熊去氧胆酸
G蛋白偶联胆汁酸受体
炎症
肠道菌群
小胶质细胞
冲程(发动机)
胆汁酸
药理学
缺血性中风
医学
免疫学
内科学
缺血
机械工程
工程类
作者
Feng Zhang,Yiting Deng,Huidi Wang,Jingxiang Fu,Guangyan Wu,Zhuo Duan,Xiru Zhang,Yijia Cai,Hongwei Zhou,Jia Yin,Yan He
标识
DOI:10.1016/j.bbi.2023.11.021
摘要
Ischemic stroke has been demonstrated to cause an imbalance of gut microbiota. However, the change in gut microbiota-mediated bile acids (BAs) metabolites remains unclear. Here, we observed a decrease in gut microbiota-mediated BAs, especially ursodeoxycholic acid (UDCA), in the serum of stroke patients as well as in the intestine, serum and brain of stroke mice. Restoration of UDCA could decrease the area of infarction and improve the neurological function and cognitive function in mice in association with inhibition of NLRP3-related pro-inflammatory cytokines through TGR5/PKA pathway. Furthermore, knocking out TGR5 and inhibiting PKA activity reduce the protective effect of UDCA. Taken together, our results suggest that microbiota-mediated UDCA plays an important role in alleviating inflammatory responses and might be a promising therapeutic target in ischemic stroke.
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