Zhang Kun, Qin Xian, Qiu Juhui, Sun Tong, Qu Kai, Din Ahmad Ud, Yan Wenhua, Li Tianhan, Chen Yidan, Gu Wei, Rao Xiancai, Wang Guixue
Key Laboratory for Biorheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, College of Bioengineering, Chongqing University, Chongqing 400044, China.
College of Information and Management Sciences, Henan Agricultural University, Zhengzhou, Henan 450046, China.
Genes Dis. 2021 Oct 16;10(1):239-253. doi: 10.1016/j.gendis.2021.09.007. eCollection 2023 Jan.
It is increasingly aware that gut microbiota is closely associated with atherosclerosis. However, which and how specific gut bacteria regulate the progression of atherosclerosis is still poorly understood. In this study, modified linear discriminant analysis was performed in comparing the gut microbiota structures of atherosclerotic and non-atherosclerotic mice, and () was found to be associated with atherosclerosis. treated mice showed significantly aggravated atherosclerosis. The proatherogenic effect of was attributed to its ability to increase intestinal permeability and subsequent raise in the transit of lipopolysaccharide (LPS) from the intestine to the bloodstream. Excessive LPS in the blood can elicit local and systemic inflammation and activate Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling of endothelial cells. TAK-242, a specific inhibitor of TLR4, can ameliorate the development of -induced atherosclerosis by blocking the LPS-induced activation of TLR4/NF-κB signaling.
人们越来越意识到肠道微生物群与动脉粥样硬化密切相关。然而，具体哪些肠道细菌以及如何调节动脉粥样硬化的进展仍知之甚少。在本研究中，通过改良线性判别分析比较动脉粥样硬化小鼠和非动脉粥样硬化小鼠的肠道微生物群结构，发现（此处原文缺失相关内容）与动脉粥样硬化有关。用（此处原文缺失相关内容）处理的小鼠动脉粥样硬化明显加重。（此处原文缺失相关内容）的促动脉粥样硬化作用归因于其增加肠道通透性以及随后脂多糖（LPS）从肠道向血液转运增加的能力。血液中过量的LPS可引发局部和全身炎症，并激活内皮细胞的Toll样受体4（TLR4）/核因子-κB（NF-κB）信号通路。TAK-242是TLR4的特异性抑制剂，可通过阻断LPS诱导的TLR4/NF-κB信号通路激活来改善（此处原文缺失相关内容）诱导的动脉粥样硬化发展。
