首页 / 资料库 / 文献详情

[Role of HMGB1-RAGE/TLRs-NF-κB signaling pathway on bone mesenchymal stem cells transplantation therapy for lipopolysaccaride-induced coagulation disorder rats].

Guanghui XiuWei XiongYunyu YinXianzhong ChenPing LiuJie SunBin Ling

2018PubMedImmunology and Microbiology被引 1

出版方页面 →

摘要

OBJECTIVE: To determine the effect of bone mesenchymal stem cells (BMSCs) in transplantation therapy for lipopolysaccharide (LPS)-induced coagulation disorder and the underlying mechanism of high mobility group protein B1-receptors for advanced glycation end products/Toll-like receptors-nuclear factor-κB (HMGB1-RAGE/TLRs-NF-κB) signaling pathway. METHODS: cells via tail vein at 2 hours after LPS injection, and the rats in other groups were injected with equal volume NS. Abdominal aorta blood was collected at 1, 3 and 7 days post operation. Coagulation indexes such as platelet count (PLT), platelet volume distribution width (PDW), mean platelet volume (MPV), plateletcrit (PCT), platelet large cell ratio (P-LCR), activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), international normalized ratio (INR), and fibrinogen (FIB) were determined. The mRNA levels and contents of HMGB1, RAGE, TLR2/4 and NF-κB were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. RESULTS: ): 1.29±0.06 vs. 7.79±0.25, NF-κB content (μg/L): 1.22±0.24 vs. 2.42±0.26, all P < 0.05], till 7 days. CONCLUSIONS: BMSCs administration could ameliorate the coagulation function in LPS-induced coagulation disorder rats and these might be associated with HMGB1-RAGE/TLRs-NF-κB signaling pathway inhibition.

引用本文(GB/T 7714)

Guanghui Xiu, Wei Xiong, Yunyu Yin, 等. [Role of HMGB1-RAGE/TLRs-NF-κB signaling pathway on bone mesenchymal stem cells transplantation therapy for lipopolysaccaride-induced coagulation disorder rats].[J]. PubMed, 2018.

引文网络

参考文献与被引分析加载中…

DOI:https://doi.org/10.3760/cma.j.issn.2095-4352.2018.09.003

本站仅收录题录与摘要供学习参考,全文版权归属出版方;如有侵权请联系我们删除。