海南砂仁挥发油对2,4-二硝基氯苯与乙酸诱发的大鼠溃疡性结肠炎的治疗作用

目的观察海南砂仁挥发油(VOA)对溃疡性结肠炎(UC)的治疗作用及其机制。方法采用2,4-二硝基氯苯(DNCB)与乙酸复合灌肠法制备UC大鼠模型。将SD大鼠分为正常对照组、UC组、UC+VOA(0.42,0.84和1.68g·kg-1)和UC+柳氮磺吡啶(SSZ)0.52g·kg-1治疗组。正常组和UC组ig生理盐水,治疗组ig相应药物,连续给药21d后处死大鼠进行结肠大体形态和组织病理学评分。用邻苯三酚自氧化法测定结肠组织中超氧化物岐化酶(SOD)活性,比色法测定谷胱甘肽过氧化物酶(GSH-Px)活性和一氧化氮合酶(NOS)含量,SABC免疫组织化学法检测结肠组织肿瘤坏死因子α(TNF-α)和核因子-κBp65(NF-κBp65)阳性细胞百分率。结果与正常组比较,UC大鼠结肠组织学评分升高;结肠出现黏膜层缺损、淋巴组织增生、腺体排列紊乱以及以淋巴细胞为主的炎症细胞浸润和血管扩张等病理变化。结肠组织SOD和GSH-Px活性明显降低,NOS显著升高,TNF-α和NF-κBp65免疫阳性细胞百分率明显增加。与UC组比较,VOA0.84和1.68g·kg-1治疗后,明显降低UC大鼠结肠形态和组织学评分,减轻结肠病理变化,使UC结肠组织SOD和GSH-Px升高,NOS降低,结肠组织TNF-α和NF-κBp65免疫阳性细胞明显减少。结论VOA可减轻UC大鼠结肠炎症反应和黏膜损伤,作用机制可能与其抑制TNF-α和NF-κBp65表达从而抑制炎症级联反应有关。     

TLR9和NF-κBp65在大鼠溃疡性结肠炎模型结肠组织中的表达

目的观察TLR9(Toll样受体9)、NF-κBp65(核因子-κBp65)在大鼠溃疡性结肠炎(UC)模型结肠组织中的表达。方法应用复合法(2,4-二硝基氯苯+乙酸)制备大鼠UC模型,观察和评估结肠黏膜的大体形态和组织学变化。以免疫组化Elivision法检测TLR9、NF-κBp65的表达。结果造模后可见大鼠肠黏膜有大量炎性细胞浸润,累及黏膜下层和固有层。与正常对照组相比,模型组结肠组织TLR9、NF-κBp65表达显著升高(P0.01)。结论 TLR9、NF-κBp65在UC发病机制中具有重要作用。     

5-氨基水杨酸治疗结肠炎的抗氧化作用及对细胞因子表达的影响

目的探讨5-氨基水杨酸(5-ASA)灌肠治疗对三硝基苯磺酸(TNBS)诱导大鼠结肠炎的抗氧化作用及对细胞因子表达的影响。方法建立TNBS结肠炎模型,给予5-ASA灌肠治疗,同时设正常对照组和模型组。于治疗后1、2周,评价结肠大体、组织学损伤及髓过氧化物酶(MPO)活性,检测超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平,逆转录-多聚酶链反应(RT-PCR)检测结肠组织白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-αmRNA表达水平。结果5-ASA灌肠治疗能明显降低结肠炎大鼠的大体、组织学评分及MPO活性(P<0.05),升高SOD活性(P<0.05),降低MDA水平(P<0.05),降低IL-1β和TNF-α表达水平(P<0.05)。结论5-ASA灌肠治疗TNBS诱导的大鼠结肠炎疗效显著,其机制与抗氧化作用及抑制IL-1β和TNF-α的表达有关。     

泻痢消片治疗实验性结肠炎的研究

目的考察泻痢消片对大鼠实验性结肠炎的保护作用。方法雄性SD大鼠随机分为6组,每组10只。除空白对照组外,其他组用2,4-二硝基氯苯和醋酸灌肠的方法制备大鼠结肠炎模型。泻痢消高、中、低剂量组分别给予泻痢消溶液0.28,0.56,1.12 g.kg-1,阳性对照组给予柳氮磺吡啶(0.27 g.kg-1),造模次日开始给药,每天1次,连续14 d。对大鼠疾病活动指数(DAI)进行评分,测定结肠组织中核因子κBp65(NF-κBp65)表达和髓过氧化物酶(MPO)水平。结果泻痢消高、中、低剂量组能够降低大鼠DAI评分,降低结肠组织中NF-κBp65表达和MPO水平(P<0.05或P<0.01)。结论泻痢消可以减轻肠道炎症,对实验性结肠炎有良好疗效。     

半夏泻心汤对溃疡性结肠炎大鼠结肠组织中TLRs/NF-κB通路相关因子表达的影响

目的:观察半夏泻心汤对溃疡性结肠炎(UC)大鼠结肠组织中核转录因子κB p65(NF-κB p65)、NF-κB抑制蛋白α(IκB-α)及Toll样受体4(TLR4)表达的影响,探讨其治疗UC的可能机制。方法:将大鼠随机分为正常组(生理盐水)、模型组(生理盐水)、柳氮磺吡啶肠溶片(SASP,阳性对照,0.3 g/kg)和半夏泻心汤低、中、高剂量组(3.9、7.8、11.7 g/kg),每组8只。除正常组外,其余各组大鼠均采用三硝基苯磺酸-乙醇法复制UC模型。成模后,ig给药,每天1次,连续3周。给药结束后,检测各组大鼠结肠组织中NF-κB p65、IκB-α、TLR4 mRNA及蛋白的表达。结果:与正常组比较,其余各组大鼠结肠组织中NF-κB p65、IκB-α、TLR4 mRNA及蛋白表达水平均显著升高(P<0.05)。与模型组比较,各给药组大鼠结肠组织中NF-κB p65、IκB-α、TLR4 mRNA及蛋白表达水平均显著降低(P<0.05);半夏泻心汤具有一定的剂量依赖性,且高剂量组大鼠结肠组织中上述水平的降低程度均高于SASP组(P<0.05)。结论:半夏泻心汤可下调UC大鼠结肠组织中NF-κB p65、IκB-α及TLR4 mRNA及蛋白的表达,这可能是其治疗UC的作用机制之一。     

Ghrelin通过核因子-κB抑制肿瘤坏死因子-α诱导的HepG2细胞PAI-1 mRNA表达

目的探讨Ghrelin对肿瘤坏死因子-α(TNF-α)诱导的HepG2细胞纤溶酶原激活物抑制剂-1(PAI-1)mRNA表达的影响及核因子-κB(NF-κB)在其中的作用.方法HepG2细胞培养,加入不同浓度TNF-α,采用逆转录-聚合酶链反应测定(RT-PCR)检测PAI-1 mRNA的水平;免疫印迹法检测胞浆胞核NF-κBp65和胞浆κB抑制蛋白(IκB)的表达.给予Ghrelin预处理1 h后,加入TNF-α检测NF-κKBp65和IκB表达的变化.结果TNF-α(0.1,1,10μg·L-1)浓度依赖地增高HepG2细胞PAI-1 mRNA的表达;Ghrelin组的PAI-1 mRNA表达减少.TNF-α组胞核NF-κBp65表达增加,胞浆IκBα的表达减少;Ghrelin组较TNF-α组胞核NF-κBp65减少,胞浆IκBα的表达增加.结论TNF-α通过NF-κB介导HepG2 PAl-1mRNA的表达;Ghrelin通过抑制NF-κB而抑制TNF-α诱导PAI-1mRNA的表达.     

黄芩汤对溃疡性结肠炎大鼠NF-κBp65调控作用研究

研究黄芩汤对溃疡性结肠炎(UC)大鼠细胞因子、NF-κB p65蛋白表达的影响,探讨其治疗效果及作用机制。运用复合法(三硝基苯磺酸+乙醇)制备细胞免疫反应性UC大鼠模型,大鼠随机分成正常对照组、模型组、柳氮磺胺吡啶(SASP)组和黄芩汤高、中、低剂量组(20、10、5 g·kg-1)。治疗5天后评估各组大鼠饮食量、体重变化及组织损伤程度,采用Griess法测定血清中NO含量,ELISA法测定IL-6、TNF-α、PGE2含量,运用免疫组化法检测NF-κB p65蛋白表达情况。结果显示,模型组大鼠饮食量及体重显著低于正常组;血清中NO、IL-6、TNF-α、PGE2水平、结肠组织NF-κB p65蛋白表达量及组织损伤程度显著高于正常组。黄芩汤高、中剂量组大鼠上述指标均较模型组显著好转。黄芩汤对溃疡性结肠炎的治疗作用可能是通过抑制NF-κB P65通路活化,进而下调促炎细胞因子NO、IL-6、TNF-α和PGE2表达实现的。     

雷公藤多苷对溃疡性结肠炎大鼠炎症因子及结肠组织丝裂原p38活化蛋白激酶和核因子-κBp65蛋白表达的影响北大核心CSCD

目的研究雷公藤多苷对溃疡性结肠炎大鼠炎性因子及结肠组织丝裂原p38活化蛋白激酶(p38MAPK)和核因子-κBp65(NF-κBp65)蛋白表达的影响。方法从32只Wistar大鼠中随机选取8只为正常组不做任何处理,24只构建溃疡性结肠炎大鼠模型,死亡2只,将剩余22只模型大鼠随机分为模型组(n=7)、实验组(n=8)和阳性对照组(n=7)。正常组和模型组均灌胃生理盐水10 m L·kg^(-1),试验组灌胃雷公藤多苷20 mg·kg-1,阳性对照组灌胃柳氮磺砒啶片0.5 mg·kg^(-1),连续灌服14 d。用酶联免疫吸附实验测定各组大鼠血清炎症因子水平,用苏木精-伊红染色法观察各组大鼠结肠组织病理变化,用蛋白质免疫印迹法检测结肠组织p38MAPK、NF-κBp65蛋白的表达。结果模型组大鼠血清IL-4水平低于正常组,实验组和阳性对照组IL-4水平高于模型组(P<0.01);模型组大鼠血清IL-6水平高于正常组、实验组和阳性对照组(P<0.01);模型组、实验组和阳性对照组大鼠血清IL-1β水平高于正常对照组,实验组和阳性对照组IL-1β水平低于模型组(P<0.01)。模型组、实验组和阳性对照组结肠组织损伤评分分别为(4.56±0.88),(1.65±0.53),(1.50±0.54)分,明显高于对照组的(0.23±0.32)分(P<0.01);与模型组比较,实验组和阳性对照组结肠组织损伤评分均降低(均P<0.01)。模型组p38MAPK和NF-κBp65蛋白相对表达量分别为1.62±2.39,1.53±3.21,明显高于正常对照组的0.74±0.11,0.63±0.09;实验组和阳性对照组p38MAPK蛋白相对表达量分别为0.93±0.16,0.78±0.19,NF-κBp65蛋白相对表达量分别为0.81±0.23,0.72±0.16,均显著低于模型组(均P<0.01)。结论雷公藤多苷可有效降低溃疡性结肠炎大鼠血清炎症因子水平,改善结肠黏膜组织形态,其分子实质可能与降低p38MAPK及NF-κBp65蛋白表达量,调控其所介导的炎症反应通路有关。     

己酮可可碱对小鼠溃疡性结肠炎NF-κB的影响

目的:观察己酮可可碱(pentoxifylline,PTX)治疗小鼠溃疡性结肠炎(ulcerative colitis,UC)的治疗作用,探讨PTX对三硝基苯磺酸(TNBS)诱导的小鼠UC NF-κB的影响.方法:用TNBS局部灌肠法建立小鼠UC模型,随机分为正常组、模型组、PTX组、柳氮磺胺吡啶(SASP)组,评价疾病活动指数(DAI),观察结肠组织学损伤,用ELISA法测定结肠组织NF-κB的水平.结果:用TNBS灌肠可使小鼠结肠炎性改变;PTX治疗可使小鼠疾病活动指数、结肠黏膜大体形态学损伤评分及组织学评分、结肠黏膜组织NF-κB的表达明显下降,与SASP相比较差异无统计学意义(P＞0.05).结论:PTX对以TNBS诱发的小鼠UC有良好的治疗作用,其作用机制可能是通过抑制小鼠结肠黏膜组织NF-κB的表达而减轻其炎症性损害.     

黄芩汤对溃疡性结肠炎大鼠的保护作用及其影响NF-κB p65蛋白和相关炎症因子表达的机制研究

目的:研究黄芩汤对DSS所致溃疡性结肠炎大鼠细胞因子、NF-κBp65蛋白表达的影响,探讨其作用效果及机制。方法:运用右旋葡聚糖硫酸钠(Sodium dextran sulfate,DSS)制备UC大鼠模型,大鼠随机分成正常对照组、模型组、柳氮磺胺吡啶组和黄芩汤高、中、低剂量组。治疗7天后,取结肠组织,评估各组大鼠结肠长度、体重变化及组织损伤程度,采用ELISA法测定结肠组织中肿瘤坏死因子-α (Tumor Necrosis Factor-α,TNF-α)、白介素-6 (Interleukin6,IL-6)、白介素-1β (Interleukin1β,IL-1β)含量,运用Western blot法检测NF-κB p65蛋白表达情况。结果:模型组大鼠体重及结肠长度均明显低于正常组大鼠(P0.01);血清中TNF-α、IL-6、IL-1β水平、结肠组织NF-κB p65蛋白表达量及组织损伤程度显著高于正常组(P0.01)。与模型组大鼠相比,柳氮磺胺吡啶组大鼠上述指标均减轻,黄芩汤高、中剂量大鼠上述指标较模型组显著改善(P0.01)。结论:黄芩汤能明显改善模型大鼠精神、体重、肠上皮损伤等,对溃疡性结肠炎的治疗作用可能是通过抑制NF-κB通路活化,进而下调促炎细胞因子TNF-α、IL-6、IL-1β表达实现的。     

Proanthocyanidins from grape seeds modulates the nuclear factor-kappa B signal transduction pathways in rats with TNBS-induced recurrent ulcerative colitis

The aim of this study was to elucidate the molecular mechanisms involved in the therapeutic effects of proanthocyanidins from grape seeds (GSPE) on recurrent ulcerative colitis (UC) in rats. GSPE in doses of 100, 200, and 400 mg/kg were intragastrically administered per day for 7 days after recurrent colitis was twice-induced by TNBS. The levels of GSH, as well as the activity of GSH-Px and SOD in colon tissues were measured by biochemical methods. The expression levels of tumor necrosis factor-α (TNF-α) and the nuclear translocation levels of nuclear factor-kappa B (NF-κB) in the colon tissues were measured by enzyme-linked immunosorbent assay methods. Western blotting analysis was used to determine the protein expression levels of inhibitory kappa B-alpha (IκBα), inhibitor kappa B kinase (IKKα/β), phosphorylated IκBα and phosphorylated IKKα/β. GSPE treatment was associated with a remarkable increased the activity of GSH-Px and SOD with GSH levels in TNBS-induced recurrent colitis rats as compared to the model group. GSPE also significantly reduced the expression levels of TNF-α, p-IKKα/β, p-IκBα and the translocation of NF-κB in the colon mucosa. GSPE exerted a protective effect on recurrent colitis in rats by modifying the inflammatory response and promoting damaged tissue repair to improve colonic oxidative stress. Moreover, GSPE inhibited the TNBS-induced inflammatory of recurrent colitis though blocking NF-κB signaling pathways.     

Effects of mimic of manganese superoxide dismutase on 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats

The mimic of manganese superoxide dismutase (MnSODm) has been synthesized and reported to have anti-inflammatory properties. However, whether MnSODm has anti-inflammatory effects on colitis and any underlying mechanisms are poorly understood. This study was to investigate therapeutic effects and mechanism of MnSODm on 2,4,6-trinitrobenzenesulfonic acid (TNBS) induced colitis model in rats. Rats were intragastrically administered MnSODm (10, 20, and 40 mg/kg) per day for 7 days after colitis was induced by TNBS. After treated with MnSODm, the colonic macroscopic and microscopic damage scores and colonic weight/length ratios were significantly decreased compared with colitis model group. Myeloperoxidase (MPO) activity, malonyldialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-8 levels in colon tissues were also significantly decreased in MnSODm treatment groups. However, superoxide dismutase (SOD) activity significantly increased and phosphorylated inhibitory kappa B-alpha (IκBα), inhibitor kappa B kinase (IKKα/β), and nuclear factor-kappa Bp65 (NF-κBp65) as well as Toll-like receptor 4 (TLR4) and myeloid differentiation actor 88 (MyD88) in the colonic mucosa were significantly inhibited by MnSODm treatment. Thus, MnSODm was protective against colitis via antioxidant activity and by inhibiting inflammatory mediators by down-regulating TLR4/MyD88/NF-κB signaling pathways. These data suggest a potential therapeutic effect of MnSODm in colitis.     

Therapeutic efficacy of carboxyamidotriazole on 2,4,6-trinitrobenzene sulfonic acid-induced colitis model is associated with the inhibition of NLRP3 inflammasome and NF-κB activation

Excess proinflammatory cytokines owing to the activation of NF-κB and NLRP3 inflammasome play the key role in inflammatory bowel disease (IBD). Previously, we reported the anti-inflammatory activity of carboxyamidotriazole (CAI) resulting from decreasing cytokines. Therefore, we investigated the therapeutic effects of CAI in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat colitis and the involvement of CAI action with NLRP3 inflammasome and NF-κB pathway. CAI was orally administered to TNBS-induced colitis rat. The severity of colitis was assessed, and NLRP3 inflammasome, NF-κB pathway and cytokines were determined. Our results showed that CAI significantly reduced weight loss and disease activity index (DAI) scores in colitis rats and alleviated the colonic macroscopic signs and pathological damage. In addition, the intestinal inflammatory markers and permeability index were markedly ameliorated by CAI treatment. The decreased levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-18 were also detected in the colon tissues of CAI-treated colitis rats. Moreover, the activation of NLRP3 inflammasome in inflamed colon was significantly suppressed by showing an obvious reduction in the NLRP3 and activated caspase-1 levels. Furthermore, CAI reduced NF-κB p65 expression and IκBα phosphorylation and degradation in colitis rats. Therefore, CAI attenuates TNBS-induced colitis, which may be attributed to its inhibition of NLRP3 inflammasome and NF-κB activation, and down-regulation of proinflammatory cytokines. These results provide further understanding of the intestinal anti-inflammatory effect of CAI and highlight it as a potential drug for the treatment of IBD.     

Ameliorative effects of 3,4-oxo-isopropylidene-shikimic acid on experimental colitis and their mechanisms in rats

The aim of the present study was to investigate the therapeutic effect and mechanism of 3,4-oxo-isopropylidene-shikimic acid (ISA) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. (50, 100, 200 mg/kg) was administered for 14 days, 1 day after the induction of colitis by TNBS. The colonic injury and inflammation were assessed by macroscopic damage scores and myeloperoxidase (MPO) activity. Malondialdehyde (MDA) and nitric oxide (NO) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in plasma were measured with biochemical methods. Prostaglandin E₂ (PGE₂) level in colon was determined by radioimmunoassay. Expressions of inducible nitric oxide synthase (iNOS), cyclo-oxygenase-2 (COX-2), inhibitor kappa B-alpha (IκBα) and nuclear factor kappa B (NF-κB) p65 proteins in the colonic tissue were detected with immunohistochemistry. Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with TNBS, which was manifested as the significant increase in colon mucosal damage index, MPO activity, levels of MDA, NO and PGE₂, as well as the expressions of iNOS, COX-2 and NF-κB p65 proteins in the colonic mucosa, and the significant decrease in expressions of IκBα proteins in the colonic mucosa. However, these parameters were found to be significantly ameliorated in rats treated with ISA at given doses, especially at 100 mg/kg and 200 mg/kg. Administration of ISA may have significant therapeutic effects on experimental colitis in rats, probably due to its mechanism of antioxidation, its inhibition of arachidonic acid metabolism and its modulation of the IκBα/NF-κB p65 expression.     

阿魏酸钠对结肠炎大鼠结肠组织一氧化氮合酶和环氧合酶的影响

目的　研究阿魏酸钠 (SF)对大鼠结肠炎的抗炎保护作用及其机制。方法　建立大鼠乙酸性结肠炎模型。SF与5 氨基水杨酸灌肠给药 1wk后评价大鼠结肠黏膜损伤指数(CMDI) ,采用试剂盒及免疫组化方法检测结肠组织NO、MPO、PGE2 含量及结构型一氧化氮合酶 (cNOS) ,诱生型一氧化氮合酶 (iNOS) ,环氧合酶 1(COX 1) ,环氧合酶 2 (COX 2 )和核因子 κBp6 5 (NF κBp6 5 )的表达水平。 结果　SF(2 0 0、4 0 0、80 0mg·kg-1)灌肠用药均降低模型组大鼠升高的CMDI及结肠组织NO、MPO、PGE2 含量 ,下调iNOS、COX 2、NF κBp6 5的过度表达 ,亦抑制cNOS的正常表达水平 ,对COX 1表达影响不明显。SF用药呈现一定量效关系。结论　SF为一氧化氮合酶及部分选择性COX 2抑制剂 ,对大鼠结肠炎具有一定抗炎保护作用。     

薯蓣皂苷对大鼠胶原性关节炎治疗作用的实验研究

目的评价薯蓣皂苷对大鼠胶原性关节炎(collegeninduced arthritis,CIA)的治疗作用并探讨其可能的作用机制。方法于大鼠左后足底皮内注射胶原乳剂制备CIA模型造模两周后灌胃给药14 d,每4天测量1次右后足跖容积。处死后取右后足作病理切片。Western blot法测定踝关节滑膜组织中NF-κBp65亚基和环氧化酶-2蛋白表达。用放射免疫法检测了足爪TNF-α及PGE2含量。结果薯蓣皂苷可抑制CIA大鼠的足趾肿胀,与模型相比差异有显著性;降低足爪TNF-α及PGE2含量;明显降低NF-κBp65亚基和COX-2的水平。结论薯蓣皂苷对CIA大鼠具有较强的抗炎作用,机制可能与抑制NF-κBp65亚基和COX-2的表达有关。     

孕烷X受体/NF-κB信号通路在美沙拉嗪改善大鼠溃疡性结肠炎中的作用

目的研究孕烷X受体/NF-κB(PXR/NF-κB)信号通路在美沙拉嗪(Mes)干预溃疡性结肠炎(UC)大鼠中的作用。方法SPF级雄性SD大鼠一次性结肠灌注2,4,6-三硝基苯磺酸(TNBS)每只0.8 mL,连续4 d。每天观察各组大鼠体质量,粪便性状,计算病变活动指数(DAI),DAI为正常组的2倍以上,则为造模成功。模型大鼠按照分组每天分别ig给予Mes 300 mg·kg^-1(模型+Mes组)、利福平(Rif)50 mg·kg^-1+Mes组(模型+Mes+Rif组)和酮康唑(Ket)35 mg·kg^-1+Mes组(模型+Mes+Ket组),均先给Rif和Ket、给药4 d后给予Mes,连续7 d。HE染色观察结肠病理改变;ELISA法测定血浆肿瘤坏死因子α(TNF-α)、γ干扰素(IFN-γ)、白细胞介素4(IL-4)和IL-13含量;比色法检测结肠髓过氧化物酶(MPO)活性;实时PCR和Western印迹法检测结肠PXR,NF-κB,NF-κB p65和κB抑制因子α(IκB-α)蛋白和mRNA水平。结果模型组大鼠体质量明显下降,并伴有稀便和血便的症状。与UC模型组相比,模型+Mes组大鼠体质量明显升高(P<0.05),HE染色见结肠组织病变程度减轻;血浆TNF-α与IFN-γ含量、结肠组织中MPO活性、NF-κB mRNA及p-P65蛋白水平显著降低(P<0.05),而血浆IL-4和IL-13含量及结肠组织Pxr,NF-κB p65和IκB-αmRNA水平均显著升高(P<0.05)。与模型+Mes组相比,模型+Mes+Rif组结肠组织Pxr和NF-κB通路相关靶基因表达水平差异无统计学意义,而模型+Mes+Ket组结肠中Pxr和IκB-αmRNA水平显著下降(P<0.05)。结论Mes对UC的治疗效果很可能与激活PXR/NF-κB信号通路有关。     

安肠汤对TNBS致溃疡性结肠炎模型大鼠TLR4/NF-κB信号通路及粪钙卫蛋白表达的影响

目的:研究安肠汤对2,4,6-三硝基苯磺酸(TNBS)致溃疡性结肠炎(UC)模型大鼠Toll样受体4(TLR4)/核因子κB(NF-κB)信号通路及粪钙卫蛋白(FC)表达的影响.方法:将SD大鼠随机分为空白组、模型组、阳性对照组[双歧杆菌活菌胶囊,5 mL(含双歧杆菌活菌0.35 g)]和安肠汤低、中、高剂量组(1、5...