开口箭提取物对结肠炎大鼠血小板活性的影响

[目的]研究中药开口箭有效成分对实验性结肠炎大鼠血小板活性的影响.[方法]建立三硝基苯磺酸大鼠结肠炎模型,用开口箭醇提物(主要成分为甾体皂苷)灌肠治疗2周后评价大鼠血小板表面P-选择素以及血小板聚集率改变.[结果]治疗组与模型组比较,血小板聚集率和血小板表面P-选择素下降(P＜0.05).[结论]开口箭醇提物可以抑制血小板的聚集与活化.     

罗格列酮对大鼠溃疡性结肠炎的疗效及其机制

目的观察罗格列酮对大鼠溃疡性结肠炎的疗效并探讨其可能存在的机制。方法应用三硝基苯磺酸(TNB)/乙醇灌肠制备大鼠溃疡性结肠炎模型。实验设正常对照组、模型对照组、阳性药物组(柳氮磺胺吡啶组,100 mg/kg)、罗格列酮给药组(2 mg、4mg、8 mg/kg),每天灌胃给药1次,给药时间从造模后第2天开始至实验结束共8 d,观察大鼠疾病活动指数(DAI)、结肠黏膜损伤指数(CMDI)及组织学评分(HS)。生化法检测大鼠结肠组织髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)的含量。结果与正常组相比,模型组大鼠DAI、CMDI、HS明显增加(P<0.01),结肠组织MPO活性、MDA水平显著升高(P<0.01),SOD活性下降(P<0.01)。罗格列酮4 mg、8 mg/kg和SASP可不同程度改善DAI、CMDI和HS(P<0.05,P<0.01),降低MPO活性和MDA水平(P<0.01),增加SOD活性(P<0.01)。结论罗格列酮对大鼠溃疡性结肠炎有保护作用,其机制可能与减少脂质氧化,增加清除氧自由基的能力有关。     

姜黄素对大鼠小肠炎组织MPO、SOD作用的影响

目的 研究姜黄素对受损肠黏膜大鼠小肠组织髓过氧化物酶(MPO),超氧化物歧化酶(SOD) 活性的影响,探讨姜黄素的抗炎机制.方法 应用氨甲碟呤制备大鼠小肠炎模型.实验设正常对照组,模型对照组,柳氮磺胺吡啶(SASP,100 mg/kg)组,姜黄素(100 mg/kg)组.后2组每天灌冒给药1次.给药时间从造模后第2天开始至实验结束,共6 d,第4天、第7天分别观察大鼠疾病活动指数(DAI)和结肠黏膜损伤指数(CMDI),光镜下组织学评分(HS),生化法检测大鼠小肠组织髓过氧化酶(MPO)及超氧化物歧化酶(SOD)活性.结果 与正常组相比,模型组大鼠DAI、CMDI和Hs明显增加(P相似文献   

阿魏酸钠对结肠炎大鼠结肠巨噬细胞功能的影响

目的探讨阿魏酸钠在整体水平对结肠炎大鼠结肠巨噬细胞功能的影响及其机制。方法建立大鼠免疫性结肠炎模型。阿魏酸钠（SF）灌肠用药21d后检测结肠组织MDA、NO、PGE2含量，SOD、IL-1，TNF-α、MPO活性及NF-κB p65表达水平。结果阿魏酸钠（200，400，800mg／kg）灌肠后呈剂量依赖型降低模型组大鼠的MDA、NO、PGE2含量，IL-1、TNF—α、MPO活性及NF-κB p65表达水平，同时升高SOD活性。结论SF可减弱结肠炎大鼠结肠活化巨噬细胞的生物活性，缓解结肠炎症反应，机制可能与抑制NF-κB表达有关。     

痛泻要方治疗溃疡性结肠炎模型大鼠的药效学机制

目的探讨痛泻要方治疗溃疡性结肠炎(UC)大鼠的疗效及其机制。方法将实验动物分为3组:空白组、模型组、痛泻要方组,采用TNBS/乙醇溶液灌肠加束缚法制作UC肝郁脾虚证大鼠模型,光镜观察结肠组织病理形态变化,免疫组化法观察结肠组织过氧化物酶体增殖物激活受体(PPAR-γ)蛋白表达变化,并以大鼠胸腺指数、脾脏指数、结肠组织髓过氧化物酶(MPO)、丙二醛(MDA)、超氧化物歧化酶(SOD)、总抗氧化能力(TAOC)为观察指标。结果与空白组比较,模型组大鼠结肠组织损伤程度严重(P0.01),大鼠结肠组织PPAR-γ蛋白表达下调(P0.01),脾脏和胸腺指数降低(P0.05),MPO和T-AOC活性降低(P0.05,P0.01),SOD活性升高(P0.05),MDA含量下降(P0.01);与模型组比较,痛泻要方组的结肠损伤明显修复(P0.05),大鼠结肠组织PPAR-γ蛋白表达上调(P0.01);脾脏和胸腺指数升高,MPO和T-AOC活性升高(P0.05),SOD活性降低(P0.05),MDA含量增加(P0.05)。结论痛泻要方能够有效治疗实验性UC,其药效作用可能是通过提高结肠组织抗氧化能力和调节结肠组织紊乱的免疫功能以及提高结肠组织PPAR-γ的表达实现。     

丹参注射液对心脑血管病自由基损害和血栓烷等水平的影响

目的：探讨丹参注射液对心脑血管疾病患者血超氧化物歧化酶（SOD）、丙二醛（MDA）、P-选择素、血栓烷B2（TXB2）水平的影响。方法：选择26例心脑血管疾病患者，在常规治疗基础上加用丹参注射液，测定治疗前、后血SOD、MDA、P-选择索、TXB2水平，并与正常人进行对比分析。结果：心脑血管疾病患者血SOD浓度较正常对照组降低，MDA、P-选择素、TXB：水平较正常对照组升高非常显著（P〈0．01）。丹参注射液治疗后上述各指标均显著改善（P〈0．01）。结论：丹参注射液能防止自由基脂质过氧化，抑制P-选择素活化及血小板粘附、聚集。     

奥扎格雷钠对TNBS诱导的结肠炎大鼠的治疗作用

背景:近期研究证实血小板活化在炎症性肠病(IBD)的发病中起重要作用。目的:探讨血栓烷合成酶抑制剂奥扎格雷钠对三硝基苯磺酸(TNBS)诱导的大鼠结肠炎模型的治疗作用。方法:21只Sprague-Dawley(SD)大鼠随机分为结肠炎模型组、地塞米松治疗组、奥扎格雷钠治疗组,每组7只;另取4只大鼠作为正常对照组。TNBS建模后第2～6 d分别给予地塞米松、奥扎格雷钠和0.9%NaCl溶液皮下注射,于第7 d处死所有大鼠。检测大鼠体质量改变、结肠重量长度比、结肠大体和病理评分,以放射免疫法检测血浆P-选择素(CD62P)、血栓烷B_2(TXB_2)和6-酮-前列腺素F(6-kPGF)1α,化学比色法测定结肠组织髓过氧化物酶(MPO)、丙二醛(MDA)、诱生型一氧化氮合酶(iNOS)。结果:地塞米松治疗组和奥扎格雷钠治疗组的肠道病理损伤较结肠炎模型组明显减轻,血浆CD62P、TXB_2、TXB_2/6-k-PGF1α和结肠组织MPO、MDA、iNOS明显降低(P0.05),血浆6-k-PGF1α水平明显增高(P0.05)。结论:奥扎格雷钠可通过抑制血小板活化明显减轻TNBS结肠炎大鼠的肠道炎症损伤,提示抗血小板治疗有望成为IBD新的治疗方法。     

银杏叶提取物对实验性结肠炎大鼠肠组织IL-6表达的影响

目的探讨银杏叶提取物(EGB)对实验性结肠炎大鼠肠组织大体形态组织学及炎性指标的影响。方法利用三硝基苯磺酸灌肠制备大鼠实验性结肠炎模型。实验设正常对照组、模型组、5-氨基水杨酸组、EGB组。4周后评价结肠组织大体形态和组织学评分,检测髓过氧化物酶(MPO)活性和IL-6、IL-6 mRNA表达。结果模型组大鼠结肠组织大体形态和组织学评分较对照组显著增加,MPO活性、IL-6、IL-6 mRNA表达水平显著升高;EGB组上述指标较模型组显著下降。结论EGB对大鼠实验性结肠炎有一定治疗作用,其作用机制可能与其降低结肠组织细胞因子IL-6水平有关。     

复方刺五加注射液对大鼠实验性脑缺血的影响

目的观察复方刺五加注射液(CASI)对大鼠实验性脑缺血的保护作用。方法采用大鼠结扎双侧颈总动脉伴低血压模型,探讨CASI对实验性脑缺血大鼠脑含水量、脑指数、血小板黏附及聚集功能,脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)、钙离子(Ca2 )及乳酸(LA)等指标的影响。结果CASI可使实验性脑缺血大鼠的脑含水量及脑指数明显降低,能抑制血小板黏附和聚集功能,提高脑组织SOD活性,降低MDA、Ca2 及LA含量。结论CASI对大鼠实验性脑缺血具有明显保护作用,可能与其抑制脂质过氧化物损害、提高抗氧化酶活性及降低乳酸酸中毒和细胞内钙超载有关。     

雷公藤内酯醇对大鼠实验性结肠炎的治疗作用

背景:炎症性肠病(IBD)病程迁延,传统的药物治疗效果均不理想,寻找新型而有效的药物一直是该领域研究的热点.目的:观察不同剂量雷公藤内酯醇对大鼠实验性结肠炎的治疗作用和不良反应.方法:60只Sprague-Dawley大鼠随机分为6组:模型组、低剂量(0.1 mg/kg)雷公藤内酯醇组、中剂量(0.2 mg/kg)雷公藤内酯醇组、高剂量(0.4 mg/kg)雷公藤内酯醇组、丙二醇(20%,5 ml/kg)对照组和地塞米松(0.2 mg/kg)对照组.应用三硝基苯磺酸(TNBS)/乙醇溶液诱导产生大鼠结肠炎模型,以相应药物处理2周后处死大鼠.处死大鼠前1天行白细胞计数检查,处死后直接称取胸腺重量.计算结肠溃疡面积和湿干比;测定结肠黏膜超氧化物歧化酶(SOD)和髓过氧化物酶(MP0)活性;采用酶联免疫吸附(ELISA)法测定结肠组织白细胞介素(IL)-1和肿瘤坏死因子(TNF)-α水平.结果:不同剂量雷公藤内酯醇治疗后,能显著减少大鼠结肠黏膜的溃疡面积,降低结肠湿干比;显著升高结肠黏膜SOD活性、降低MP0活性;显著降低IL-1和TNF-α的水平;使大鼠胸腺明显缩小,白细胞计数显著减少.结论:雷公藤内酯醇对TNBS/乙醇溶液诱导的大鼠实验性结肠炎具有显著的治疗作用,同时剂量大时亦有明显的不良反应.     

Protective effect of angelica sinensis polysaccharide on experimental immunological colon injury in rats

AIM: To study the effect of angelica sinensis polysaccharide (ASP) on immunological colon injury and its mechanisms in rats.METHODS: Immunological colitis model of rats was induced by intracolon enema with 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) and ethanol. The experimental animals were randomly divided into normal control, model control, 5-aminosalicylic acid therapy groups and three doses of ASP therapy groups. The 6 groups were treated intracolonically with normal saline, normal saline, 5-aminosalicylic acid (100 mg.kg-1), and ASP daily (8:00 am) at the doses of 200, 400 and 800 mg.kg-1 respectively for 21 days 7 d following induction of colitis. The rat colon mucosa damage index (CMDI), the histopathological score (HS), the score of occult blood test (OBT), and the colonic MPO activity were evaluated. The levels of SOD, MDA, NO, TNF-α, IL-2 and IL-10 in colonic tissues were detected biochemically and immunoradiometrically. The expressions of TGF-β and EGF in colonic tissues were also determined immunochemically.RESULTS: Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in colitis rats,which manifested as significant increases of CMDI, HS, OBT,MPO activity, MDA and NO contents, as well as the levels of TNF-α and IL-2 in colonic tissues, although colonic TGF-β protein expression, SOD activity and TL-10 content were significantly decreased compared with the normal control (P＜0.01). However, these parameters were found to be significantly ameliorated in colitis rats treated intracolicly with ASP at the doses of 400 and 800 mg@kg-1 (P＜0.05-0.01).Meantime, colonic EGF protein expression in colitis rats was remarkably up-regulated.CONCLUSION: ASP has a protective effect on immunological colon injury induced by TNBS and ethanol enema in rats,which was propably due to the mechanism of antioxidation,immunomodulation and promotion of wound repair.     

Ameliorative effects of sodium ferulate on experimental colitis and their mechanisms in rats

AIM: To investigate the ameliorative effects of sodium ferulate (SF) on acetic acid-induced colitis and their mechanisms in rats.METHODS: The colitis model of Sprague-Dawley rats was induced by intracolon enema with 8 % (WV) of acetic acid.The experimental animals were randomly divided into model control, 5-aminosalicylic acid therapy group and three dose of SF therapy groups. The 5 groups were treated intracolonically and daily (8:00 am) for 7 days 24 h following the induction of colitis. A normal control group of rats clystered with normal saline instead of acetic acid was also included in the study.Pathological changes of the colonic mucosa were evaluated by the colon mucosa damage index (CMDI) and the histopathological score (HS). The insulted colonic mucosa was sampled for a variety of determinations at the end of experiment when the animals were sacrificed by decapitation.Colonic activities of myeloperoxidase (MPO) and superoxide dismutase (SOD), and levels of malondialdehyde (MDA)and nitric oxide (NO) were assayed with ultraviolet spectrophotometry. Colonic contents of prostaglandin E2 (PGE2) and thromboxane B2 (TXB2)were determined by radioimmunoassay. The expressions of inducible nitric oxide synthase (iNOS), cyclo-oxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB) p65 proteins in the colonic tissue were detected with immunohistochemistry.RESULTS: Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with acetic acid, which manifested as the significant increase of CMDI, HS, MPO activities, MDA and NO levels,PGE2 and TXB2 contents, as well as the expressions of iNOS,COX-2 and NF-κB p65 proteins in the colonic mucosa,although the colonic SOD activity was significantly decreased compared with the normal control (CMDI: 2.9±0.6 vs0.0±0.0;HS: 4.3±0.9 vs0.7±1.1; MPO: 98.1±26.9 vs24.8±11.5; MDA:57.53±12.36 vs9.21±3.85; NO: 0.331±0.092 vs0.176±0.045;PGE2: 186.2±96.2 vs 42.8±32.8; TXB2: 34.26±13.51 vs 8.83±3.75; iNOS: 0.365±0.026 vs0.053±0.015; COX-2:0.296±0.028 vs0.034±0.013; NF-κB p65:0.314±0.026 vs 0.039±0.012; SOD: 28.33±1.17 vs36.14±1.91; P<0.01).However, these parameters were found to be significantly ameliorated in rats treated locally with SF at the given dose (CMDI: 1.8±0.8, 1.6±0.9; HS: 3.3±0.9, 3.1±1.0; MPO:63.8±30.5, 36.2±14.2; MDA: 41.84±10.62, 37.34±8.58; NO:0.247±0.042; 0.216±0.033; PGE2: 77.2±26.9, 58.4±23.9;TXB2:18.07±14.83; 15.52±8.62; iNOS:0.175±0.018, 0.106±0.019;COX-2: 0.064±0.018, 0.056±0.014; NF-κBp65: 0.215±0.019,0.189±0.016; SOD: 32.15±4.26, 33.24±3.69; P<0.05-0.01).amelioration of colonic mucosal injury as evaluated by CMDI and HS.CONCLUSION: Administration of SF intracolonically may have significant therapeutic effects on the rat model of colitis induced by acetic acid enema, which was probably due to the mechanism of antioxidation, inhibition of arachidonic acid metabolism and NF-κB expression.     

微生态制剂对实验性大鼠结肠炎的治疗

目的 评价微生态制剂双歧三联活菌对三硝基苯磺酸钠(TNBS)诱导的大鼠结肠炎的疗效,探索炎症性肠病(IBD)治疗的新方法.方法 成年雌性SD大鼠50只,随机分为对照组(G1)、模型组(G2)、双歧三联活菌治疗组(G3)、奥沙拉秦治疗组(G4)、双歧三联活菌和奥沙拉秦联合治疗组(G5),每组10只.ELISA法检测各组的血清C反应蛋白(CRP)、TNFα、IL-10水平,分光光度法检测肠组织髓过氧化物酶(MPO)活力,并对肠组织进行病理组织学分析.结果 治疗后,G1组肠组织结构正常,血清CRP、TNFα、IL-10水平、结肠黏膜损伤指数(CMDI)及肠组织MPO活力显著低于G2组(P<0.001);G2组肠组织炎症程度最莺,血清CRP、TNFα、IL-10水平、CMDI及肠组织MPO活力最高,P<0.05;3个治疗组G3、G4、G5组的肠组织炎症呈不同程度消散,血清CRP、TNFα、IL-10水平及肠组织MPO活力呈不同程度下降,以G5组最显著,P<0.05;G2组血清CRP、TNFα、IL-10及肠组织MPO活力均分别与CMDI呈正相关,P<0.001.结论 双歧三联活菌能有效改善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.     

Effects of low molecular weight heparin on platelet surface P-selectin expression and serum interleukin-8 production in rats with trinitrobenzene sulphonic acid-induced colitis

AIM:To observe the effects of low molecular weight heparin(LMWH) on platelet surface P-selectin expression and serum interleukin-8 production in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis.METHODS:Colitis was induced in female Sprauge-Dawley rats by colonic administration of 2, 4, 6-TNBS. LMWH, a dalteparin (150U/kg, 300U/kg) was subcutaneously administrated one hour before induction of colitis and went on once a day for 6 days. Then a half dose was given for the next 7 days. Control animals received the same volume of normal saline once a day for 14 days after treated by TNBS.Animals were sacrificed at 24h, days 7 and 14 after induction of colitis. The colon was excised for the evaluation of macroscopic and histological findings and TNF-α immunohistochemical assay. Platelet surface P-selectin expression was determined by radioimmunoassay and serum IL-8 production was assayed by ELISA method.RESULTS:LMWH treatment in a dose of 300U/kg for 14 days significantly improved colonic inflammation by histological examination. Serum IL-8 production in the 300U/kg treatment group was more significantly decreased at day 14 than that at 24h (P&lt;0.05). However, platelet surface P-selectin expression and TNF-α staining in colonic tissue were not significantly different among the three groups.CONCLUSION:LMWH has an anti-infiammatory effect on TNBS induced colitis in rats. The effect is possibly related to inhibition of proinflammatory cytokine IL-8, but not involved platelet surface P-selectin expression.     

The effect of sildenafil, a phosphodiesterase-5 inhibitor, on acetic acid-induced colonic inflammation in the rat

Background and Aim:  Sildenafil, a selective and potent inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase (PDE)5, has a relaxant effect on the smooth muscle cells of the arterioles supplying the human corpus cavernosum acting via nitric oxide (NO)-dependent mechanism. This study aimed to investigate the possible protective effect of sildenafil citrate on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis.
Methods:  Colitis was induced by intrarectal administration of 1 mL of 5% acetic acid to Sprague-Dawley rats (200–250 g; n  = 7–8/group). Control rats received an equal volume of saline intrarectally. In treatment groups, the rats were treated with either sildenafil citrate (5 mg/kg/day; subcutaneously) or saline for 3 days. After decapitation, distal colon was weighed and scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and oxidant production. Trunk blood was collected for the assessment of serum tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels.
Results:  In the colitis group, the colonic tissue was characterized by lesions, increased lipid peroxidation with a concomitant reduction in GSH content, increased MPO activity and oxidant production. Serum TNF-α and IL-1β levels were higher in the colitis group compared to control values. Sildenafil reversed these inflammatory parameters nearly back to control values.
Conclusions:  Sildenafil citrate administration to rats with acetic acid-induced colitis seems to be beneficial via prevention of lipid peroxidation, oxidant generation, cytokine production and neutrophil accumulation.     

参苓白术散对脾虚湿困型溃疡性结肠炎大鼠血清EGF、SOD、MDA的影响

目的:观察参苓白术散对脾虚湿困型溃疡性结肠炎(UC)大鼠表皮生长因子(EGF)、超氧化物歧化酶(SOD)、丙二醛(MDA)的影响,以期探明其治疗脾虚湿困型UC大鼠的部分作用机制.方法:参照文献复制脾虚湿困型UC模型,将大鼠随机分为正常对照组、模型对照组、参苓白术散组,每组10只,观察大鼠一般情况、结肠病理改变,检测各组大鼠血清EGF、SOD、MDA含量.结果:参苓白术散组大鼠症状、体征及结肠黏膜病理变化较模型对照组明显改善.模型对照组大鼠EGF含量与正常对照组比较,差异有统计学意义(1.67±0.17 vs 1.92±0.23,P<0.05),S O D、M DA含量与正常对照组比较的差异有非常显著性(1.11±0.13 vs 1.40±0.14,16.42±1.77 vs 13.26±0.99,P<0.01);参苓白术散组大鼠EGF含量与模型对照组比较,差异有统计学意义(1.89±0.19 vs 1.67±0.17,P<0.05),SOD、MDA水平的差异有非常显著性(1.38±0.15 vs 1.11±0.13,13.40±1.25 vs16.42±1.77,P<0.01).结论:参苓白术散能显著改善脾虚湿困型UC大鼠血清EGF、SOD、MDA的水平,可能是其发挥临床疗效的重要作用机制之一.     

硫酸锌溶液对大鼠三硝基苯硫酸实验性结肠炎治疗作用的研究

目的 动物实验表明硫酸锌具有抗炎作用，但对结肠炎的作用仍不十分清楚。现评估硫酸锌灌肠对大鼠2，4，6三硝基苯硫酸(TNB)结肠炎的抗炎作用，并探讨其机制。方法Spragur—Dawley雌性大鼠直肠内给予TNB制备成结肠炎模型，第1天开始每天给予硫酸锌溶液灌肠1次，共6d，第8天处死大鼠，与对照组比较，评价硫酸锌灌肠对TNB结肠炎黏膜病变面积、黏膜髓过氧化物酶(MPO)及超氧化物歧化酶(SOD)活性、黏膜前列腺素E2(PGE2)及白三烯B4(LTB4)水平的影响。结果 大鼠TNB结肠炎黏膜病变面积、黏膜MPO活性、黏膜PGE2和LTB4水平均明显升高，硫酸锌灌肠可以改善这些异常，但是对黏膜SOD活性没有影响。结论 硫酸锌灌肠对大鼠实验性结肠炎具有一定的抗炎及促黏膜修复作用。