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1.
李新莉  吴大畅  张翠丽  辛毅 《中国药房》2012,(33):3089-3091
目的:比较盐酸林可霉素(LIH)与头孢拉定(CED)对BALB/c小鼠肠道菌群的影响。方法:将BALB/c小鼠随机分为LIH(330mg·kg-1)组和CED(165mg·kg-1)组,每组10只,分别灌服相应药物10d,停药7d,应用聚合酶链式反应-变性梯度凝胶电泳(PCR-DGGE)技术,对给药前和给药3、10d以及停药7d后2组小鼠粪便中的肠道菌群进行相似性、多样性分析及优势条带的序列分析。结果:2组给药前和停药7d后的肠道菌群结构相似,给药3、10d的肠道菌群结构相似,但2组给药前后菌群结构差异较大。实验期间2组肠道菌群均分为4个菌簇,其中LIH组给药前粪便标本中Clostridium carboxidivorans是定植菌,给药3d后卟啉单胞菌成为定植菌,Clostridium carboxidivorans消失;CED组给药前和给药3d的粪便标本中Clostridium carboxidivorans是定植菌,给药10d后卟啉单胞菌成为定植菌,Clostridium carboxidivorans消失;另2个菌簇在2组给药前后均变化不大。结论:2种药均可杀灭肠道中的定植菌Clostridium carboxidivorans,并在用药过程中产生致病菌卟啉单胞菌,导致肠道菌群失调。  相似文献   

2.
目的:研究锦灯笼提取物对抗菌药物致小鼠肠道菌群失调的预防作用。方法:48只BALB/c小鼠随机均分为正常对照(等容生理盐水)组、模型(等容生理盐水)组、丽珠肠乐(2 mg/kg)组与锦灯笼提取物高、中、低剂量(80、40、20 mg/kg)组,灌胃给药,每天1次,连续7 d。末次给药后第2天灌胃盐酸左氧氟沙星(1.3 mg/kg),每天1次,连续7 d以致小鼠肠道菌群失调。收集小鼠粪便,提取基因组DNA,采用聚合酶链反应-变性梯度凝胶电泳(PCR-DGGE)法获得肠道菌群指纹图谱,进行相似性及优势条带的序列分析。结果:灌胃抗菌药物前,小鼠肠道优势菌型为内普雷沃氏菌和乳酸杆菌,高、中、低剂量锦灯笼提取物可增加其乳酸杆菌数量;灌胃抗菌药物后,高、中、低剂量锦灯笼提取物可促进模型小鼠肠道内拟杆菌的生长,使其成为优势菌型。结论:锦灯笼提取物能增加肠道乳酸杆菌的数量,对抗菌药物致小鼠肠道菌群失调有预防作用。  相似文献   

3.
目的研究丹参提取物DS对小鼠化疗诱导性肠黏膜炎的治疗作用,并探讨其可能的作用机制。方法雄性BALB/c小鼠腹腔注射5-氟尿嘧啶(25 mg·kg~(-1))与伊利替康(25 mg·kg~(-1))4 d制备化疗诱导性肠黏膜炎模型,造模第2天开始DS灌胃给药8 d。给药期间测定小鼠体质量、3 h排便量、疾病活动指数。给药结束后收集血清及结肠黏膜上皮组织,测定炎症因子表达。结肠组织甲醛固定、石蜡包埋切片,HE染色进行病理学评分。提取粪便样本总DNA,16SrDNA测序分析粪便菌群。结果DS显著增加化疗性肠黏膜炎小鼠3 h排便量,抑制体重下降及结肠炎疾病活动指数。DS显著降低小鼠血清及黏膜蛋白中IL-6、TNFα、MPO的含量。病理评分显示,DS显著减轻模型组动物黏膜炎症及伴发的黏膜变性/萎缩。粪便菌群分析显示,DS可有效提高化疗性肠黏膜炎小鼠粪便菌群多样性,使治疗组小鼠粪便菌群构成恢复至接近正常水平。DS显著降低化疗性肠黏膜炎小鼠粪便拟杆菌属和链球菌属丰度,提高变形菌属、乳杆菌属和肠杆菌属丰度。结论 DS可有效治疗小鼠化疗诱导性肠黏膜炎,这一作用可能是通过调节肠道菌群、修复结肠黏膜及抑制炎症因子表达实现的。  相似文献   

4.
目的研究丹参破壁饮片、丹参常规饮片及丹参传统粉末对小鼠肠道菌群的影响。方法 C57BL/6小鼠50只,随机分为5组,分别为空白组、常规饮片组、低剂量破壁饮片组、高剂量破壁饮片组及传统粉末组。连续灌胃给药14 d后,选择性分离培养粪便中双歧杆菌、乳酸杆菌、肠球菌及肠杆菌,鉴定和计数;并提取回盲部粪便的总DNA,进行PCR-DGGE(PCR-梯度凝胶电泳)分析,以观察小鼠肠道菌群的变化。结果细菌培养结果显示低剂量破壁饮片组及常规饮片组双歧杆菌及乳酸杆菌数量增加、肠球菌和肠杆菌数量则减少,差异有显著性意义;高剂量破壁饮片组及传统粉末中4种菌均无显著性差异。PCRDGGE结果显示,低剂量破壁饮片组的物种丰度和多样性指标均高于其他各组。结论丹参破壁饮片、常规饮片及传统粉末对肠道菌群无不良影响,且低剂量长期服用丹参破壁饮片对肠道菌群具有调整作用。  相似文献   

5.
本实验用抗生素造成小鼠肠道菌群失调的模型,然后给小鼠灌喂厌氧-1号菌液(1亿活菌/ml)0.5ml,7d后查肠道菌群与自然恢复组比有显著差别,说明厌氧-1号活菌制剂对菌群失调小鼠肠道菌群具有调整作用.  相似文献   

6.
目的研究BLE对化疗性肠黏膜炎(CIM)小鼠肠道菌群的影响,探讨BLE改善CIM模型小鼠的作用与肠道菌群的关系。方法选取24只雄性Balb/c小鼠随机均分为正常对照组、模型组和BLE给药组,联合5-氟尿嘧啶(25 mg·kg~(-1))及伊利替康(25 mg·kg~(-1))腹腔注射4 d制备CIM小鼠模型。给药期间监测小鼠体重及疾病活动指数。给药8 d后,收集小鼠血清,ELISA法测定血清炎性因子含量。采集24只小鼠的粪便样本,提取粪便样本总DNA,采用16SrRNA高通量测序技术,检测小鼠粪便菌群。结果 BLE给药组显著降低疾病活动指数,抑制血清中IL-6、TNF-α含量。粪便菌群分析:通过Alpha多样性分析、Beta多样性分析和物种差异分析得出3组小鼠肠道菌群组成存在明显差异;与对照组相比,模型组毛螺菌属、瘤胃菌属显著降低(P<0.05),拟杆菌属、大肠杆菌属、志贺氏菌属、副杆菌属、肠球菌、梭状芽孢杆菌属和乳球菌属显著升高(P<0.05);与模型组相比较,BLE给药组拟杆菌属、大肠杆菌属、志贺氏菌属、副杆菌属、肠球菌、梭状芽孢杆菌属和乳球菌属均显著降低(P<0.05),Muribaculaceae显著升高(P<0.05);结合环境因子db-RDA、Heatmap图关联性分析得出3组小鼠血清中IL-6、TNF-α的含量与样本肠道菌群的分布呈正相关(P<0.01),且与梭状芽孢杆菌属、乳球菌属、拟杆菌属等相关性显著(P<0.05)。结论 BLE可有效改善小鼠化疗性肠黏膜炎,这一作用与调节肠道菌群密切相关。  相似文献   

7.
目的 对比破伤风疫苗在BALB/c与NIH小鼠中的免疫效果,探讨将BALB/c小鼠用于破伤风疫苗效力实验的可能。方法 将破伤风毒素系列稀释至适当的浓度范围,根据小鼠存活情况摸索合适的毒素浓度,重复实验,测定BALB/c和NIH小鼠的破伤风毒素半数致死量(median lethal dose,LD50)。分别用BALB/c和NIH小鼠的破伤风毒素2 LD50同时攻击BALB/c与NIH小鼠,考察BALB/c和NIH小鼠对破伤风毒素的敏感性。将破伤风疫苗稀释50、100、200倍,分别作为高剂量组、中剂量组、低剂量组免疫BALB/c和NIH小鼠,免疫4周后用50 LD50破伤风毒素攻毒,观察小鼠死亡情况。结果   BALB/c小鼠的破伤风毒素2 LD50为0.16 μg/ml;NIH小鼠的破伤风毒素2 LD50为0.23 μg/ml。用0.16 μg/ml的破伤风毒素分别注射BALB/c和NIH小鼠各3组,每组6只,BALB/c小鼠死亡动物数为3、3、2,NIH小鼠死亡动物数为0、0、0。用0.23 μg/ml的破伤风毒素分别注射BALB/c和NIH小鼠各3组,每组6只,BALB/c小鼠死亡动物数为6、6、6,NIH小鼠死亡动物数为3、2、3。3批破伤风疫苗免疫后的BALB/c与NIH小鼠采用相同攻毒剂量,每组14只,BALB/c小鼠攻毒后,高剂量组存活数为13、14、14,中剂量组存活数为10、10、9,低剂量组存活数为4、3、4;NIH小鼠攻毒后,高剂量组存活数为10、10、10,中剂量组存活数为6、7、6,低剂量组存活数为0、0、1。结论   BALB/c小鼠比NIH小鼠对破伤风毒素具有更高的敏感性,能更好地对破伤风疫苗产生免疫应答,在破伤风疫苗效价测定实验中是一种较为理想的小鼠品系。  相似文献   

8.
桑叶多糖调节小鼠肠道菌群失调的研究   总被引:1,自引:0,他引:1  
目的研究桑叶多糖对小鼠肠道菌群失调的调节作用。方法利用盐酸林可霉素诱导小鼠肠道菌群失调。将造模成功的小鼠随机分为桑叶多糖组、乳酶生组、模型组,另设置对照组。桑叶多糖组小鼠ig 6.0 mg/m L桑叶多糖溶液0.6 m L(剂量0.144 mg/g),乳酶生组小鼠ig 5.5 mg/m L乳酶生混悬液0.6 m L(剂量0.132 mg/g)。2次/d,连续给药7 d。模型组、对照组小鼠自行饮水。取小鼠的新鲜粪便,提取肠道菌DNA。16S段DNA序列扩增,变性梯度凝胶电泳(DGGE)法分析。比对各条带及样品,进行聚类分析,对各组小鼠肠道微生物群落结构进行主成分分析。结果 DGGE直观图分析,经过自然恢复、桑叶多糖和乳酶生的作用,小鼠肠道菌群种类有了明显的增加,但与对照组小鼠的肠道菌群比较仍然有差别,并不能完全恢复到原来的水平。聚类分析结果可以看出,与对照组最接近的是乳酶生组,其次是桑叶多糖组,最后是自然恢复组。菌群落结构的主成分分析可以直观地看出,桑叶多糖、乳酶生组小鼠肠道菌群与对照组关系最近,模型组与对照组肠道菌群及其他组肠道菌群的差异明显。结论桑叶多糖对小鼠肠道菌群失调有调节作用。  相似文献   

9.
目的研究氨苄西林钠和盐酸林可霉素对小鼠肠道菌群的影响,为科学研究提供依据。方法以氨苄西林钠和盐酸林可霉素连续灌胃小鼠5 d,分别于停药后第1、3、7、10和第15天检测小鼠直肠球菌、肠杆菌、乳酸菌及双歧杆菌数。结果各给药组小鼠均发生肠道菌群失调,氨苄西林钠组小鼠恢复过程缓慢。结论两种抗生素皆可造成小鼠肠道菌群紊乱。  相似文献   

10.
罗红霉素对兔体内稳态时氨茶碱药代动力学的影响   总被引:1,自引:0,他引:1  
目的 观察 6只新西兰白兔灌服罗红霉素前后对氨茶碱稳态血药浓度及药代动力学的影响。方法 实验分二期 :Ⅰ期为d 1~ 4单独灌服氨茶碱至稳态 ;Ⅱ期为d 5~ 10合用罗红霉素与氨茶碱 ,血药浓度采用HPLC法测定。结果 各期测得氨茶碱药代动力学参数 ,与Ⅰ期比较 ,Ⅱ期的AUC、CL/Fs、Ka、Ke、T1/ 2 (ka) 、Tmax差异有显著性 (P <0 0 5 ,P <0 0 1) ,而Cmax、V/Fc、T1/ 2 (ke) 在两期间差异均无显著性(P >0 0 5 )。结论 长期合用罗红霉素和氨茶碱 ,罗红霉素能延缓氨茶碱在兔体内稳态时的吸收和消除 ,提示合并用药时应对氨茶碱进行临床给药监测。  相似文献   

11.
To test the role of bacterial fractions released from intestinal flora during immunomodulation by antimicrobial agents, BALB/c mice were treated with the non-absorbable antibiotics polymyxin B or teicoplanin by the intragastric route. The composition of faecal microbiota and the capacity of spleen cells to proliferate in response to B-cell and T-cell mitogens were assessed at several times during the treatment. Both antibiotics lowered the count of some bacteria of the intestinal flora and induced significant modifications in spleen cell ability to proliferate in response to mitogens. Thus, the active fractions released from intestinal bacteria during antibiotic treatments may be able to induce immunomodulating effects.  相似文献   

12.
Fumonisins are a kind of mycotoxin that has harmful influence on the health of humans and animals. Although some research studies associated with fumonisins have been reported, the regulatory limits of fumonisins are imperfect, and the effects of fumonisins on fecal bacterial flora of mice have not been suggested. In this study, in order to investigate the effects of fumonisin B1 (FB1) on fecal bacterial flora, BALB/c mice were randomly divided into seven groups, which were fed intragastrically with 0 mg/kg, 0.018 mg/kg, 0.054 mg/kg, 0.162 mg/kg, 0.486 mg/kg, 1.458 mg/kg and 4.374 mg/kg of FB1 solutions, once a day for 8 weeks. Subsequently, feces were collected for analysis of microflora. The V3-V4 16S rRNA of fecal bacterial flora was sequenced using the Illumina MiSeq platform. The results revealed that fecal bacterial flora of mice treated with FB1 presented high diversity. Additionally, the composition of fecal bacterial flora of FB1 exposure groups showed marked differences from that of the control group, especially for the genus types including Alloprevotella, Prevotellaceae_NK3B31_group, Rikenellaceae_RC9_gut_group, Parabacteroides and phylum types including Cyanobacteria. In conclusion, our data indicate that FB1 alters the diversity and composition of fecal microbiota in mice. Moreover, the minimum dose of FB1 exposure also causes changes in fecal microbiota to some extent. This study is the first to focus on the dose-related effect of FB1 exposure on fecal microbiota in rodent animals and gives references to the regulatory doses of fumonisins for better protection of human and animal health.  相似文献   

13.
目的 建立稳定有效的抗生素相关性腹泻(antibiotic-associated diarrhea, AAD)小鼠模型,为抗生素相关腹泻的机制及药物的研究提供支持。方法 各抗生素按约临床剂量的8倍,每日灌胃2次,连续5d;停止抗生素后,再观察8d;观察小鼠的腹泻情况;根据单用抗生素的结果,选取致腹泻较明显的进行组合:头孢拉定(1.00g/kg)+庆大霉素(0.16g/kg),头孢呋辛(0.26g/kg) +左氧氟沙星(0.20g/kg),头孢克肟(0.10g/kg)+罗红霉素(0.08g/kg),每日灌胃给药2次,连续5d,观察小鼠腹泻情况、肠道微生物菌群和结肠组织等。结果 各抗生素单用,剂量达到约临床的8倍,小鼠腹泻率低,恢复快,不适于作为AAD模型继续研究。抗生素联用,小鼠腹泻出现时间提早、腹泻率高,其中头孢呋辛+左氧氟沙星于第3天出现明显腹泻症状,到第5天腹泻率达到100%,腹泻评分最高。停止抗生素6d后,即实验的第11天,该组小鼠全部可见腹泻症状,且无小鼠死亡。结肠组织观察发现,头孢呋辛+左氧氟沙星组小鼠结肠组织出现炎性细胞浸润;进一步发现结肠组织紧密连接蛋白表达下降。肠道菌群分析发现,该组小鼠与正常组比,肠道菌群结构发生显著变化,多样性显著降低,有益菌群显著降低。结论 头孢呋辛+左氧氟沙星灌胃小鼠,每日2次,可复制稳定的抗生素相关腹泻模型,肠道菌群紊乱、抗生素对肠黏膜的直接损坏及二者共同作用导致了腹泻。  相似文献   

14.
李欢  闫波  王金坤  袁丽萍 《天津医药》2021,49(12):1265-1270
目的 探讨粪菌移植对母婴分离诱导的肠易激综合征(IBS)大鼠内脏敏感性的影响并观察酸敏感离子通 道3(ASIC3)抑制剂APETx2对其作用及可能机制。方法 取SD孕鼠10只,待其生产后取仔鼠,采用母婴分离法构 建IBS模型,收集建模成功的大鼠粪便制成粪菌液。18只健康雄性SD大鼠按照随机数字表法分为正常对照(Con) 组、母婴分离(NMS)组、NMS+APETx2 处理组,每组 6 只。NMS 组、NMS+APETx2 组均予以含有抗生素的鸡尾酒 (ABX-water)连续灌胃5 d,构建伪无菌鼠模型,之后给予NMS大鼠粪菌液(1.6 mL/kg)灌胃;Con组给予等体积生理盐 水灌胃,每天1次,连续灌胃5 d。灌胃结束后,NMS+APETx2组给予100 μg/kg APETx2连续腹腔注射7 d,每天1次。 采用墨汁推进实验测定肠道推进率,结直肠扩张刺激后评估内脏敏感性。免疫组化染色法检测结肠组织中ASIC3、 c-kit蛋白表达。分离3组大鼠结肠cajal间质细胞(ICC),显微镜观察细胞形态学和数量变化。结果 与Con组比较, NMS组肠道推进率减慢,腹部回撤反射(AWR)评分升高,内脏敏感性增加,结肠组织ASIC3、c-kit表达上调,ICC形态 改变。与NMS组相比,NMS+APETx2组肠道推进率加快,AWR评分下降,内脏敏感性降低,结肠组织ASIC3、c-kit表 达下调,ICC形态趋于正常,数量明显减少。结论 IBS粪菌移植可以诱导内脏高敏感发生和降低肠道传输速率, APETx2可改善其内脏敏感性和肠道传输速率,其机制可能与APETx2下调ASIC3表达、抑制与ICC相关的c-kit信号 有关。  相似文献   

15.

BACKGROUND AND PURPOSE

Dersalazine sodium (DS) is a new chemical entity formed by combining, through an azo bond, a potent platelet activating factor (PAF) antagonist (UR-12715) with 5-aminosalicylic acid (5-ASA). DS has been demonstrated to have anti-inflammatory effects on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats and recently in UC patients in phase II PoC. There is Increasing evidence that Th17 cells have an important role in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to further characterize the anti-inflammatory effects of DS.

EXPERIMENTAL APPROACH

Effect of DS (10 or 30 mg·kg−1 b.i.d.) on TNBS-induced colitis in rats was studied after 2 and 7 days with special focus on inflammatory mediators. Additionally, its anti-inflammatory properties were analysed in two different models of dextran sodium sulphate (DSS)-induced colitis, BALB/c and C57BL/6 mice, the latter being dependent on IL-17.

KEY RESULTS

DS, when administered for 7 days, showed intestinal anti-inflammatory effects in TNBS-induced colitis; these effects were observed both macroscopically and through the profile of inflammatory mediators (TNF, IL-1β, IL-6 and IL-17). Although the 2 day treatment with DS did not induce intestinal anti-inflammatory effects, it was sufficient to reduce the enhanced IL-17 expression. DS showed beneficial effects on DSS-induced colitis in C57BL/6 mice and reduced colonic pro-inflammatory cytokines IL-1β, IL-6 and IL-17. In contrast, it did not exert intestinal anti-inflammatory effects on DSS-induced colitis in BALB/c mice.

CONCLUSIONS AND IMPLICATIONS

DS exerts intestinal anti-inflammatory activity in different rodent models of colitis through down-regulation of IL-17 expression.  相似文献   

16.
Background: Chronic kidney disease (CKD) is a renal disorder characterized by the accumulation of uremic toxins with limited strategies to reduce their concentrations. A large amount of data supports the pivotal role of intestinal microbiota in CKD complications and as a major source of uremic toxins production. Here, we explored whether fecal microbiota transplantation (FMT) could be attenuated in metabolic complication and uremic toxin accumulation in mice with CKD. Methods: Kidney failure was chemically induced by a diet containing 0.25% (w/w) of adenine for four weeks. Mice were randomized into three groups: control, CKD and CKD + FMT groups. After four weeks, CKD mice underwent fecal microbiota transplantation (FMT) from healthy mice or phosphate buffered saline as control. The gut microbiota structure, uremic toxins plasmatic concentrations, and metabolic profiles were explored three weeks after transplantation. Results: Associated with the increase of alpha diversity, we observed a noticeable improvement of gut microbiota disturbance, after FMT treatment. FMT further decreased p-cresyl sulfate accumulation and improved glucose tolerance. There was no change in kidney function. Conclusions: These data indicate that FMT limited the accumulation of uremic toxins issued from intestinal cresol pathway by a beneficial effect on gut microbiota diversity. Further studies are needed to investigate the FMT efficiency, the timing and feces amount for the transplantation before, to become a therapeutic option in CKD patients.  相似文献   

17.
Metabolic profiling of the fecal extracts of male mice was carried out to assess the effects of probiotics on colonic inflammation using 1H NMR spectroscopy coupled with multivariate data analysis. The control group (n = 5) was administered phosphate buffered saline for 14 days. Acute colitis was induced with dextran sulfate sodium (DSS) for 7 days following administration of phosphate buffered saline for 7 days (DSS-treated group, n = 5). LAB + DSS-treated group (n = 5) was administered lactic acid bacteria (LAB) daily for 7 days followed by treatment with DSS for 7 days to investigate protective effect of LAB against DSS-inducible colitis. Histological damage, myeloperoxidase activity, and malondialdehyde content of colon tissue were reduced, whereas colon length increased in LAB + DSS-treated mice compared to those in DSS-treated mice. DSS treatment was associated with fecal excretion of amino acids, short chain fatty acids, and nucleotides, revealing significant decreases of threonine, alanine, glutamate, glutamine, aspartate, lysine, glycine, butyrate, uracil, and hypoxanthine together with increases of monosaccharides, glucose, and trimethylamine in the feces of mice with DSS-induced colitis. Increased levels of acetate, butyrate, and glutamine and decreased levels of trimethylamine were found in the feces of LAB + DSS-treated mice compared to DSS-treated mice alone. The increased short chain fatty acids levels in the feces of mice fed with LAB indicate that the probiotics have protective effects against DSS-induced colitis via modulation of the gut microbiota. This work highlights the possibility for alternative approach of metabonomics in feces for assessing the probiotic effect in an animal model of inflammatory bowel disease.  相似文献   

18.
摘 要 目的:研究高木二糖、木三糖含量的低聚木糖对小鼠肠道菌群及免疫功能的影响。方法:利用高木二糖、木三糖含量的低聚木糖和普通低聚木糖为碳源,分别接种两种双歧杆菌和两种乳杆菌,测定其48 h活菌数,比较两种低聚木糖对双歧杆菌和乳杆菌生长的影响。以BALB/C小鼠为试验对象,在连续给予不同剂量[100、200 mg·(kg·bw)-1]的两种低聚木糖14 d后,利用选择培养基测定小鼠粪便中双歧杆菌、乳杆菌、肠球菌、肠杆菌和产气荚膜菌的菌数,同时测定粪便中短链脂肪酸乙酸、丙酸和丁酸的含量,并利用酶联免疫吸附测定法(ELISA)检测小鼠血清中免疫球蛋白IgG、IgA和IgM的含量。结果:与普通的低聚木糖相比,高木二糖、木三糖含量的低聚木糖对双歧杆菌和乳杆菌具有更强的增殖作用。连续给予低聚木糖14 d后,与普通低聚木糖组相比,高木二糖、木三糖含量的低聚木糖对小鼠肠道内双歧杆菌和乳杆菌具有更强的增殖作用,而且小鼠肠道代谢产生的乙酸、丙酸和丁酸分别提高了24.4%、50%和36.4%。与模型组相比,两种低聚木糖都增加了小鼠血清中IgG和IgM的含量,并且与普通低聚木糖高剂量组相比,高木二糖、木三糖含量低聚木糖高剂量组的IgG和IgM含量分别提高了6.9%和17.5%。结论:木二糖和木三糖相比于低聚木糖的其他组分具有更强的生物活性,为高品质低聚木糖的开发及应用提供了依据。  相似文献   

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