前列腺Ⅰ号水丸对慢性细菌性前列腺炎大鼠组织内菌落数量和NO、NOS浓度的影响

目的:探讨前列腺I号水丸对慢性细菌性前列腺炎(CMP)大鼠组织内菌落数量、一氧化氮(NO)浓度和一氧化氮合酶(NOS)活力的影响。方法:健康成年雄性Wistar大鼠120只,体重250~300 g,随机分为6组,分别为空白对照组、模型对照组、阳性对照组、水丸高剂量组、水丸中剂量组、水丸低剂量组,每组20只。前列腺注射大肠杆菌(107个/ml)建立CMP大鼠动物模型。造模成功1个月后,用前列腺水丸高[4.4 g/(kg.day)]、中[2.2 g/(kg.day)]、低[1.1 g/(kg.day)]剂量灌胃治疗,阳性对照组用美满霉素[0.018 g/(kg.day)]灌胃,模型组和空白组用生理盐水灌胃。连续治疗35 d后,计算大鼠前列腺组织匀浆菌落数。采用亚硝酸盐还原酶法检测前列腺组织中NO变化并计算NOS活力的变化。结果:前列腺Ⅰ号水丸高、中、低剂量组大鼠组织内菌落数的水平和前列腺组织内NO含量及NOS活力明显低于模型组,与模型组比较差异显著(P<0.01)。结论:前列腺Ⅰ号水丸对慢性细菌性前列腺炎模型大鼠有一定治疗作用。其作用机制可能与抑制前列腺内细菌生长以及降低前列腺组织内NO含量和NOS活力有关。     

磷霉素氨丁三醇散对慢性细菌性前列腺炎模型大鼠前列腺组织TNF-α、IL-8、IL-6含量的影响

目的:探讨磷霉素氨丁三醇散(FT)对慢性细菌性前列腺炎模型大鼠肿瘤坏死因子-α(TNF-α)、白介素8(IL-8)、白介素6(IL-6)表达水平的影响。方法:70只雄性SD大鼠随机分为7组,每组10只。A组:假手术组;B组:模型对照组;C组:阳性对照组[左氧氟沙星:100 mg/(kg·d),30 d];D组:FT低剂量、14 d疗程组[200 mg/(kg·d),14 d];E组:FT低剂量、7 d疗程组[200 mg/(kg·d),7 d];F组:FT高剂量、14 d疗程组[300 mg/(kg·d),14 d];G组:FT高剂量、7 d疗程组[300 mg/(kg·d),7 d],各组均采用灌胃给药。实验结束后留取各组大鼠前列腺组织,制作病理切片并使用酶联免疫吸附实验(ELISA)检测各组大鼠前列腺组织匀浆中TNF-α、IL-8、IL-6的含量。结果:与空白对照组比较,模型组大鼠前列腺组织匀浆中的TNF-α、IL-8、IL-6含量均明显升高,差异均有统计学意义[(19.83±6.1)ng/g prot vs(32.93±6.21)ng/gprot,(8.26±0.52)ng/g prot vs(16.2±2.84)ng/g prot,(1.55±0.11)ng/g prot vs(2.51±1.06)ng/g prot,P0.05或0.01];与模型组[(32.93±6.21)ng/g prot、(16.2±2.84)ng/g prot]相比,各治疗组大鼠前列腺组织匀浆中的TNF-α、IL-8含量[(20.54±5.78)ng/g prot、(21.95±6.48)ng/g prot、(23.8±6.93)ng/g prot、(19.97±2.58)ng/g prot、(21.97±3.38)ng/g prot;(12.43±3.64)ng/g prot、(11.11±2.86)ng/g prot、(12.43±4.02)ng/g prot、(8.83±1.32)ng/g prot、(12.68±1.97)ng/g prot]明显降低,差异具有统计学意义(P0.05或0.01);各治疗组大鼠前列腺组织匀浆的TNF-α、IL-8、IL-6含量与阳性对照组比较差异均无统计学意义(P0.05);F组大鼠前列腺组织匀浆中的IL-6的表达量较模型组显著减少[(2.51±1.06)ng/g prot vs(1.76±0.46)ng/g prot,P0.05],其余治疗组及阳性对照组前列腺组织匀浆中的IL-6的表达与模型组比较均无显著性差异(P0.05),但较模型组均有下降趋势。结论:FT通过抑制TNF-α、IL-8、IL-6的表达,减轻前列腺组织的炎症反应,达到治疗大鼠CBP的目的,为临床研究提供了实验依据。     

姜黄素对慢性非细菌性前列腺炎大鼠TNF-α、IL-6和IL-8表达的影响

目的:研究姜黄素对慢性非细菌性前列腺炎大鼠血清及前列腺组织中TNF-α、IL-6、IL-8影响。方法:健康雄性SD大鼠60只,体重200～220g,随机均分为5组:正常对照组、模型组、口服姜黄素组、腹腔注射姜黄素组、塞来昔布(西乐葆)组(阳性对照组)。大鼠去势术后皮下注射苯甲酸雌二醇[0.25mg/(kg·d),30d]建立慢性非细菌性前列腺炎模型。造模成功后,分别用姜黄素200mg/(kg·d)灌胃及腹腔注射治疗,阳性对照组用西乐葆250mg/(kg·d)灌胃;正常对照组和模型组用生理盐水灌胃。连续治疗7d后,采用ELISA法检测大鼠血清和前列腺组织匀浆内TNF-α、IL-6、IL-8的表达。结果:腹腔注射姜黄素组血清和前列腺组织中TNF-α、IL-8表达显著低于阳性对照组(P<0.05),而IL-6的表达与阳性对照组没有差异(P>0.05)。结论:姜黄素对大鼠慢性非细菌性前列腺炎有一定治疗作用,其作用机制可能与降低血液及组织中细胞因子IL-8、TNF-α水平有关。     

IL-18和TNF-α在大鼠酒精性肝病中的表达

目的观察酒精性肝病大鼠血清中白细胞介素18(IL-18)和肿瘤坏死因子α(TNF-α)水平的变化。方法大鼠随机分为:⑴实验组,用56%乙醇[5~9 g/(kg.d)]灌胃,共12周;(2)对照组,灌等容量生理盐水。实验第4,8,12周末分批处死动物。用HE染色观察肝脏病理学改变;用ELISA法检测血清中IL-18和TNF-α的浓度。结果实验组大鼠肝组织于4,8,12周时出现慢性酒精性肝病的各种表现,如脂肪变性、炎性改变及肝纤维化等。实验组血清ALT、AST含量高于对照组(P0.05);实验组血清IL-18浓度明显降低而TNF-α明显升高,且其变化随病变程度的改变而变化。结论酒精性肝病大鼠血清细胞因子IL-18和TNF-α浓度的变化与病情严重程度有关,故可望作为酒精性肝病病情变化的动态指标。     

同种异体皮肤移植家兔注射重组人IL-10后血清IL-17家族水平的变化观察

目的:观察同种异体皮肤移植家兔注射重组人IL-10后血清IL-17家族水平的变化,探究重组人IL-10抑制免疫反应的机制。方法:30只健康新西兰白兔依据随机平均原则分为A组[重组人IL-10低剂量组,5μg/(kg·d)]、B组[重组人IL-10高剂量组,10μg/(kg·d)]、C组[环孢菌素低剂量组,5mg/(kg·d)]、D组[环孢菌素低剂量组,10mg/(kg·d)]、E组[重组人IL-10低剂量,5μg/(kg·d)+环孢菌素低剂量组,5mg/(kg·d)]、F组[生理盐水空白对照组,0.9%氯化钠溶液1ml/d]六组,每组5只,均经肌肉注射于皮肤移植术前1d给药,共给药10d,各组分别于术前1d,术后1d、4d、1周、2周、3周、4周取兔耳中动脉血,分离制得血清后,依酶联免疫法测定IL-17家族各成员(IL-17A~F)的浓度。结果:家兔同种异体皮肤移植术后IL-17A、IL-27(IL-17B/C/D)、IL-17E(IL-25)、IL-17F的浓度均高于术前,且在术后2周达到高峰,随后逐渐降低;rhIL-10能抑制IL-17A、IL-27、IL-17F的分泌,且抑制效应随着rhIL-10剂量的增多而加强;rhIL-10可促进IL-25的分泌,但无明显量效关系。结论:同种异体皮肤移植家兔注射rhIL-10后血清IL-17家族水平明显提高,rhIL-10对免疫反应的抑制作用可能与IL-17家族介导的炎性反应及炎性因子分泌有关。     

复方玄驹胶囊治疗自身免疫性前列腺炎大鼠的实验研究

目的:研究复方玄驹胶囊对自身免疫性前列腺炎大鼠的治疗效果。方法:健康Wistar大鼠60只,随机分为5组,对照组、低浓度蛋白免疫模型组、低浓度蛋白免疫+复方玄驹胶囊全方治疗组、高浓度蛋白免疫模型组、高浓度蛋白免疫+复方玄驹胶囊全方治疗组。除对照组外,其余4组用高低两种浓度(15 mg/ml及80 mg/ml)的同种大鼠前列腺匀浆蛋白提纯液进行注射造模。造模(30 d)成功后,对照组和模型组生理盐水[1 ml/(200 g·d)]灌胃,治疗组用生理盐水溶解的复方玄驹胶囊全方[0.068 g/(ml·d)]灌胃,随后分别于30、45、60 d分批处死大鼠。用ELISA法检测大鼠血清中的IL-8、IL-10及TNF-α的表达,并观察大鼠前列腺组织病理切片。结果:与模型组相比,经复方玄驹胶囊全方灌胃治疗的高浓度蛋白免疫大鼠血清中IL-8、TNF-α在造模45 d时由(148.54±17.23)pg/ml、(62.14±5.59)pg/ml下降到(100.77±11.08)pg/ml、(32.63±2.91)pg/ml(P0.05);60 d时由(143.69±17.28)pg/ml、(59.38±5.50)pg/ml降到(95.77±10.53)pg/ml、(29.63±2.66)pg/ml(P0.05)。低浓度组造模45 d时IL-8、TNF-α亦由(128.47±12.21)pg/ml、(40.43±3.64)pg/ml下降至(111.76±10.07)pg/ml、(35.44±3.17)pg/ml(P0.05),60 d时由(131.07±10.93)pg/ml、(43.34±3.91)pg/ml降至(97.46±8.75)pg/ml、(30.44±2.75)pg/ml(P0.05)。高浓度蛋白免疫的治疗组大鼠血清IL-10在造模45 d、60 d分别由(189.14±16.78)pg/ml、(184.14±15.89)pg/ml上升至(230.48±29.96)pg/ml、(248.48±31.03)pg/ml(P0.05),低浓度组由(223.14±17.87)pg/ml、(224.14±17.93)pg/ml升高至(231.42±23.18)pg/ml、(249.42±24.97)pg/ml(P0.05)。病理切片示对照组无明显变化;实验组病理切片显示大鼠前列腺组织腺体结构破坏,炎性细胞浸润;治疗组治疗15 d后光镜下观察病变逐步改善,腺腔增大,上皮细胞轻度增生,间质中无明显炎性细胞浸润,可见少量纤维组织。结论:复方玄驹胶囊能降低自身免疫性前列腺炎大鼠前列腺组织炎性改变,并有效改善炎性因子表达,对大鼠自身免疫性前列腺炎有一定疗效。     

白藜芦醇对前列腺炎大鼠模型前列腺组织中细胞因子的干预研究

目的探讨白藜芦醇对慢性前列腺炎大鼠模型的治疗机制。方法 50只体质量(150±15)g的雄性SD大鼠随机分为5组:阴性对照组和模型假性对照组、白藜芦醇低、中、高剂量模型组。模型组分别在第0、30天于大鼠皮下注射大鼠前列腺蛋白提纯液和弗氏完全佐剂的混悬液,同时腹腔注射百白破疫苗造模;阴性对照组以生理盐水注射参照。第45天开始,白藜芦醇低、中和高剂量模型组每日按照白藜芦醇4 mg/kg、20 mg/kg、40mg/kg灌胃给药,阴性对照组和模型假性对照组以生理盐水灌胃。第55天后处死大鼠取左侧前列腺组织,10%甲醛溶液固定,做石蜡包埋切片,HE染色,镜下观察大鼠前列腺病理形态的改变。右侧前列腺打成组织匀浆,免疫组化ELISA法检测白介素-1β(IL-1β)、IL-6、IL-8、IL-10和肿瘤坏死因子(TNF-α)的含量。计量数据用(x±s),统计分析用t检验。结果白藜芦醇高、中剂量组与模型假性对照组比较,前列腺间质中炎细胞数量显著降低,成纤维细胞数量轻度下降,腺体数量与腺腔面积明显升高;前列腺匀浆中IL-1β、IL-8、TNF-α明显降低,IL-6、IL-10含量显著上升(P0.01)。结论白藜芦醇对慢性免疫性前列腺炎大鼠模型的治疗是通过降低前列腺内促炎性细胞因子IL-1?、IL-8、TNF-α,提高抑炎性细胞因子IL-6、1L-10来减轻炎细胞浸润,抑制纤维组织增生完成。     

麝香配伍乳香促虎杖提取物治疗慢性非细菌性前列腺炎的动物实验研究

目的:观察麝香、乳香配伍组合对虎杖提取物治疗慢性非细菌性前列腺炎模型大鼠前列腺组织病理及炎症因子表达的影响。方法:53只健康雄性Wistar大鼠,5只用于大鼠前列腺蛋白提纯液的制备,48只随机分为麝香配伍乳香+虎杖提取物组、虎杖提取物、模型组、正常对照组共4组。除正常对照组外,应用大鼠前列腺蛋白提纯液辅以免疫佐剂制备实验性慢性非细菌性前列腺炎大鼠模型,造模60 d时正常对照组、模型组予生理盐水,虎杖提取物、麝香配伍乳香+虎杖提取物组分别予生药量虎杖1.575 g/(kg.d)、麝香0.021 g/(kg.d)、乳香1.05 g/(kg.d)按组别选用连续灌胃,各组给药14 d时处死,检测指标包括病理学,ELISA法检测前列腺组织匀浆TNF-α、IL-1β、IL-6、IL-8水平,RT-PCR及Western印迹方法检测炎症因子MCP-1(CCL2)、CCR2 mRNA及蛋白表达。结果:麝香配伍乳香+虎杖提取物组前列腺组织结构改善,无明显炎性细胞浸润,虎杖提取物组可见炎性细胞浸润。麝香配伍乳香+虎杖提取物组明显降低前列腺组织炎症因子(TNF-α:11.04±4.07、IL-1β:16.94±4.26、IL-6:110.08±28.42、IL-8:26.28±7.36,pg/ml),优于单纯虎杖提取物组(TNF-α:63.21±21.37、IL-1β:41.32±14.62、IL-6:177.64±42.65、IL-8:96.37±37.61,pg/ml),差异有统计学意义(P<0.05,P<0.01)。麝香配伍乳香+虎杖提取物组大鼠前列腺组织炎症趋化因子MCP-1(CCL2)及其受体CCR2的mRNA(MCP-1:0.32±0.17;CCR2:0.28±0.11)及蛋白(MCP-1:0.28±0.15;CCR2:0.11±0.04)表达水平与模型组(MCP-1 mRNA:1.15±0.39;MCP-1蛋白:0.93±0.34;CCR2 mRNA:0.83±0.26;CCR2蛋白:0.93±0.34)比较显著降低(P<0.01),显著优于虎杖提取物组(MCP-1 mRNA:0.65±0.27;MCP-1蛋白:0.56±0.22;CCR2 mRNA:0.78±0.24;CCR2蛋白:0.25±0.09),差异有统计学意义(P<0.05,P<0.01)。结论:麝香乳香配伍组合的应用具有促进虎杖提取物对慢性前列腺炎的治疗,降低炎症反应程度,从而促进前列腺组织结构修复的作用。     

苦豆子调节JNK信号通路对抗GBM肾炎大鼠的作用研究

目的:研究苦豆子对抗肾小球基底膜(glomerular basement membrane,GBM)肾炎大鼠的作用及机制研究。方法:30只健康雄性大鼠,随机分为5组,每组6只,分别为对照组、模型组、苦豆子低、中、高剂量组,除对照组外,其余各组采用尾静脉注射给予大鼠兔抗大鼠GBM血清的方法建立大鼠抗GBM肾炎模型,然后根据大鼠体重按照1 g/kg、2 g/kg、4 g/kg灌胃给予大鼠苦豆子提取物,对照组及模型组灌胃给予等量生理盐水,1次/d,连续给药21 d,并于给药第14天和21天测定各组大鼠24 h尿量及尿蛋白量,给药结束后,测定大鼠血浆TNF-α、IL-6及IL-1β水平,血清尿素氮及血肌酐水平,苏木精-伊红染色法对大鼠肾脏进行组织病理学观察,western blot检测大鼠肾脏组织JNK、p-JNK水平,实时定量PCR检测各组大鼠肾脏组织中c-Jun及AP-1 mR NA水平。结果:与模型组比较,苦豆子各剂量组大鼠24 h尿量显著增加(P 0.05),24 h尿蛋白量、血清尿素氮、血肌酐水平、血清尿素氮水平、血肌酐水平及其血浆TNF-α、IL-6及IL-1β水平、肾组织JNK及p-JNK水平、c-Jun及AP-1 mR NA水平均显著降低(P 0.05),大鼠肾组织病理学明显改善。结论:苦豆子能够改善抗GBM肾炎大鼠的疾病状态,其作用机制可能与调节抗GBM肾炎大鼠体内JNK信号通路有关。     

夏荔芪胶囊对良性前列腺增生模型大鼠PCNA、caspase-3表达水平的影响

目的:探讨夏荔芪胶囊对良性前列腺增生(BPH)模型大鼠增殖细胞核抗原(PCNA)、半胱氨酸蛋白酶3(caspase-3)表达水平的影响。方法:50只雄性SD大鼠,随机分为5组,每组10只:空白组(假手术组),模型组,夏荔芪高、低剂量治疗组[1.20 g/(kg·d)、0.61 g/(kg·d)]及非那雄胺治疗组[0.8 mg/(kg·d)]。采用去势后皮下注射丙酸睾酮[0.5 mg/(kg·d),30 d],建立大鼠BPH模型。空白组及模型组予以生理盐水,治疗组予以相应药物,造模成功后连续灌胃30 d。实验结束后将各组大鼠于麻醉下留取双侧前列腺组织后处死,计算大鼠前列腺指数(前列腺湿重/体重);免疫组化法检测大鼠前列腺组织中PCNA的表达情况;免疫荧光法检测大鼠前列腺组织中caspase-3的表达水平。结果:与空白组相比,模型组的前列腺湿重(g)及前列腺指数(mg/g)明显增加(1 326±60 vs 471±17;2.89±0.18 vs 1.06±0.06,P均0.01);与模型组比较,各治疗组的前列腺湿重及前列腺指数则明显降低,其中,夏荔芪高剂量组较低剂量组下降更明显(914±36 vs 1 099±46;2.02±0.08 vs 2.39±0.11,P均0.01),而各治疗组中以非那雄胺组(817±53 vs 471±17;1.83±0.10 vs 1.06±0.06,P均0.01)降低最明显。免疫组化结果显示,与空白组相比,模型组大鼠前列腺组织中PCNA表达明显增多,各治疗组与模型组相比,前列腺组织中PCNA表达均有明显减少,其中夏荔芪高剂量治疗组减少较为明显。免疫荧光结果显示,与空白组相比,模型组大鼠前列腺组织caspase-3表达量降低,各治疗组与模型组相比,前列腺组织中caspase-3表达明显增高,其中非那雄胺治疗组增高较为明显。结论:夏荔芪胶囊能明显降低BPH大鼠前列腺湿重及前列腺指数,通过降低前列腺组织中PCNA的表达水平,增高前列腺组织中caspase-3的表达,可能是其治疗BPH大鼠的机制。     

葛仙汤治疗大鼠溃疡性结肠炎

目的:探讨葛仙汤对大鼠溃疡性结肠炎的治疗作用及其机制.方法:将SD大鼠按均衡随机原则分为正常对照组、模型对照组和葛仙汤低、中、高剂量组,采用大肠杆菌加乙酸免疫复合法造成大鼠溃疡性结肠炎模型.连续给药21 d,观察动物的一般情况,进行疾病活动指数(DAI)评估、结肠病理学评分(HS),检测血清中IL-6、IL-10含量.结果:葛仙汤低、中、高剂量3个治疗组DAI和HS均明显低于模型对照组(P<0.05或P<0.01),IL-6含量与模型对照组比较均明显减少(P<0.01);中剂量组IL-6含量明显低于高、低剂量组(P<0.05).3个治疗组IL-10均较模型对照组明显升高(P<0.01);中、低剂量组IL-10明显高于高剂量组(P<0.05).结论:低、中、高剂量葛仙汤均能缓解溃疡性结肠炎大鼠的症状,减轻其结肠病理损伤,促进溃疡面愈合,其中以中剂量效果为更好.     

Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome, severe pneumonia, and controls

BACKGROUND: The inflammatory response has been widely investigated in patients with acute respiratory distress syndrome (ARDS) and pneumonia. Studies investigating the diagnostic values of serum cytokine levels have yielded conflicting results and only little information is available for the differential diagnosis between ARDS and pneumonia. METHODS: Clinical and physiological data, serum concentrations of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6, and quantitative cultures of lower respiratory tract specimens were obtained from 46 patients with ARDS and 20 with severe pneumonia within 24 hours of the onset of the disease and from 10 control subjects with no inflammatory lung disease. Cytokine concentrations were compared between groups and determinants in addition to the diagnosis were tested. RESULTS: Serum TNF-alpha levels were significantly higher in ARDS patients (67 (57) pg/ml) than in patients with severe pneumonia (35 (20) pg/ml; p = 0.031) or controls (17 (8) pg/ml; p = 0.007). For IL-1beta and IL-6 the observed differences were not statistically significant between patients with ARDS (IL-1beta: 34 (65) pg/ml; IL-6: 712 (1058) pg/ml), those with severe pneumonia (IL-1beta: 3 (4) pg/ml, p = 0.071; IL-6: 834 (1165) pg/ml, p = 1.0), and controls (IL-1beta: 6 (11) pg/ml, p = 0.359; IL-6: 94 (110) pg/ml, p = 0.262). TNF-alpha (standardised coefficient beta = 0.410, p<0.001) and IL-1beta (standardised coefficient beta = 0.311, p = 0.006) were most strongly associated with the degree of lung injury, even when the diagnostic group was included in the statistical model. CONCLUSIONS: Serum TNF-alpha levels were higher in patients with ARDS than in those with severe pneumonia or in control subjects. Multivariate results suggest that the levels of systemic TNF-alpha and IL-1beta reflect the severity of the lung injury rather than the diagnosis.     

前列腺按摩液中IL-8和TNF-α测定在慢性前列腺炎诊断、分型中的临床意义

目的 :探讨检测前列腺按摩液 (EPS)中细胞因子白细胞介素 8(IL 8)和肿瘤坏死因子α(TNF α)在慢性前列腺炎诊断、分型中的意义。　方法 :ELISA法检测 78例临床诊断的慢性前列腺炎患者 [其中慢性前列腺炎(CBP)组 12例 ,慢性非细菌性前列腺炎 /慢性骨盆疼痛综合征 (CPPS)ⅢA组 38例 ,CPPSⅢB组 2 8例 ]和 12例正常对照者EPS中IL 8和TNF α浓度。分析各组EPS中IL 8和TNF α浓度差异。　结果 :CBP组和CPPSⅢA组EPS中IL 8水平 [(10 96 7.5± 3477.7) pg/ml;(92 6 8.4± 2 0 34.6 ) pg/ml]和TNF α水平 [(84 .1± 5 4 .7) pg/ml;(32 .6± 18.6 ) pg/ml]显著高于CPPSⅢB组和正常对照组EPS中的IL 8水平 [(2 72 6 .1± 2 77.5 ) pg/ml;(2 80 0 .0± 32 0 .2 )pg/ml]和TNF α水平 [(12 .6± 7.1)pg/ml;(12 .9± 10 .1)pg/ml](P均 <0 .0 1)。　结论 :检测EPS中IL 8、TNF α水平可能有助于CBP、慢性非细菌性前列腺炎 /慢性骨盆疼痛综合征的分型诊断。     

极化液对严重烫伤伴多器官功能障碍综合征大鼠炎性细胞因子水平及预后的影响

目的观察早期极化液治疗对烫伤伴多器官功能障碍综合征(MODS)大鼠炎性细胞因子水平及预后的影响,探讨其防治机制。方法将120只SD大鼠造成30%TBSAⅢ度烫伤,伤后2h腹腔注射内毒素,制作烫伤伴MODS大鼠模型,随机分为极化液组、葡萄糖组和盐水组,每组40只。观察3组大鼠伤后1~7d血浆中血糖、乳酸、肿瘤坏死因子α(TNF-α)、一氧化氮(NO)以及白细胞介素6(IL-6)含量的变化;并计算伤后7d内各组大鼠的死亡率。结果极化液组大鼠伤后1~7d血糖、乳酸、TNF-α、IL-6和NO含量均明显低于其他组(P<0.01),伤后6~7d其TNF-α、IL-6和NO含量达到最低值,分别为(2.37±0.54)μg/L、(0.28±0.17)μg/L及(29±9)μmol/L;葡萄糖组血糖、乳酸含量明显高于盐水组(P<0.01),而两组TNF-α、IL-6和NO含量相近(P>0.05).极化液组伤后7d内死亡率为20.0%,明显低于葡萄糖组与盐水组(分别为37.5%、47.5%,P<0.05).结论极化液通过改善烫伤引起的糖代谢障碍,降低机体炎性细胞因子水平,可作为防治烫伤伴MODS的辅助措施。     

连续性血液净化对重症急性胰腺炎血浆炎症介质的影响

【摘要】　目的 探讨连续性血液净化(CBP)对重症急性胰腺炎(SAP)患者血浆炎症介质的影响。方法 对36例重症急性胰腺炎患者进行CBP治疗,使用ELISA法检测治疗前和治疗后24 h、48 h血浆TNF -α、IL -1β、IL -6、IL -8的浓度,并与同期健康人群做比较。结果 31例患者好转出院,存活率为86.1%,血生化指标明显改善;SAP患者血浆TNF -α、IL -1β、IL -6、IL -8浓度显著高于正常对照组,CBP治疗24 h后四种细胞因子明显低于治疗前水平(P<0.05),治疗48 h后有不同程度的回升,但仍低于治疗前水平(P<0.05)。结论 CBP可有效清除SAP患者血浆炎症介质,从而阻断全身炎症反应,改善预后。     

Effect of CO2 pneumoperitoneum on the systemic and peritoneal cytokine response in a LPS-induced sepsis model

We studied the effect of carbon dioxide (CO2) pneumoperitoneum on the systemic and peritoneal cytokine response in a rat model of intraperitoneal sepsis. After intraperitoneal injection of bacterial lipopolysaccharide (LPS, 10 mg/kg), rats were divided into 3 groups (n = 49 in each group): control (abdominal puncture); CO2 pneumoperitoneum, and laparotomy. Blood and peritoneal lavage fluid (PLF) were sampled at 0, 1, 2, 3, 4, 6, and 8 h after LPS challenge. Blood cell counts, plasma endotoxin level, and the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) in the plasma and PLF were measured. Blood cell counts did not differ between the 3 groups. Plasma endotoxin levels in the pneumoperitoneum group were significantly increased immediately after the procedure (p < 0.05). Although peak plasma TNF-alpha levels in the pneumoperitoneum group were seen immediately after the procedure, other changes in plasma cytokine levels did not differ significantly between the 3 groups. PLF TNF-alpha and IL-1beta levels in the pneumoperitoneum group were significantly lower than levels in the control and laparotomy groups soon after the procedure (p < 0.05). PLF IL-6 levels in the pneumoperitoneum group tended to be lower than those in the laparotomy group. In conclusion, CO2 pneumoperitoneum might induce different responses between systemic and peritoneal cytokines soon after the procedure in a rat model of intraperitoneal sepsis.     

Elevation of urinary IL-1β levels during transplant associated nephropathy in rat model of the nephrotic syndrome

A recurrence of nephrotic syndrome is a well-known phenomenon in patients who receive kidney transplantation. In this study, we attempt to establish a rat model of recurrent nephrotic change after renal transplantation using puromycin aminonucleoside (PA) induced nephrotic rats. We then examine the mechanism leading to recurrence. Female Sprague-Dawley rats (8 weeks) were divided into four groups: group A, allogenic renal transplantation of a normal kidney to PA-induced nephrotic rats; group B, PA injection only as a nephrotic control; group C, allogenic transplantation of a normal kidney to rats receiving a saline injection; group D, rats receiving only a saline injection. The serum and urinary levels of protein, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-2 and interferon (IFN)-gamma were measured. The cytokine levels were assessed by performing enzyme-linked immunosorbent assays. Six days after renal transplantation, the kidneys were excised, tissue sections were stained with hematoxylin-eosin and the specimens were studied for pathological alterations. The urinary protein levels and the histological results of protein casts in renal tubules of the autologous kidneys of the nephrotic rats and the transplanted kidneys confirmed the recurrence of nephrotic syndrome in the transplanted kidney. After renal transplantation, urinary protein and IL-1beta levels were significantly elevated in recurrent transplanted kidney groups compared with those in the control groups, while the TNF-alpha, IL-2, and IFN-gamma levels were not elevated. In addition, serum levels of TNFalpha and IL-1beta were not elevated. These results suggested that IL-1beta may relate to the recurrent nephropathy in the transplanted kidney in the nephrotic rat.     

大鼠重症急性胰腺炎肺泡巨噬细胞的活化和调控作用

目的 观察巨噬细胞中p38蛋白活化激酶对大鼠重症急性胰腺炎肺损伤的影响.方法 假手术组仅胆胰管注射生理盐水0.1 ml/100 g;5%的牛黄胆酸(0.1 ml/100 g)逆行注射到SD大鼠的胆胰管内,造成重症急性胰腺炎(SAP)分为SAP组和SB03580组(SB203580,0.5 mg/kg,静注).在6 h剖杀大鼠,查腹水,抽血检测血清淀粉酶(AMS)和肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6[酶联免疫吸附试验(ELISA)法];同时分别离心收集全肺肺泡巨噬细胞,免疫组织化学检测肺组织及其巨噬细胞中p38 MAPK的表达,同时检测肺组织中的TNF-α和IL-6;光镜下检测胰腺组织损害.结果 SAP组及SB组中AMS在6 h分别为(4865.12±890.35)IU/L和(2918.24±614.58)IU/L,差异有统计学意义.血清TNF-α分别为(106.59±43.71)ng/L和(76.43±38.43)ng/L;IL-6是(2203.76±640.85)ng/L和(1254.76±459.35)ng/L,差异有统计学意义(P<0.01).肺组织中的TNF-α和IL-6的升高与血中的一致.光镜下,胰腺组织内可见炎细胞浸润、充血、水肿和坏死;在SAP组中肺组织及其巨噬细胞中p38 MAPK强烈表达,TNF-α和IL-6的表达一致,SB治疗组表达下降.结论 TNF-α和IL-6在重症急性胰腺炎肺损伤起着重要作用;肺泡巨噬细胞中p38 MAPK表达对TNF-α和IL-6的转录和合成起重要作用.