德尔布鲁氏乳杆菌亚种的抑菌作用。kappa - carrage胶诱导小鼠血栓形成及氧化损伤的调控作用。

IF 3.4 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Cardiovascular Therapeutics Pub Date : 2022-06-15 eCollection Date: 2022-01-01 DOI:10.1155/2022/4415876
Pan Wang, Fang Tan, Jianfei Mu, Hongjiang Chen, Xin Zhao, Yanan Xu
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引用次数: 1

摘要

采用卡帕-卡拉胶建立小鼠血栓形成模型,观察其对德尔布鲁氏乳杆菌亚种的抑制作用。KSFY07 (LDSB-KSFY07)对血栓形成和氧化应激反应的影响通过生化试剂盒、切片观察和定量聚合酶链反应(qPCR)实验检测小鼠粪便中微生物的表达,检测小鼠血清、肝组织相关指标和肠道微生物组成。结果表明,LDSB-KSFY07能有效降低血栓形成小鼠的黑尾程度,提高活化的部分凝血活素时间(APTT),降低血栓形成小鼠的凝血酶时间(TT)、纤维蛋白原(FIB)、凝血酶原时间(PT)。LDSB-KSFY07还能够降低血栓形成小鼠血清和肝脏组织中的丙二醛(MDA)水平,增加超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)水平。病理观察显示,LDSB-KSFY07可减轻肝组织病变和尾静脉血栓形成。进一步,实验结果表明,LDSB-KSFY07能够上调血栓形成小鼠肝组织中铜/锌- sod (Cu/Zn-SOD)、锰- sod和GSH-Px mRNA的表达。此外,LDSB-KSFY07还能下调尾静脉血管组织中NF-κB p65、细胞间细胞粘附分子-1 (ICAM-1)、血管细胞粘附分子-1 (VCAM-1)和e-选择素的mRNA表达。同时,LDSB-KSFY07可提高血栓形成小鼠心脏和尾静脉血管组织中纤溶酶原激活物抑制剂-1 (PAI-1) mRNA表达,降低组织型纤溶酶原激活物(t-PA)表达。小鼠粪便检测显示,LDSB-KSFY07还可以上调肠道中拟杆菌、乳杆菌和双歧杆菌的微生物表达,下调厚壁菌门的表达。这些结果表明,LDSB-KSFY07能够抑制小鼠血栓形成,减轻血栓小鼠肝脏氧化应激损伤,并且高浓度的LDSB-KSFY07具有与药物肝素类似的更好的反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Inhibitory Effect of <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.

Inhibitory Effect of <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.

Inhibitory Effect of <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.

Inhibitory Effect of Lactobacillus delbrueckii subsp. bulgaricus KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.

A mouse thrombosis model was established by kappa-carrageenan to observe the inhibitory effect of Lactobacillus delbrueckii subsp. bulgaricus KSFY07 (LDSB-KSFY07) on thrombosis and the oxidative stress response. Mouse serum, liver tissue-related indicators, and intestinal microbial composition were measured by examining the expression of microbes in mouse faeces using a biochemical kit, slice observations, and quantitative polymerase chain reaction (qPCR) experiments. The results showed that LDSB-KSFY07 effectively reduced the degree of black tail in thrombotic mice, increased activated partial thromboplastin time (APTT), and decreased thrombin time (TT), fibrinogen (FIB), and prothrombin time (PT) in thrombotic mice. LDSB-KSFY07 was also able to reduce malondialdehyde (MDA) levels and increase superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the serum and liver tissues of thrombotic mice. Pathological observations showed that LDSB-KSFY07 reduced liver tissue lesions and tail vein thrombosis. Further, experimental results showed that LDSB-KSFY07 was able to upregulate the mRNA expression of copper/zinc-SOD (Cu/Zn-SOD), manganese-SOD, and GSH-Px in the liver tissue of thrombotic mice. Moreover, LDSB-KSFY07 was also able to downregulate the mRNA expression of NF-κB p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in tail vein vascular tissue. Meanwhile, LDSB-KSFY07 could raise plasminogen activator inhibitor-1 (PAI-1) mRNA expression and reduce tissue plasminogen activator (t-PA) expression in heart and tail vein vascular tissues of thrombotic mice. A mouse faeces examination revealed that LDSB-KSFY07 could also upregulate Bacteroides, Lactobacterium, and Bifidobacterium microbial expression and downregulate Firmicutes expression in the gut. These results indicate that LDSB-KSFY07 was able to inhibit mouse thrombosis and reduce liver oxidative stress damage in thrombus mice and show that high concentrations of LDSB-KSFY07 provided a better response similar to that of the drug heparin.

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来源期刊
Cardiovascular Therapeutics
Cardiovascular Therapeutics 医学-心血管系统
CiteScore
5.60
自引率
0.00%
发文量
55
审稿时长
6 months
期刊介绍: Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged. Subject areas include (but are by no means limited to): Acute coronary syndrome Arrhythmias Atherosclerosis Basic cardiac electrophysiology Cardiac catheterization Cardiac remodeling Coagulation and thrombosis Diabetic cardiovascular disease Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF) Hyperlipidemia Hypertension Ischemic heart disease Vascular biology Ventricular assist devices Molecular cardio-biology Myocardial regeneration Lipoprotein metabolism Radial artery access Percutaneous coronary intervention Transcatheter aortic and mitral valve replacement.
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