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发酵乳杆菌CQPC04减轻小鼠血栓形成和调节肠道菌群的效果
引用本文:易若琨,刘佳,冯霞,赵欣.发酵乳杆菌CQPC04减轻小鼠血栓形成和调节肠道菌群的效果[J].食品科学,2023,44(1):149-159.
作者姓名:易若琨  刘佳  冯霞  赵欣
作者单位:(重庆第二师范学院 重庆市功能性食品协同创新中心,重庆 400067)
基金项目:重庆市高校创新研究群体项目(CXQTP20033);重庆市教育委员会科学技术研究项目重大项目(KJZD-M202201601); 重庆市自然科学基金面上项目(CSTB2022NSCQ-MSX0848); 重庆市留学人员回国创业创新支持计划项目(2205012980094776)
摘    要:本研究通过给小鼠注射0.01 mL/(g mb·d)质量分数0.2%的角叉菜胶建立血栓形成模型,分析以0.2 mL/(g mb·d)不同浓度(1×108 CFU/mL和1×109 CFU/mL)发酵乳杆菌(Lactobacillus fermentum)CQPC04(以下简称LF-CQPC04)菌悬液干预10 d对小鼠凝血情况、氧化应激水平、炎症水平及肠道微生物组成的影响。分别采用生化试剂盒、苏木精-伊红染色切片观察、定量聚合酶链式反应分析小鼠血清和组织的相关指标,并通过高通量测序分析小鼠肠道微生物组成。结果表明,LF-CQPC04干预可以缩短血栓性小鼠的黑尾长度、凝血酶原时间、凝血酶时间,同时减少血液中纤维蛋白原质量浓度,延长血栓性小鼠的活化部分凝血活酶时间。LF-CQPC04干预还可降低血栓性小鼠血清中丙二醛、肿瘤坏死因子(tumor necrosis factor,TNF)-α、白细胞介素(interleukin,IL)-6、核因子(nuclear factor,NF)-κB和IL-1β的水平,并提高超氧化物歧化酶和过氧化氢酶(cata...

关 键 词:血栓  发酵乳杆菌  肠道菌群  氧化应激  炎症

Effect of Lactobacillus fermentum CQPC04 on Reducing Thrombosis and Regulating Intestinal Flora in Mice
YI Ruokun,LIU Jia,FENG Xia,ZHAO Xin.Effect of Lactobacillus fermentum CQPC04 on Reducing Thrombosis and Regulating Intestinal Flora in Mice[J].Food Science,2023,44(1):149-159.
Authors:YI Ruokun  LIU Jia  FENG Xia  ZHAO Xin
Affiliation:(Chongqing Collaborative Innovation Center for Functional Food, Chongqing University of Education, Chongqing 400067, China)
Abstract:In this study, the effect of 10-day intragastric administration of different concentrations (1 × 108 and 1 × 109 CFU/mL) of Lactobacillus fermentum CQPC04 (LF-CQPC04) suspension at a dose of 0.2 mL/(g mb·d) on blood coagulation, oxidative stress levels, inflammation levels and intestinal microbial composition in a mouse model of thrombosis induced by injecting 0.01 mL/(g mb·d) of 0.2% carrageenan was analyzed. Biochemical kits, hematoxylin-eosin (H&E) staining, and quantitative polymerase chain reaction (qPCR) were used to detect related indicators in serum and tissues, and high-throughput sequencing was used to observe the composition of gut microbiota. The experimental results showed that LF-CQPC04 could shorten the length of black tail, prothrombin time and thrombin time in mice with thrombosis, reduce the blood fibrinogen (FIB) concentration, and increase the activated partial thromboplastin time (APTT). LF-CQPC04 could also reduce malondialdehyde (MDA), tumor necrosis factor (TNF)-α, interleukin (IL)-6, nuclear factor (NF)-κB and IL-1β levels in serum, and increase superoxide dismutase (SOD) and catalase (CAT) activities. H&E staining showed that LF-CQPC04 could reduce tissue damage caused by tail vein thrombosis. LF-CQPC04 down-regulated the mRNA expression of the NF-κB p65, IL-6, TNF-α and IFN-γ genes in colon tissue, and up-regulated the mRNA expression of the genes encoding copper-zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD) and CAT. LF-CQPC04 could also down-regulate the mRNA expression of the genes encoding NF-κB p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in tail vein tissue. The gene sequencing results of gut microbiota showed that LF-CQPC04 could increase the relative abundance of beneficial bacteria such as norank_f_Muribaculaceae, Lactobacillus, Bacteroides, Lachnospiraceae NK4A136, unclassified_f__Lachnospiraceae. These results indicated that LF-CQPC04 could inhibit thrombosis in mice, reduce oxidative stress and intestinal inflammation in mice with thrombosis, and regulate the intestinal flora, and high concentrations of LF-CQPC04 showed more pronounced effects, close to those of the drug heparin.
Keywords:thrombosis  Lactobacillus fermentum  gut flora  oxidative stress  inflammation  
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