Zymosan足底炎性疼痛大鼠模型的建立及其脊髓背角COX-2表达水平变化

目的评价该模型大鼠的疼痛行为学特点和炎性水肿程度,并对该模型大鼠脊髓背角COX-2表达水平进行分析。方法 SD大鼠48只,随机分为3组,即对照组(n=8)、假手术组(n=16)及zymosan组(n=24)。按Meller方法制作zymosan足底炎性疼痛模型,假手术组在左侧后足皮下注射同等容积的PBS。采用电子VonFrey压力测痛仪、热板和电子数显卡尺分别于制模后0.5h、1h、2h、4h、8h、24h和48h测定各组大鼠左侧后足机械刺激缩足阈值、热敏缩足反射阈值和左足最大厚度。各组大鼠在指定时间点处死后取制模侧腰段脊髓背角,采用Western blot方法测定脊髓背角中COX-2表达水平。结果与对照组和假手术组比较,zymosan组大鼠制模侧后足机械刺激缩足阈值和热敏缩足反射阈值显著降低(P<0.05,P<0.01),最大厚度显著增加(P<0.01),提示zymosan组大鼠出现机械痛敏、热痛敏和炎性水肿。Zymosan组大鼠制模侧脊髓背角COX-2表达水平显著增加,与对照组和假手术组比较有显著性差异(P<0.05)。结论 Zymosan足底炎性疼痛大鼠模型可以产生持续的、可信的痛觉过敏,与人体损伤后情况基本一致,并诱导脊髓背角COX-2表达水平增加,是研究组织损伤诱发炎性疼痛机制的较佳选择。

Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction

AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administration of normal saline(SS group); sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P < 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P < 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P < 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P < 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P < 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.

Inhibition of zymosan-induced cytokine and chemokine expression in human corneal fibroblasts by triptolide

AIM：To investigate the effects of triptolide on proinflammatory cytokine and chemokine expression induced by the fungal component zymosan in cultured human corneal fibroblasts（HCFs）.·METHODS：HCFs were cultured in the absence or presence of zymosan or triptolide.The release of interleukin（IL）-6,IL-8,and monocyte chemoattractant protein-1（MCP-1）into culture supernatants was measured with enzyme-linked immunosorbent assays.The cellular abundance of the m RNAs for these proteins was determined by reverse transcription and real-time polymerase chain reaction analysis.The phosphorylation of mitogen-activated protein kinases（MAPKs）and the endogenous nuclear factor-κB（NF-κB）inhibitor IκB-αwas examined by immunoblot analysis.The release of lactate dehydrogenase（LDH）activity from HCFs was measured with a colorimetric assay.·R ESULTS：Triptolide inhibited the zymosan-induced release of IL-6,IL-8,and MCP-1 from HCFs in a concentration-and time-dependent manner.It also inhibited the zymosan-induced up-regulation of IL-6,IL-8,and MCP-1 m RNA abundance in these cells.Furthermore,triptolide attenuated zymosan-induced phosphorylation of the MAPKs extracellular signalregulated kinase（ERK）,c-Jun NH2-terminal kinase（JNK）,and p38 as well as the phosphorylation and degradation of IκB-α.Triptolide did not exhibit cytotoxicity for HCFs.·C ONCLUSION：Triptolide inhibited proinflammatory cytokine and chemokine production by HCFs exposed tozymosan,with this action likely being mediated by suppression of MAPK and NF-κB signaling pathways.This compound might thus be expected to limit the infiltration of inflammatory cells into the cornea associated with fungal infection.

Effect of zymosan on the expression and function of the gap-junction protein connexin 43 in human corneal fibroblasts

AIM:To study the effect of zymosan,a ligand found on the surface of fungi,on gap junctional intercellular communication(GJIC)in cultured human corneal fibroblasts(HCFs).METHODS:Zymosan was added to the medium of cultured HCFs with or without the administration of mitogenactivated protein kinase(MAPK)inhibitors or the inhibitor kappa B kinase 2(IKK2)inhibitor IV.The protein and m RNA levels of connexin 43(Cx43)in HCFs were measured by Western blot,immunofluorescence,and quantitative reverse transcription-polymerase chain reaction(q RT-PCR)analyses.The GJIC activity was tested using a dye-coupling assay.RESULTS:The reduction of Cx43 protein and m RNA levels as well as a significant decrease in GJIC activity were observed in cultured HCFs when zymosan was added into the culture medium.Compared with controls(no zymosan),the protein level of Cx43 was reduced by 45%and 54%in the presence of zymosan at 200 and 600μg/m L,respectively(P<0.05);and it was reduced by 45%,48%,and 75%in the presence of zymosan(600μg/m L)for 24,36,and 48 h,respectively(P<0.05).The m RNA expression of Cx43 was reduced by 98%in the presence of zymosan(P<0.05).The effects of zymosan on Cx43 expression and GJIC activity were attenuated by the administration of PD98059[an extracellular signal-regulated kinase(ERK)signaling inhibitor](P<0.05),c-Jun NH2-terminal kinase(JNK)inhibitor II(P<0.05),and IKK2 inhibitor IV(P<0.05).CONCLUSION:Zymosan inhibits the activity of GJIC in cultured HCFs.This effect is likely regulated via the nuclear factor-κB(NF-κB),MAPK/ERK,and JNK signaling pathways.The inhibitory effects of zymosan on Cx43 expression and GJIC activity in HCFs may induce damage of corneal stroma during corneal fungal infection.

基于TLR2/MyD88信号通路探究五味子乙素对全身炎症反应综合征的影响

目的观察五味子乙素(Schisandrin B,SchB)通过TLR2/MyD88信号通路对酵母聚糖诱导的小鼠全身炎症反应综合征(Systemic inflammatory response syndrome,SIRS)的影响。方法采用腹腔注射酵母聚糖方法造模,记录小鼠体温及白细胞变化,应用酶联免疫吸附法检测血清中TNF-α、IL-1β及IL-6水平,应用试剂盒检测ALT、AST、Cr、BUN含量;HE染色观察各组织病理学变化;应用Western Blot法检测组织中TLR2、MyD88、NF-κB、HMGB1蛋白表达水平。结果SchB使小鼠体温升高显著(P<0.01),白细胞数量增多明显(P<0.01);SchB能显著降低TNF-α、IL-1β、IL-6、ALT、AST、Cr、BUN水平(P<0.001);Western Blot结果显示,SchB能显著降低组织中TLR2、MyD88、NF-κB、HMGB1的表达水平(P<0.01)。结论SchB能够减轻由酵母聚糖导致的SIRS,其作用机制主要是通过调控TLR2/MyD88信号通路缓解炎症。

Relationship between HMGB1 content and MHC-II expression in circulating monocytes and spleen of mice challenged with zymosan

Objective： To observe the regularity of change in high mobility group protein box 1 （HMGB 1） content in serum and spleen of mice with multiple organ dysfunction syndrome （MODS）, to analyze the correlation between HMGB 1 content and major histocompatibility complex （MHC）-II-I-Ab expression on monocytes in blood and spleen, and to explore the effect of HMGB 1 on immune function of circulating monocytes and splenocytes. Methods： One hundred 8-week-old male 57BL/6 mice were randomly divided into normal group and experimental group subdivided into 8 subgroups： 3, 8, 12 hours, 1, 2, 3, 5- 7 days and 10-12 days post zymosan injection （PZI）. MODS model was replicated by injecting zymosan into the peritoneal cavity. At each time point, blood and spleen were collected to detect HMGB 1 content and the rate of I-A^b positive monocytes. Results： In normal and PZI 3-hour, 8-hour mice, serum HMGB 1 was not detected, but it significantly increased at PZI 12 hours. In spleen of normal mice, there was low level of HMGB 1 expression. In zymosan-treated mice, HMGB 1 started to rise in spleen at PZI 3 hours. Subsequently, HMGB 1 content in both serum and spleen significantly increased, and it reached the peak level in 1-2 days, decreased in 5 days, and then increased in 10-12 days. The number of I-Ab positive monocytes in circulating blood and spleen decreased at 1-2 days （t=9.589, 4.432, P〈0.01） and 10-12 days following the challenge, forming a two trough like decrease, just corresponding with two-peak increase of HMGB 1. However, at 3 hours after zymosan challenge, I-Ab expression on circulating monocytes was downregulated （t=5.977, P〈0.01）, while that in spleen upregulated （t=4.814, P〈0.01）. Conclusion： In mice with MODS, up-regulated HMGB lexpression can regulate I-Ab expression on monocytes to depress their ability of presenting antigen, which results in immune disturbance contributing development of MODS.

酵母多糖对小鼠腹腔巨噬细胞产生一氧化氮和白细胞介素-1的影响

目的探讨酵母多糖对小鼠腹腔巨噬细胞产生一氧化氮 (NO)和白细胞介素 1(IL 1)的影响。方法将不同剂量的酵母多糖加入体外培养的小鼠腹腔巨噬细胞中 ,取细胞培养上清液根据Griess反应检测NO-2 的量 ,间接反映巨噬细胞产生NO的生成量 ,并用溴化四唑蓝 (MTT)比色法检测上清液中IL 1的生成量。结果酵母多糖可明显促进小鼠腹腔巨细胞产生NO和IL 1,NO的生成量呈现剂量依赖关系。结论酵母多糖可诱导小鼠腹腔巨噬细胞产生NO和IL 1,可能是酵母多糖调节机体免疫功能。

小剂量酵母多糖诱发肠缺血-再灌注后全身炎症反应和多器官功能障碍综合征

目的 :研究肠缺血再灌注 (I R)损伤后腹腔注射小剂量酵母多糖对全身炎症反应和远隔器官的影响。方法 :将雄性 Wistar大鼠随机分为 3组。二次打击组 (M组 )先阻断肠系膜上动脉血流 6 0 m in,于恢复肠道血流 12 h腹腔注射小剂量酵母多糖 (12 5 m g/ kg) ;对照组分别实施单纯肠缺血再灌注损伤 (I R)或腹腔注射酵母多糖 (Z)。观察 3组动物炎症介质、脏器功能及死亡率的变化。结果 :3组动物均出现全身炎症反应综合征 ,M组动物血肿瘤坏死因子、内毒素含量以及肺和小肠髓过氧化物酶活性均显著高于 I R组和 Z组。二次打击组 72 h多器官功能障碍综合征 (MODS)发病率和死亡率分别为 4 8%和 6 8% ,显著高于两个单次打击组。结论 :小剂量酵母多糖能诱发肠缺血再灌注后全身炎症反应和 MODS。

小鼠迟发型多器官功能障碍综合征模型复制及病理学观察

目的 :建立一种小鼠多器官功能障碍综合征 (MODS)模型。方法 :选用昆明种小鼠 ,按抽签法随机分为正常对照组和模型实验组 ,实验组按不同时间点又分为 6～ 4 8h及 3～ 7d和 8～ 12 d组。实验组小鼠腹腔注射酵母多糖 ,观察各组动物的症状、体征、生存率、脏器功能指标〔如丙氨酸转氨酶 (AL T)、血尿素氮 (BUN )、血肌酐 (Cr)和肌酸激酶 (CK)〕与组织病理变化。结果 :8～ 12 d组实验小鼠的症状、体征与功能指标 (AL T、BUN及 Cr)均发生明显变化 ,肺、肝、心、肾及胃肠道等脏器病理改变严重。结论 :采用腹腔注射酵母多糖的方法 ,可以成功地复制出迟发型小鼠 MODS模型。

炎症诱导的新型大鼠动脉粥样硬化模型的建立及Rb1的防治作用

目的通过激发大鼠炎症反应建立新型动脉粥样硬化(AS)动物模型并观察人参皂苷Rb1的抗AS作用。方法模型组采用酵母多糖混悬液(20 mg/kg)每隔3d腹腔注射一次,引发大鼠持续性炎症;相同方法注射无菌石蜡液作为对照组;Rb1组同时腹腔注射Rb1(40 mg/kg);所有大鼠均喂食高脂饲料,实验共10周。分别通过苏丹染色、透射电镜、real time PCR、免疫组化、ELISA观察大鼠主动脉壁大体标本、超微结构、NFκB、TNFα、IL6的表达。结果模型组可见红染的脂纹、斑块形成,电镜显示内膜下层出现吞噬脂滴的泡沫细胞,NFκB/P65高表达于主动脉壁的内膜层,TNFα、IL6水平均明显高于对照组,经Rb1干预后大体标本可见AS病变明显减轻,电镜下未见泡沫细胞,NFκB、TNFα、IL6水平均较模型组显著降低。结论在高脂喂饲的基础上持续炎症刺激能够成功诱导大鼠AS模型,人参皂苷Rb1能够通过抑制炎症反应抗AS。

丹参素、黄芩甙等对大鼠腹腔巨噬细胞产生PGE_2及TXB_2的影响

酵母多糖刺激大鼠腹腔细胞合成与释放PGE_2及TXB_2,经短期培养(0～4h),静止的细胞合成的PGE_2虽随时间的延长而增加,但无显著差别,而TXB_2的增长有明显差别。经酵母多糖刺激后二者均有显著增加,但以TXB_2之增加更迅速。角叉菜、硅胶、钙离子载体A_(23187)均能显著促进培养24h的腹腔巨噬细胞合成与释放PGE_2和TXB_2。消炎痛、丹参素、硝苯吡啶及黄芩甙明显抑制A_(23187)诱导的PGE_2合成增加。

炎症因素在泡沫细胞形成中的作用及三七皂苷对其影响

目的 探讨炎症因素在小鼠腹腔巨噬细胞来源泡沫细胞形成中的作用及三七皂苷对其影响。方法 在传统泡沫细胞形成模型基础上添加炎症刺激因素及三七皂苷,培养后,油红O染色观察泡沫细胞的形成,检测细胞内总胆固醇的含量,取细胞培养液测定TNF α和IL 1的含量。结果 酵母多糖能够明显增加细胞内脂质的沉积,同时伴有细胞产生TNF α和IL 1的增加,三七皂苷可以明显减少由炎症因素引起的脂质沉积的增加,并同时减少炎症细胞因子的产生。结论 炎症因素可以明显促进泡沫细胞的生成,三七皂苷可通过其抗炎活性干预这一过程。

吴茱萸碱对酵母多糖诱导急性腹膜炎小鼠的保护作用

目的探讨吴茱萸碱(evodiamine,EVO)对酵母多糖(zymosan,ZYM)诱导的小鼠腹膜炎中炎症反应及中性粒细胞(polymorphonuclear neutrophil,PMN)浸润的影响。方法将54只成年雄性C57BL/6小鼠按随机数字表法分为正常对照组、模型组和EVO治疗组。模型组腹腔注射1 mg/m L ZYM溶液(1 m L)建立急性腹膜炎小鼠模型,EVO治疗组则同时腹腔注射10 mg/kg EVO及1 mg/m L ZYM溶液,正常对照组腹腔注射等量磷酸盐缓冲液。各组处理后2、6、12 h处死6只小鼠,收集眼眶血及腹腔灌洗液。采用酶联免疫吸附法检测血清及腹腔灌洗液中白介素6(interleukin-6,IL-6)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、角化细胞来源趋化因子(keratinocyte-derived chemokine,KC)及巨噬细胞炎性蛋白2(macrophage inflammatory protein 2,MIP-2)的含量;通过血细胞计数板计数腹腔灌洗液中混合细胞总数;利用流式细胞仪检测腹腔灌洗液中PMN比例及PMN中活性氧(reactive oxygen species,ROS)水平;采用Western blot检测6 h时腹腔灌洗液混合细胞中核转录因子-k B(nuclear factor-κB,NF-κB)p65入核情况。结果建模后2、6、12 h,模型组血清及腹腔灌洗液中IL-6、TNF-α、KC及MIP-2含量均高于正常对照组(P<0.05),EVO治疗组上述指标均较模型组明显降低(P<0.05),其中,血清中IL-6、KC及MIP-2均于2 h达高峰,随后逐渐下降,而TNF-α在2 h逐渐上升,6 h达到高峰,随后逐渐下降;腹腔灌洗液中TNF-α、KC及MIP-2均于2 h达高峰,随后逐渐下降,而IL-6在2 h逐渐上升,6 h达到高峰,随后逐渐下降。制模后6 h,EVO治疗组可显著降低腹腔混合细胞数与PMN数及其百分比(P<0.05),且PMN中ROS显著降低(P<0.05)。另EVO治疗可显著降低腹腔混合细胞中细胞核的NF-κB p65表达(P<0.05)。结论 EVO可抑制ZYM诱导急性小鼠腹膜炎模型中血清及腹腔灌洗液中炎症因子及趋化因子的分泌,减轻腹腔PMN的浸润,并抑制PMN中ROS的产生,该作用可能是通过抑制NF-k B p65入核实现的。

九孔鲍血细胞吞噬能力的研究

在体外研究九孔鲍（Haliotis diversicolor supertexta）血细胞的吞噬能力，初步了解九孔鲍血细胞的吞噬功能。结果表明，在室温20～22℃下，不同反应时间（30、60、90min）对血细胞吞噬作用的影响不显著；不同吞噬物比例（酵母聚糖与血细胞数量之比为2、5、10）对血细胞吞噬作用有显著影响，吞噬率和吞噬指数随着吞噬物比例的增大而上升。测定不同温度（10、20、30℃）下血细胞对酵母聚糖的吞噬作用，20℃时血细胞的吞噬率、吞噬指数最高；10℃与30℃时的吞噬率、吞噬指数均较低，但与20℃的相比没有显著差异。电镜观察证实酵母聚糖颗粒位于血细胞的吞噬体内。在室温20～22℃、反应时间60min的条件下，测定血细胞对金黄色葡萄球菌（10个菌／每个血细胞）的吞噬作用（吞噬率为23．7％、吞噬指数为0．51）。在硝基四氮唑蓝（NBT）还原试验中，血细胞在酵母聚糖的刺激下，发生呼吸暴发产生了超氧阴离子。

多器官功能障碍综合征小鼠血清多种细胞因子含量变化及其与病程进展的关系

目的分析小鼠多器官功能障碍综合征(MODS)病程发展中血清多种细胞因子含量的变化规律及其与病程进展的关系。方法采用酵母多糖腹腔注射制作C57BL/6小鼠MODS模型,观察伤后不同阶段动物脏器功能的变化和死亡率,并监测血清多种细胞因子含量的变化。结果酵母多糖腹腔注射致伤后12h^2d,血清中反映脏器功能的丙氨酸转氨酶(ALT)、尿素氮(BUN)、肌酐(Cr)和肌酸激酶(CK)等指标维持在较高水平,明显高于对照组(P<0.05),伤后5~7d恢复至接近正常值,而伤后10~12d再次升高(P<0.05或P<0.01),与动物在伤后1~2d和10~12d两个阶段的死亡高峰对应。血清细胞因子含量随病程进展呈序贯性变化:伤后6~12h,TNF和IL-1含量增加;1d后HMGB1含量增加;伤后5d,IL-10大幅增加;IL-2和IL-12在病程发展中呈降低趋势;病程晚期即伤后10d,致炎和抗炎因子含量均在较高水平,而IL-2和IL-12大幅降低。结论 MODS病程进展过程中,血清多种致炎、抗炎细胞因子含量呈序贯性变化,表现为早期免疫活化为主、晚期免疫耐受占优势的特征,与病情发展密切相关。动态观察血清细胞因子含量的变化有助于判断病情发展及采取相应的防治策略。

酵母多糖致老年大鼠多器官功能不全模型细胞因子的变化

目的研究酵母多糖(Zym)致老年大鼠多器官功能不全综合征(MODSE)模型细胞因子的变化。方法成年和老年SD大鼠,腹腔注射不同剂量Zym制作MODS模型,采用放射免疫分析法(RIA)和酶联免疫法(ELISA)分别进行血清肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和白细胞介素10(IL-10)的检测。结果与成年和老年正常对照组相比,成年和老年不同剂量Zym组TNF-α、IL-6和IL-10均出现不同程度的升高;老年Zym0.5g/kg组TNF-α高于相应成年组,IL-10则低于成年组。结论Zym腹腔注射可致成年和老年大鼠MODS炎症紊乱,在相同剂量下,老年模型组比成年模型组更易发生全身炎症反应综合征(SIRS)和MODS。

吴茱萸碱对脓毒症小鼠急性肺损伤的保护作用

目的探究吴茱萸碱（evodiamine,EVO）对酵母多糖（zymosan）诱导的急性肺损伤的保护效应及其作用机制。方法 24只6-8周龄雄性C57BL/6小鼠,按随机数字表法分为正常对照组、EVO对照组、模型组、EVO治疗组,每组6只。各组分别于处理作用12 h后处死小鼠,收集眼眶血及肺组织。酶联免疫吸附法（ELISA）检测血液及肺组织中白介素-6（interleukin-6,IL-6）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）水平及肺组织髓过氧化物酶（myeloperoxidase,MPO）活性及核转录因子NF-κB p65的DNA结合活性,TUNEL法检测肺组织细胞凋亡情况,HE染色观察肺组织病理改变并测量肺湿干质量比。结果酵母多糖作用12 h后,小鼠出现精神萎靡、活动减少等症状。EVO治疗组小鼠状态有所好转。EVO可明显改善酵母多糖所致的肺泡壁毛细血管扩张充血及炎性细胞浸润,降低肺湿干质量比,并显著下调酵母多糖刺激下血清和肺脏中IL-6和TNF-α的含量（P〈0.01）,同时抑制肺组织中MPO含量以及NF-κB p65的DNA结合活性（P〈0.01）。结论 EVO可缓解酵母多糖诱导的急性肺损伤。该作用可能是通过抑制NF-κB的活性以减少炎症介质释放实现。

抗小鼠TLR2胞外段单表位抗体TSP-2对酵母多糖诱发小鼠腹膜炎的影响

目的观察抗小鼠TLR2胞外段(mTLR2ECD)单表位抗体TSP-2对酵母多糖诱发的小鼠腹膜炎的主要作用。方法用腹腔灌洗、细胞计数及特异染色、免疫组化、ELISA等各种方法检测了抗体TSP-2对模型动物的扭身次数、腹腔灌洗液的伊文思兰渗出、腹腔白细胞浸润的数量变化、腹腔肥大细胞脱颗粒情况以及腹腔灌洗液离心上清中PAF和TNFα水平的影响。结果与PBS处理组和正常兔IgG组相比,抗体TSP-2能促使小鼠因腹腔炎症引起的扭身次数减少,腹腔灌洗液中伊文思蓝OD值降低,腹腔灌洗液中白细胞渗透减少以及C48/80诱导的腹腔肥大细胞脱颗粒降低。结论抗体TSP-2可能通过对肥大细胞脱颗粒的抑制作用减轻酵母多糖诱导的小鼠腹膜炎炎症症状。

酵母多糖A性腹膜炎时的肺损伤及大承气汤的保护作用

目的：了解大承气汤对酵母多糖Ａ性腹膜炎时肺损伤的保护作用。方法：用酵母多糖Ａ腹腔注射制备大鼠急性无菌性腹膜炎模型。随机分为４组：（１）模型组；（２）大承气汤组；（３）大黄组；（４）抗生素组（氨苄青霉素组），并与正常组进行对比，观察实验性腹膜炎时的肺损伤及中药的保护作用。结果：中药组内毒素、肺匀浆脂质过氧化物，以及白细胞计数均明显低于模型组，接近正常组；而还原谷胱甘肽（ＧＳＨ）明显高于模型组，（Ｐ＜０．０５）。结论：中药可能通过降低外周、门脉血内毒素，抑制脂质过氧化的产生与加强自由基的清除，从而显著减轻急性腹膜炎引起的肺损伤。

酵母多糖对S_(180)荷瘤小鼠抗氧化作用和免疫机能的影响

目的:研究酵母多糖(zymosan)对S180荷瘤小鼠抗氧化状态和免疫功能的影响。方法:将昆明小鼠70只随机分为7组,第1组作为正常组,另6组将S180瘤细胞悬液接种于小鼠右前肢腋皮下制备荷瘤小鼠动物模型,分为zymosan低、中、高剂量组和环磷酰胺(Cy)组、肿瘤对照组及zymosan联合Cy治疗组,灌胃第7 d接种S180瘤,第19 d后测定小鼠肝匀浆中丙二醛(MDA)含量、谷胱甘肽过氧化酶(GSH-Px)和超氧化物歧化酶(SOD)活力,评价zymosan对小鼠抗氧化能力的作用。采用逆转录-聚合酶链反应(RT-PCR)检测IL-2、TNF-α、TGF-β1mRNA的表达,评价zymosan对小鼠免疫功能的影响。结果:zymosan各剂量组均能提高肝脏中GSH-Px活性和SOD活力,但zymosan高剂量组显著降低MDA水平(P<0.01)。zymosan各剂量组荷瘤小鼠肿瘤组织内TNF-α、IL-2 mRNA相对表达量明显高于Cy组和肿瘤对照组(P<0.01),同时下调TGF-β1水平。zymosan高剂量对小鼠S180瘤有明显抑制作用,且与Cy合用后有协同作用,并提高了小鼠的TNF-α、IL-2 mRNA的表达。结论:zymosan的抑瘤机制可能主要是抗氧化作用和免疫调节作用,且作用与剂量有关。