黑木耳黑色素对缺铁性贫血诱导溃疡性结肠炎小鼠的保护作用  

Protective Effect of Auricularia auricula Melanin on Iron Deficiency Anemia Induced Ulcerative Colitis in Mice

作　　者：王雨亭 王淼[1] 李元敬 施树良[3] 雷虹[1] 冯磊[4] WANG Yuting;WANG Miao;LI Yuanjing;SHI Shuliang;LEI Hong;FENG Lei(Engineering Research Center of Agricultural Microbiology Technology,Ministry of Education,Heilongjiang Provincial Key Laboratory of Ecological Restoration and Resource Utilization for Cold Region,Key Laboratory of Molecular Biology,College of Heilongjiang Province,School of Life Sciences,Heilongjiang University,Harbin 150080,China;School of Materials and New Energy,South China Normal University,Shanwei 516600,China;School of Life Science and Technology,Harbin Institute of Technology,Harbin 150001,China;Teaching Research Office,Heilongjiang Academy of Forestry,Harbin 150081,China)

机构地区：[1]黑龙江大学生命科学学院,农业微生物技术教育部工程研究中心,黑龙江省寒地生态修复与资源利用重点实验室,黑龙江省普通高校分子生物学重点实验室,黑龙江哈尔滨150080 [2]华南师范大学材料与新能源学院,广东汕尾516600 [3]哈尔滨工业大学生命科学与技术学院,黑龙江哈尔滨150001 [4]黑龙江省林业科学院科研处,黑龙江哈尔滨150081

出　　处：《食品科学》2023年第17期110-117,共8页Food Science

基　　金：黑龙江省自然科学基金资助项目(C2015023);黑龙江省森林工业总局科技计划项目(sgzjY2015016);黑龙江大学横向课题(17016);“三区”科技人才项目;华南师范大学学生课外科研一般课题(22XZGB01)。

摘　　要：目的:探究黑木耳黑色素对缺铁性贫血(iron deficiency anemia,IDA)诱导溃疡性结肠炎(ulcerative colitis,UC)小鼠的保护作用机制。方法:将45只昆明种雄性小鼠随机分成空白对照组、模型组、黑木耳黑色素组。除空白对照组外,其他两组采用低铁饮食建立IDA诱导UC小鼠模型。造模2周后,对黑木耳黑色素组连续灌胃给药3周,模型组继续低铁饮食,分析黑木耳黑色素对UC小鼠贫血指标、结肠炎症特征、氧化应激程度、炎症因子表达水平以及炎症信号通路的影响。结果:与模型组相比,黑木耳黑色素组小鼠贫血症状改善,体质量恢复至正常水平,结肠组织病理学评分显著降低(P<0.0001)。此外,与模型组相比,黑木耳黑色素组小鼠结肠总抗氧化能力(total antioxidant capacity,TAC)及超氧化物歧化酶(superoxide dismutase,SOD)活力显著增强(P<0.0001),丙二醛(malondialdehyde,MDA)、羟自由基(·OH)、超氧阴离子自由基(O_(2)^(-)·)水平显著下降(P<0.0001、P<0.01、P<0.001),表明黑木耳黑色素有助于增强小鼠抗氧化能力,减轻氧化损伤。进一步的机制研究表明,黑木耳黑色素的干预可显著调控Toll样受体4(Toll-like receptors 4,TLR4)/核转录因子-κB(nuclear factor-kappa B,NF-κB)信号通路的表达,使促炎因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的基因表达量显著降低(P<0.01),抗炎细胞因子白细胞介素10(interleukin-10,IL-10)的基因表达量显著增加(P<0.05)。结论:黑木耳黑色素可能通过调节氧化应激以及调控TLR4/NF-κB信号通路,从而减少肠黏膜溃疡、结肠组织氧化应激损伤和炎症细胞浸润,减轻小鼠IDA诱导的UC。Objective:To explore the protective mechanism of Auricularia auricula melanin(AAM)on iron deficiency anemia(IDA)induced ulcerative colitis(UC)in mice.Methods:Forty-five Kunming male mice were randomly divided into blank control group,model group,and AAM group(n=15 each).The mice from all groups except the blank control one were provided with a low-iron diet to establish an IDA-induced UC model.After two weeks,AAM was administered by gavage to the mice from the AAM group for three weeks,whereas those from the model group continued receiving the low-iron diet.The effects of AAM on anemia indexes,colonic inflammation characteristics,oxidative stress,inflammatory factor expression levels and inflammatory signaling pathways in UC mice were evaluated.Results:Compared with the model group,the symptoms of anemia in the AAM group were alleviated.The body mass returned to the normal level,and the colonic pathological score was significantly reduced(P<0.0001).In addition,the total antioxidant capacity(TAC)and superoxide dismutase(SOD)activity in the colon of mice from the AAM group were significantly enhanced compared with the model group(P<0.0001),and the levels of malondialdehyde(MDA),hydroxyl radical(·OH),and superoxide anion radical(O_(2)^(-)·)were significantly decreased(P<0.0001,P<0.01,P<0.001),indicating that AAM could enhance antioxidant capacity and attenuate oxidative damage in mice.Further mechanistic studies showed that intervention with AAM significantly regulated protein expression associated with Toll-like receptors-4/nuclear factor-kappa B(TLR4/NF-κB)signaling pathway,significantly down-regulated the gene expression of the pro-inflammatory cytokine tumor necrosis factor(TNF-α)(P<0.01),and significantly increased the gene expression level of the anti-inflammatory cytokine interleukin-10(IL-10)(P<0.05).Conclusion:Auricularia auricula melanin may regulate oxidative stress and inhibit the TLR4/NF-κB signaling pathway,thereby reducing intestinal mucosal ulcer,oxidative stress injury and inflammatory cell inf

关 键 词：黑木耳黑色素 缺铁性贫血 溃疡性结肠炎 抗氧化 Toll样受体4/核转录因子-κB 炎症因子 

分 类 号：TS201.4[轻工技术与工程—食品科学]