机构地区:[1]江苏大学附属江滨医院普外科,江苏省镇江市212001 [2]上海交通大学附属第六人民医院普外科,上海市200233
出 处:《世界华人消化杂志》2011年第8期794-799,共6页World Chinese Journal of Digestology
摘 要:目的:评估益生菌植物乳杆菌(LP)对三硝基苯磺酸(TNBS)诱导小鼠肠道炎症损伤的治疗作用,并探讨其可能的作用机制.方法:将成年♀Balb/c小鼠随机分成3组:正常对照组(Control组),TNBS灌肠诱导小鼠结肠炎组(TNBS组)和LP干预组(TNBS+LP组).TNBS诱导肠炎模型建立后,给予TNBS+LP组小鼠灌胃LP3wk,其余两组灌胃空白对照PBS液.实验结束后对大鼠一般情况、结肠大体损伤及组织学损伤进行评估,并对各组小鼠结肠组织髓过氧化物酶(MPO)活性、LTB4含量及促炎细胞因子TNF-α和IFN-γ的表达进行测定.结果:与TNBS诱导的TNBS组相比,LP明显减轻了TNBS诱导的小鼠结肠炎症,表现为疾病活动指数下降(3.37±0.36vs0.97±0.47,P<0.05),结肠大体和组织学评分显著降低(1.11±0.61vs4.62±0.40;1.48±0.40vs5.39±1.12,均P<0.05),且LP显著降低了TNBS诱导的小鼠结肠黏膜内中性粒细胞浸润,这与MPO活性降低相一致(25.14U/g±5.22U/gvs90.3U/g±7.70U/g,P<0.05).此外,LP明显降低了TNBS诱导的小鼠结肠内具有化学趋化活性的LTB4含量(3.13ng/g±0.10ng/gvs8.43ng/g±0.49ng/g,P<0.05)和增加了促炎细胞因子TNF-α和IFN-γ的表达(205ng/g±68ng/gvs375ng/g±79ng/g;446ng/g±116ng/gvs603ng/g±109ng/g,均P<0.05).结论:口服植物乳杆菌能有效缓解TNBS诱导的小鼠结肠炎症状,其作用机制可能与其降低白细胞聚集及促炎细胞因子的表达有关.AIM: To determine the effect of administration of Lactobacillus plantarum (LP) on established colitis in mice and to explore possible mechanisms involved.METHODS: A model of colitis was induced by intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid sodium salt (TNBS) in adult Balb/c mice.The mice were then treated with LP (109 CFU) or vehicle for three weeks.After treat- ment,all mice were killed and colonic damage was evaluated both histologically and biochemi-cally,including determination of the activity of myeloperoxidase (MPO) activity,and the levels of leukotriene B4 (LTB4),tumor necrosis factor α (TNF-α) and interferon-γ (IFN-γ) in colon tissue.RESULTS: LP therapy resulted in amelioration of colitis induced with TNBS in mice when compared with control mice without undergoing LP treatment.This anti-inflammatory effect of LP was evidenced by a signif icant reduction of macroscopic and microscopic colonic damage scores (1.11 ± 0.61 vs 4.62 ± 0.40,P 〈0.05;1.48 ± 0.40 vs 5.39 ± 1.12,P 〈0.05).Moreover,a reduction of neutrophil infiltrate in LP-treated mice was confi rmed biochemically by a signifi cant reduc- tion of the activity of colonic MPO (25.14 U/g ± 5.22 U/g vs 90.3 U/g ± 7.70 U/g,P 〈0.05),a marker of neutrophil infi ltration,in comparison with non-treated colitic mice.In addition,treatment with LP resulted in a lower colonic content of LTB4 and in a signifi cant reduction of proin- flammatory factors,such as TNF-α and IFN-γ,when compared with control mice (3.13 ng/g ± 0.10 ng/g vs 8.43 ng/g ± 0.49 ng/g,P〈 0.05;205 ng/g ± 68 ng/g vs 375 ng/g ± 79 ng/g,P 〈0.05;446 ng/g ± 116 ng/g vs 603 ng/g ± 109 ng/g,P〈 0.05).CONCLUSION: Administration of LP is effective in accelerating the recovery of experimental colitis in mice possibly by reducing leukocyte accumulation and proin ammatory cytokine expression.
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