs in vivo.Ⅱ. Isolated and cultured KCs of mouse, 1 h pretreatment with GdCl3; Culture medium with LPS(100ng/ml) was added and continuatively incubated 30 minute. Assay the protein expression and phosphorylation level of ERK1/2 and p38MAPK of KCs in vitro and detection effect of GdCl3 on its phagocytosis function in respectively.

Ⅰ 雄性昆明种小鼠在注射LPS(5mg/kg)前48h、24h,分别静脉注射GdCl3(10mg/kg )或等量的生理盐水,于LPS或生理盐水注射后30min,分别取出肝脏或分离KCs,检测肝脏或KCs ERK1/2、p38MAPK蛋白表达及磷酸化水平;Ⅱ体外培养小鼠KCs经GdCl3(100μM)预处理1h,加入含LPS(100ng/ml)的DMEM培养基继续孵育30min,分别检测体外培养KCs ERK1/2、p38MAPK蛋白表达及磷酸化水平和GdCl3对其吞噬、分泌功能的影响。

The response of HNEC to the stimulation of LPS shows dosage dependence, and stimulation of LPS with suitable concentration benefits HNEC secreting Th1/Th2 cell factors to maintain the balance; The stimulation of LPS with too high and too low concentrations would cause unbalanced secretion of Th1/Th2 cell factors, which might be the pathopoiesis mechanism of gram negative bacilli in chronic rhinitis and rhinosinusitis.

LPS对HNEC的刺激反应与浓度呈剂量依赖性,适当浓度的LPS刺激有利于HNEC分泌的Th1/Th2细胞因子维持平衡状态;过高或过低浓度的LPS刺激可诱导HNEC的Th1/Th2细胞因子失衡分泌,这可能是GNB在慢性鼻、鼻窦炎的致病机理。

AMs that collected, pured and cultured with contine method were stimulated by LPS of different concentration(0μg/ml,0.01μg/ml,0.1μg/ml,1μg/ml,10μg/ml) for 60min or by 1μg/ml LPS for different time stage (0min,5min,15min,30min,60min,120min) to observe the dynamic change of NF-кB intranuclear level and NO production, from which the best concentration and time point of LPS stimulation were selected. In the study, all AMs were divided into 4 groups: control group, group stimulated with LPS, group interrupted by Cal C and group inhibited by PDTC. The following parameters were measured: NF-кB level in nuclear protein extraction of AMs detected with sandwich ELISA, Inter-nuclear transposition of NF-кB observed with immunocytochemistry staining, NO content in cell culture medium quantitied with nitric acid reductase assay, Morphologic change of AMs in apoptosis observed with acridine orange staining and fragmentation at genome DNA of AMs detected with apoptotic electrophoresis assay.

分离、纯化及培养大鼠肺巨噬细胞;以不同浓度的LPS(0μg/ml,0.01μg/ml,0.1μg/ml,1μg/ml,10μg/ml)和不同作用时间(0min,5min,15min,30min,60min,120min)分别刺激小室培养的细胞单层,观察NF-κB的核内浓度及NO合成量的动态变化,选择LPS的最佳用量和作用时间;然后分成四组实验,设正常对照组,LPS处理组,特异性PKC抑制剂阻断组,NF-κB抑制剂阻断组;收集培养的单层细胞及培养液;采用夹心ELISA法定量测定细胞核提取物中的NF-κB水平;免疫组化法检测NF-κB的核内移位变化;硝酸还原酶法测定细胞培养液中NO含量;吖啶橙染色观察凋亡细胞的形态学变化,凋亡电泳实验检测细胞凋亡后基因组DNA的断裂情况。

PART Ⅱ IMMUNOPATHOLOGICAL EVIDANCE OF SIALIC ACID STRUCTURE IN CAMPYLOBACTER JEJUNI AS THE CRITICAL ANTIGEN TO INDUCE PERIPHERAL NEUROPATHY To demonstrate the critical role of NANA structure in the pathogenesis of allergic peripheral neuropathy induced by Campylobacter jejuni and provide immunopathological evidence to confirm the supposition of molecular mimicry and cross-immunity between CJ LPS and gangliosides in nerve.

LPS免疫后第2周实验豚鼠的免疫血清中,抗LPS IgG抗体滴度均明显增高,第3周达高峰,第5周仍维持在峰水平,野生株和突变株LPS免疫血清中的抗-野生株LPS IgG抗体滴度较各自免疫前分别增高8倍和4倍,抗-突变株LPS IgG抗体滴度则较各自免疫前分别增高6.5倍和15倍;(2)全身免疫后第3周和第5周,野生株LPS免疫血清中检测到较免疫前增高6倍的抗-GM1 IgG抗体,而NANA缺失的突变株LPS免疫血清中一直未检测到抗-GM1 IgG抗体;(3)野生株LPS免疫组中有17.3%的坐骨神经原纤维发生以轴索变性为主(占65%)的免疫性损伤,与突变株LPS免疫组和对照组比较均有显著性差异。

Methods: Twenty-four male SD rats were randomly divided into normal control (NC, n=6), protein C activator (PCA, n=6), lipopolysaccharide (LPS, n=6) and LPS+PCA group (n=6). NC group were given normal saline and PCA group were injected protein C activator (0.4 mg/kg) through vein of the tail. LPS group were administered lipopolysaccharide (10 mg/kg, 4h) by intraperitoneal injection method to make the model of septic shock rats. After the animal model was made, LPS+PCA group were injected protein C activator (0.4 mg/kg) through vein of the tail. 30 minutes after the injection, each rat was tested by Medlab biosignal analyzing system for observing mean arterial pressure and left ventricle function, the activity of LDH and iNOS in myocardium and the cuttings of myocardial tissues.

取SD雄性大鼠24只随机分成对照组、PCA组、LPS组和LPS+PCA组四组,对照组尾静脉注射生理盐水,PCA组尾静脉注射蝮蛇毒蛋白C激活物,LPS组腹腔注射LPS (10 mg/kg, 4h)的方法建立败血症休克的实验动物模型,在建立败血症的实验动物模型的基础上,尾静脉注射PCA (0.4 mg/kg)为LPS+PCA组,每只大鼠均于药后30 min时运用Medlab生物信号采集处理系统记录平均动脉压和左心室功能指标,并测定心肌中乳酸脱氢酶活性、诱导性一氧化氮合酶活性及心肌病理切片。

Methods Adult wistar rats were randomly divided into control group (0.9% N.S.), LPS group (10 mg/kg LPS) and LPS+PD group (10 mg/kg LPS+10 mg/kg PD), myocardial functional parameters (LVSP, LVEDP,±dp/dt max) were recorded for 7 hours, then observe the myocardial tissue with transmission electrical microscope.

正常Wistar大鼠18只,随机平均分为3组,分别为正常对照组(0.9%生理盐水), LPS组(10 mg/kg LPS)和LPS+PD组(10 mg/kg LPS+10 mg/kg PD),分别观察其心功能指标(LVSP, LVEDP,±dp/dt max)的改变,7 h后取心脏,透射电镜观察不同处理对心肌微结构的影响。

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