徐长卿对三硝基苯磺酸诱导的大鼠结肠炎的作用

目的:探讨徐长卿对2,4,6-三硝基苯磺酸(trinitrobenzenesulfonic acid,TNBS)诱导的大鼠结肠炎的作用.方法:将40只♂SD大鼠随机分为4组:正常组、模型组、徐长卿组和巴柳氮组.除正常组外,其余3组大鼠均以TNBS灌肠造模.灌肠24h后,徐长卿组开始每天给予徐长卿4g/kg;巴柳氮组给予巴柳氮钠1g/kg灌胃治疗10d.每天观察大鼠一般情况,给药结束后,观察大鼠结肠大体损伤及病理,酵素免疫分析法(enzyme-linked immunosorbant assay,ELISA)检测肠组织肿瘤坏死因子(tumor necrosis factor,TNF)-α、白介素(interleukin,IL)-1β及IL-10水平.结果:两治疗组体质量较模型组增加,但差异无统计学意义;两治疗组疾病活动指数(disease activity index,DAI)评分较模型组明显下降(0.70±1.06,0.67±0.71vs2.38±1.51,P<0.05).徐长卿组、巴柳氮组结肠大体损伤及病理评分较模型组显著下降(1.05±0.83,1.06±0.85vs2.94±0.94;1.65±1.67,2.00±1.80vs6.00±1.67,均P<0.01).徐长卿组较模型组TNF-α、IL-1β水平明显降低(P<0.01),IL-10水平无统计学差异.巴柳氮组较模型组TNF-α、IL-1β、IL-10水平均明显降低(P<0.01).结论:徐长卿能有效改善TNBS诱导的大鼠结肠炎,其机制可能与调节细胞因子水平有关.     

雷公藤红素对三硝基苯磺酸诱导的大鼠结肠炎的保护作用

背景：传统药物对炎症性肠病疗效不甚理想，寻找新型而有效的药物一直是该领域的研究热点。目的：观察雷公藤红素对三硝基苯磺酸（TNBS）诱导的大鼠结肠炎的保护作用，并初步探讨其可能机制。方法：以TNBS诱导大鼠结肠炎模型。将动物随机分为正常对照组、模型组、助溶剂对照组以及雷公藤红素低剂量组（每天0．5mg／kg）和高剂量组（每天1mg／kg）。以大体和组织学评分评价结肠炎症程度。以免疫组化方法检测结肠组织核因子（NF）-kBp65的表达，以半定量逆转录聚合酶链反应（RT-PCR）检测白细胞介素（IL）-1β和肿瘤坏死因子（TNF）-α mRNA的表达。结果：高、低剂量雷公藤红素均能显著改善结肠组织大体和组织学评分，降低NF-kB p65以及IL-1β、TNF-α mRNA的表达。结论：雷公藤红素对TNBS诱导的大鼠结肠炎具有显著保护作用，抑制促炎细胞因子的产生可能是其主要作用机制之一。     

清肠栓调节三硝基苯磺酸诱导结肠炎大鼠结肠黏膜细胞增殖的影响

[目的]从细胞增殖动力学角度探讨清肠栓促进结肠溃疡愈合的作用机制.[方法]制备三硝基苯磺酸(TNBS)诱导结肠炎大鼠.造模3 d,分为清肠栓高剂量组、清肠栓低剂量组、柳氮磺胺吡啶(SASP)组、模型对照组、模型组和正常组.给药7 d后,取大鼠结肠病变部位标本,进行组织学评价,运用AB-PAS染色观察杯状细胞数量及其分泌黏液功能,免疫组化染色法检测增殖细胞核抗原(PCNA)表达.[结果]与清肠栓低剂量组、SASP组、模型对照组和正常组比较,清肠栓高剂量组大鼠结肠黏膜炎症消除和溃疡愈合,杯状细胞数量及黏液增加,溃疡边缘腺体细胞增殖加强,PCNA表达增加(P＜0.05).[结论]清肠栓具有促进结肠炎大鼠结肠黏膜细胞增殖、增加杯状细胞的数量和分泌黏液的水平等作用,能够促进结肠溃疡愈合过程.     

三七提取物对三硝基苯磺酸诱导溃疡性结肠炎大鼠结肠血管生成的研究

[目的]从血管生成角度研究三七提取物促进结肠溃疡愈合的作用机制。[方法]制备三硝基苯磺酸（TNBS）诱导溃疡性结肠炎（UC）大鼠，分为三七提取物低、中、高剂量组，柳氮磺胺吡啶（SASP）组，模型对照组，模型组和正常对照（正常）组。其中模型组于造模3d时处死，其余6组均在给药处理7d（即造模10d）时处死。取大鼠结肠病变部位标本，进行组织学评价；运用免疫组化染色法检测血管内皮生长因子（VEGF）、fms样酪氨酸激酶受体（FLT-1）和含有激酶插入区域的受体（KDR）、低氧诱导因子（HIF-1）蛋白表达；用RT-PCR法检测VEGF、FLT-1和KDR、HIF-1的mRNA表达。[结果]与模型对照组和SASP组比较，三七提取物低、中和高剂量组大鼠结肠黏膜炎症明显消除和溃疡愈合，杯状细胞数量及黏液增加，VEGF、FLT-1和KDR、HIF-1表达显著增加。[结论]血管生成在TNBS诱导大鼠UC形成和愈合过程中起重要作用。用药后VEGF、KDR、FLT-1和HIF-1表达增加。三七提取物通过上调VEGF、KDR、FLT-1和HIF-1表达促进血管生成，是其治疗UC的主要作用机制之一。     

三硝基苯磺酸/乙醇与免疫复合物联合诱导的结肠炎动物模型

目的 建立三硝基苯磺酸/乙醇与免疫复合物联合诱导的结肠炎动物模型,探讨炎症性肠病的发病机制.方法 SD大鼠168只,雌雄各半,分为:①正常对照组42只,②三硝基苯磺酸/乙醇模型组42只,③免疫复合物组42只,④三硝基苯磺酸/乙醇与免疫复合物联合诱导的结肠炎动物模型组42只(以上每组雌雄各半).分别于造模后1、2、3、4、6,9、12周末将大鼠处死(每组每周处死6只).观察各组结肠大体形态和组织学改变,并检测肠黏膜髓过氧化物酶(MPO)活性,大便潜血实验.结果 三硝基苯磺酸/乙醇与免疫复合物联合诱导的结肠炎动物模型组大鼠大体形态损伤评分均数为5.8571±0.8431;组织学损伤评分均数为4.8571±0.3542;MPO均数为3.8588±0.8625;OBT积分均数为4.1429±0.6010皆明显高于其余各组,具有统计学意义.结论 上述联合诱导的结肠炎动物模型是一种较理想的IBD动物模型,可作为研究IBD发病机制及评估药物疗效的有益工具.     

维生素D3对三硝基苯磺酸诱导的大鼠结肠炎的作用

背景:维生素D(VitD)对炎症性肠病(IBD)的免疫调节作用日渐受到关注。目的:探讨VitD3对TNBS诱导的大鼠结肠炎的疗效及其机制。方法:66只雄性大鼠随机分为11组:空白对照组、TNBS组、5-ASA组、不同剂量VitD3组及其联合5-ASA组、活性VitD3组及其联合5-ASA组。除空白对照组外,其余10组以TNBS灌肠诱导结肠炎模型。造模后24 h,各组以不同药物灌胃进行干预。造模第10 d处死大鼠,评估疾病活动指数(DAI)、大体损伤、组织病理学评分,测定髓过氧化物酶(MPO)活性,以RT-PCR法检测T-bet、GATA-3 mRNA表达。测定血钙和血肌酐水平以监测不良反应。结果:与TNBS组相比,单次和连续大剂量VitD3联合5-ASA组大体损伤评分和组织病理学评分均明显下降(P<0.05);各药物干预组MPO活性均明显下降(P<0.001),T-bet mRNA表达无明显差异;5-ASA组、连续大剂量VitD3组GATA-3 mRNA表达明显升高(P<0.05)。连续大剂量VitD3组及其联合5-ASA组大鼠出现高钙血症,且连续大剂量VitD3组血肌酐水平明显高于其余各组(P<0.05)。结论:VitD3可通过调节T细胞免疫减轻TNBS诱导的实验性结肠炎。     

大蒜素对三硝基苯磺酸诱导大鼠结肠炎的保护作用及其机制研究

背景：溃疡性结肠炎（UC）是一种病因未明的结直肠炎症,大蒜素对其防治的作用目前尚未有结论。目的：探讨大蒜素对TNBS诱导的大鼠结肠炎的保护作用及其机制。方法：80只大鼠随机分为对照组、TNBS组、大蒜素预防组、大蒜素灌胃组、大蒜素灌肠组、地塞米松组、柳氮磺吡啶组、巴柳氮钠组。以含150mg／kgTNBS的50％乙醇溶液灌肠制备大鼠结肠炎模型。造模2周后处死大鼠。行大体评分和病理学评分,以ELISA法测定血清TNF-α、IL-1β、IL-10、IL4含量,蛋白质印迹法检测NF—κB表达。结果：与对照组相比,TNBS组大体和病理学评分均明显升高（P〈0．05）,体质量明显降低（P〈0．05）,血清TNF-α、IL-1B含量显著升高（P〈0．05）,血清IL-4、IL-10含量显著降低（P〈0．05）,NF-κB表达明显升高（P〈0．05）;给予大蒜素预防或治疗后,上述指标均明显改善（P〈0．05）,但疗效低于地塞米松组、柳氮磺吡啶组、巴柳氮钠组。结论：大蒜素对TNBS诱导的大鼠结肠炎有保护作用,可能是通过调控细胞因子和NF—κB而发挥作用的。     

肠道微生态对三硝基苯磺酸诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白occludin保护作用的研究

目的研究肠道微生态对三硝基苯磺酸(trinitro-benzen-sulfonic acid,TNBS)诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的保护作用。方法建立TNBS诱导大鼠结肠炎模型。实验分为正常组、模型组和双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)组。进行疾病活动指数(DAI)和组织学损伤评分,用ELISA法测定结肠组织TNF-α、IL-10和血清内毒素水平,采用免疫组织化学染色检测紧密连接(tight junction,TJ)相关蛋白occludin的分布。结果TNBS诱导大鼠结肠炎后,DAI和组织学损伤评分增高,结肠组织TNF-α水平升高,IL-10水平降低和血清内毒水平升高,而经双歧杆菌嗜酸乳杆菌肠球菌三联活菌处理后,DAI和组织学损伤评分有明显下降,结肠组织TNF-α水平降低,IL-10水平升高和血清内毒素水平降低,组间比较差异有显著性(P0.05)。TNBS诱导大鼠结肠炎后,TJ结构遭到破坏,TJ相关蛋白的表达亦减少,而双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)处理后可使TNBS引起的TJ结构受损减轻,相关蛋白的表达增多(P0.05)。结论肠道微生态对TNBS诱导大鼠结肠炎肠黏膜上皮细胞TJ蛋白具有明显的保护作用,其可能的机制是通过纠正肠道微生态,上调肠上皮细胞TJ蛋白occludin的表达,降低结肠组织TNF-α水平,提高IL-10水平,从而抑制内毒素通过紧密连接进入体循环。     

美沙拉嗪对2，4，6-三硝基苯磺酸诱导溃疡性结肠炎大鼠脾脏组织NF—κBp65表达的影响

目的 探讨美沙拉嗪对2,4,6-三硝基苯磺酸（TNBS）诱导的溃疡性结肠炎大鼠脾脏组织NF-κB p65表达的影响.方法 将42只SD大鼠随机分为空白对照组、结肠炎模型组和美沙拉嗪治疗组,每组各14只.除空白对照组外,其他两组均应用TNBS灌肠制作溃疡性结肠炎大鼠模型;模型建成2d后,空白对照组和结肠炎模型组均用蒸馏水、美莎拉嗪治疗组用美莎拉嗪蒸馏水混悬液3 mL灌胃;连续灌胃15 d后取脾脏组织,采用RT-PCR法检测NF-κB p65 mRNA,Western blot法检测NF-κB p65蛋白.结果 与空白对照组比较,结肠炎模型组NF-κB p65 mRNA、蛋白表达均升高（P均＜0.05）;与结肠炎模型组比较,美沙拉嗪治疗组NF-κB p65 mRNA、蛋白均下降（P均＜0.05）.结论 美沙拉嗪能通过下调TNBS诱导的溃疡性结肠炎大鼠脾脏组织NF-κB p65的表达,发挥治疗溃疡性结肠炎的作用.     

茶多酚对D-半乳糖诱导糖基化大鼠脑损害的干预作用

目的研究茶多酚（tea polyphenols，TP）对D-半乳糖诱导的糖基化大鼠并发脑损害的干预作用。方法D-半乳糖（150mg&#183;kg-1&#183;d-1）腹腔注射给药造模8W，诱导形成糖基化大鼠，并在造模第3周时分为模型组，氨基胍组，茶多酚高、中、低剂量后，灌胃给药6W。测定红细胞醛糖还原酶活性、糖化血红蛋白、血清果糖胺和晚期糖基化终末产物（AGEs）含量；脑组织中AGEs含量、SOD活性和MDA含量及脑神经细胞内钙离子水平，透射电镜观察海马神经细胞线粒体的变化。结果茶多酚高、中剂量组能明显降低模型大鼠红细胞醛糖还原酶活性，抑制糖化产物的形成，降低脑组织中AGEs及脑细胞内钙的含量，提高SOD活性，降低MDA含量，保护海马神经细胞线粒体结构的完整性。结论茶多酚具有抑制D-半乳糖诱导的糖基化反应，并对糖基化状态并发的脑神经细胞损害具有保护作用。     

Alpha-lipoic acid modulates gut inflammation induced by trinitrobenzene sulfonic acid in rats

BACKGROUND AND AIM: Alpha-lipoic acid (ALA) has been shown to combat oxidative stress by quenching a variety of reactive oxygen species. It is involved in the regeneration of exogenous and endogenous antioxidants, chelation of metal ions, and repair of oxidized proteins. This study aimed to evaluate the potential beneficial effect of ALA on trinitrobenzenesulfonic acid (TNBS)-induced gut ileitis and colitis in rats. METHOD: After 48 h of fasting, Sprague-Dawley rats underwent a laparotomy under ether anesthesia. TNBS solution 30 mg/mL in 40% ethanol (1 mL) was injected into the lumen, 10 cm proximal to the ileocolonic junction to induce ileitis or intrarectally 8 cm proximal to the anal sphincter to induce colitis. ALA (25 mg/kg intraperitoneally, twice a day) was given after induction of inflammation and continued for 3 days. All animals were decapitated 3 days after induction of the inflammation. The mucosal lesions of the ileum and colon were scored macroscopically and microscopically. Samples were taken for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, tissue-associated myeloperoxidase (MPO) activity and luminol- or lucigenin-enhanced chemiluminescence (CL). RESULTS: Macroscopic scores, morphological changes and increased tissue lipid peroxidation with a concomitant reduction in GSH of the ileitis or colitis groups were all reversed by treatment with ALA. ALA treatment was also effective in improving tissue MPO activity and CL values, which were elevated in untreated ileitis or colitis groups. CONCLUSION: ALA is beneficial in TNBS-induced gut inflammation in rats via suppression of neutrophil accumulation, preservation of endogenous glutathione and inhibition of reactive oxidant generation.     

Leukotriene D4 participates in colonic transit disturbances induced by intracolonic administration of trinitrobenzene sulfonic acid in rats.

The effects of colonic inflammation induced by trinitrobenzene sulfonic acid and influence of previous treatment with specific antagonists of inflammatory mediators (platelet-activating factor, leukotrienes, prostaglandins, and thromboxanes) on colonic transit were examined in conscious rats which were permanently fitted with an intracolonic catheter inserted into the proximal colon. Colonic inflammation was induced by intracolonic administration of trinitrobenzene acid (80 mg/kg) in 50% ethanol. Colonic transit time was evaluated by intracolonic administration of a radiolabeled marker [( 51Cr]sodium chromate) and collection of the feces per hour on a conveyor belt. Excretion of the marker was then plotted vs. time, permitting calculations of the times elapsed to recover 25%, 50%, and 75% of the marker injected (T25, T50, and T75, respectively). In control (saline) animals, excretion of the marker described a regular sigmoid curve with 50% of the marker recovered at 6.92 +/- 0.40 hours after intracolonic administration (T25 = 6.4 +/- 0.43 hours; T75 = 7.49 +/- 0.39 hours). Ethanol (vehicle), 50%, did not modify the profile of marker recovery. On the contrary, single intracolonic administration of trinitrobenzene sulfonic acid/ethanol induced a biphasic response consisting of an early pool of radiolabeled feces (T25 = 4.03 +/- 0.55 hours) with a delayed total one (T50 = 11.74 +/- 0.83 hours; T75 = 13.70 +/- 0.49 hours). Antagonists of the leukotriene pathway, i.e., MK = 886, a lipoxygenase inhibitor, and SKF 104,353 and SR 2640, two different leukotriene D4 receptor antagonists, blocked the effects of trinitrobenzene sulfonic acid on colonic transit time and restored a control profile of radiolabeled marker excretion. In contrast, indomethacin, a cyclooxygenase inhibitor, and SC 19220, a specific prostaglandin E2 receptor antagonist, were inefficient in blocking the effects of trinitrobenzene sulfonic acid on colonic transit time. Specific thromboxane A2 receptor antagonists, KT1-32 and GR 32191B, did not show any improvement in colonic transit after trinitrobenzene sulfonic acid administration. Previous injection of the specific platelet-activating factor receptor antagonists, BN 52021 or BN 50730, was also unable to restore a normal marker excretion profile after administration of trinitrobenzene sulfonic acid. It is concluded that the alterations of colonic transit immediately observed after intracolonic trinitrobenzene sulfonic acid administration are mediated through the release of leukotriene D4. In contrast, platelet-activating factor, prostaglandins, and thromboxanes are not involved in the mediation of these transit disturbances.     

Effect of leukotriene C4D4 antagonist on colonic damage induced by intracolonic administration of trinitrobenzene sulfonic acid in rats

We examined the effects of eicosanoid antagonists on colonic damage induced by trinitrobenzene sulfonic acid (TNB) in a rat inflammatory bowel model. TNB (30 mg) dissolved in 0.25 ml of 50% ethanol, was given intrarectally. The appropriate doses of ONO-1078 (a leukotriene C₄D₄ antagonist), ONO-4057 (a leukotriene B₄ antagonist), and OKY-046 (a thromboxane A₂ synthetase inhibitor) were given to obtain the same blood level, either 4 h before (pre-treatment model) or 24 h after (the post-treatment model) the administration of TNB (n=8 in all groups). Drugs were given once daily for 6 days through a gastric feeding tube. Autopsy was performed on the 7th day. Colonie damage was assessed in terms of colonie damage scores, and myeloperoxidase (MPO) activity and eicosanoid concentrations in colonie tissues were measured. Compared with the group given TNB alone, the colonie damage score was reduced to 10% in the pre-treatment model with ONO-1078, but the score was not reduced in other groups, MPO activity was not changed in any group. The concentration of leukotriene C₄ was reduced with ONO-1078 treatment, in both pre- and post-treatment models. These results demonstrated that a leukotriene C₄D₄ antagonist reduced colonie inflammation; however, its anti-inflammatory effect was limited in this colitis model.     

白头翁醇提物对大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的保护作用

目的:探讨白头翁醇提物对三硝基苯磺酸诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的调控,进一步阐明白头翁醇提物对大鼠实验性结肠炎的肠黏膜屏障的保护作用.方法:建立TNBS诱导大鼠结肠炎模型.实验分为正常组、模型组、白头翁醇提物治疗组和双歧杆菌嗜酸乳杆茵肠球菌三联活菌(金双歧)组.进行疾病活动指数(DAI)和组织学损伤评分,用ELISA法测定结肠组织TNF-α、IL-10和血清内毒素,采用免疫组织学染色检测紧密连接(tight iunction,TJ)相关蛋白occludin的分布.结果:TNBS诱导大鼠结肠炎后,DAI和组织学损伤评分增高,结肠组织TNF-α水平升高、IL-10水平降低和血清内毒素水平升高,而经白头翁醇提物和双歧杆菌嗜酸乳杆菌肠球菌三联活菌处理后,DAI和组织学损伤评分有明显下降(6.50±1.27,5.90±1.67 vs 9.20±1.75:5.00±1.05,4.80±1.25 vs 7.10±0.99,均P<0.05),结肠组织TNF-α水平降低(521.24±109.37 ng/L,503.98±126.63 ng/L vs 657.54±149.60 ng/L,均P＜0.05)、血清内毒素水平降低(0.148±0.093EU/mL,0.153±0.106 EU/mL vs 0.213±0.023EU/mL,均P＜0.05)和IL-10水平升高(92.19±30.09 ng/L,95.57±27.71 ng/L vs 42.92±23.74ng/L,均P＜0.05);TNBS诱导大鼠结肠炎后,TJ结构遭到破坏,TJ相关蛋白的表达减少,而白头翁醇提物和双歧杆菌嗜酸乳杆菌肠球菌三联活茵(金双歧)处理后可使TNBS引起的TJ结构受损减轻,相关蛋白的表达增多.结论:白头翁醇提物可以对TNBS诱导大鼠结肠炎肠黏膜屏障具有明显的保护作用,其机制可能是通过调节肠道微生态、上调肠上皮细胞紧密连接蛋白ocluudin的表达、降低结肠组织TNF-α含量、提高IL-10水平,从而抑制内毒素通过紧密连接进入体循环.     

银杏叶提取物对脂多糖诱导D-半乳糖致衰老大鼠急性肺损伤的保护作用

目的　观察脂多糖 (LPS)诱导D 半乳糖 (D gal)致衰老大鼠急性肺损伤 (ALI)及银杏叶提取物 (GBE)对其是否有保护作用。方法　大鼠 2 4只随机分成两部分 ,6只为正常对照组 ;18只经腹腔注D gal复制衰老动物模型。后者再随机分成三组 :衰老对照组 (6只 ) ;LPS组 (6只 ,静脉注射LPS诱导形成ALI) ;GBE +LPS组 (6只 ,注LPS前 7天开始每天灌胃给GBE一次 ,按所含黄酮甙计算 ,8mg/kg体重 ,实验当日在给LPS前 2h再给一次GBE)。注LPS后 2h收集标本待测。结果　D gal致衰老大鼠较正常大鼠血中超氧化物歧化酶 (SOD)及肺组织Na+ K+ ATPase活性均显著降低 (P均 <0 0 5 ) ,而血中乳酸脱氢酶 (LDH)活性升高 (P <0 0 5 )。衰老大鼠注LPS后 2h已形成ALI。肺间质及肺泡中有较多炎性细胞 ;肺泡灌洗液中蛋白含量及肺通透指数增加 ;血中乳酸 (LD) ,丙二醛 (MDA) ,一氧化氮 (NO) ,内皮素 1(ET 1) ,肿瘤坏死因子 α(TNF α)含量和LDH活性以及肺组织中髓过氧化物酶 (MPO)活性 ,均显著升高 ;而血中超氧化物歧化酶活性及肺组织Na+ K+ ATPase活性均下降 (P <0 0 5 ,P <0 0 1)。预先给予GBE可显著地缓解除SOD活性外的上述其它指标的变化 (P <0 0 5 )。结论　D gal致衰老大鼠体内抗氧化能力降低。静注LPS可引起衰老大鼠明显的A     

选择性环氧合酶-2抑制剂塞来昔布在实验性结肠炎中的作用机制

目的　明确选择性环氧合酶 (COX) 2抑制剂—塞来昔布对 2 ,4 ,6 三硝基苯磺酸 (TNBS)诱导的大鼠结肠炎的作用 ,并初步探讨其作用机制。方法　将大鼠分为四组 :第 1组和第 2组为造模组 ,第 3组和第 4组为对照组。用 0 .2 5mlTNBS乙醇溶液 (TNBS浓度 2 5mg/ml,乙醇浓度 5 0 % )灌肠 ,诱导大鼠慢性实验性结肠炎模型。造模组大鼠于造模前 3h开始 ,分别给予塞来昔布 (1.2 5mg/kg ,第 1组 )和蒸馏水 (第 2组 ) ,每天 2次 ,共 7d。第 3组大鼠为正常对照组。第 4组大鼠以塞来昔布 (1.2 5mg/kg)灌胃 ,每天 2次 ,共 7d。于第 7天实验结束时处死所有存活动物 ,观察结肠黏膜的损伤程度 ,同时用放射免疫分析法测定结肠黏膜前列腺素E2 (PGE2 )水平。结果　造模组大鼠结肠损伤积分分别为11.15± 3.30 (第 1组 )和 8.5 0± 2 .82 (第 2组 ) ,均显著高于正常对照组 0 .6 2± 0 .0 9(P值均 <0 .0 1)。第 1组的结肠损伤积分显著高于第 2组 (P <0 .0 5 )。第 3组和第 4组的积分差异无显著性。造模组大鼠结肠黏膜PGE2浓度分别为 (12 .0 0± 4 .33)pg/ μg(第 1组 )和 (17.2 0± 9.6 2 ) pg/ μg(第 2组 ) ,均显著高于正常对照组的 (6 .0 2± 3.39) pg/ μg ,(P值均 <0 .0 5 )。第 1组的PGE2浓度显著低于第 2组 (P <0 .0 5 )