神经炎症
TLR4型
缺血
药理学
炎症
医学
小胶质细胞
再灌注损伤
肠道菌群
内科学
免疫学
作者
Shuxia Zhang,Qiuyan Chen,Meiqi Jin,Jiahui Ren,Xiao Sun,Zhixiu Zhang,Yun Luo,Xiaobo Sun,Xiaobo Sun,Xiaobo Sun
出处
期刊:Phytomedicine
[Elsevier]
日期:2024-03-11
卷期号:128: 155530-155530
被引量:45
标识
DOI:10.1016/j.phymed.2024.155530
摘要
In summary, NG-R1 treatment resulted in the restoration of the structure of the blood-brain barrier (BBB) and reduction in neuroinflammation via suppressing the stimulation of astrocytes and microglia in the cerebral ischemic area. Mechanistic research demonstrated that NG-R1 treatment suppressed the toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor kappa B (TLR4/MyD88/NF-κB) signaling pathway in both the ischemic brain and colon. NG-R1 treatment enhanced microbiota dysbiosis by inhibiting the TLR4 signaling pathway to protect MCAO/R models. These findings elucidate the mechanisms by which NG-R1 improve stroke outcomes and provide some basis for Panax notoginseng saponins in clinical treatment.
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