粪便细菌疗法
粪便
移植
砷
疾病
医学
阿尔茨海默病
免疫学
生物
内科学
微生物学
抗生素
化学
艰难梭菌
有机化学
作者
Shuyuan Li,Jia Li,Kun Chen,Jing Wang,Longmei Wang,Chao Feng,Kunbo Wang,Yifan Xu,Yi Gao,Xiaoyan Yan,Qian Zhao,Ben Li,Yulan Qiu
摘要
ABSTRACT Arsenic exposure and intestinal microbiota disorders may be related with Alzheimer's disease ( AD ), but the mechanism has not been elucidated. This study conducted chronic arsenic exposure from rat's maternal body to adult offspring to investigate the mechanisms of the characteristic effects of chronic arsenic exposure on AD, and further explored the intervention effect of fecal microbiota transplantation (FMT) on arsenic‐mediated neurotoxicity. Transmission electron microscopy, HE staining, and related indicators were measured in the control group, the exposed group, and the FMT intervention group. Western blot was used to determine microtubule‐associated proteins Tau and p‐Tau 396 , intestinal–brain barrier–related proteins Claudin‐1 and Occludin, ELISA was used to detect the content of Aβ 1–42 , and 16S rRNA sequencing was used to detect the intestinal flora of feces. Results showed that chronic arsenic exposure could lead to neurobehavioral defects in rats, increase the expression levels of Tau, p‐Tau 396 , and Aβ 1–42 in hippocampus ( p < 0.05), increase the abundance of Clostridium _ UCG‐014, decrease the abundance of Roseburia , and decrease the expression levels of Claudin‐1 and Occludin in colon and hippocampus ( p < 0.05). After FMT intervention, the expression levels of Tau and p‐Tau 396 were decreased ( p < 0.05), and the abundance of Roseburia was increased. In summary, chronic arsenic exposure caused intestinal flora disorder by changing the abundance of inflammation‐related flora, thereby destroying the gut–brain barrier and causing AD characteristic effects in rats. Although the bacterial specific genus was improved and the expression of AD ‐related proteins was reduced after transplantation, it could not alleviate the neurobehavioral defects and neurotoxicity caused by arsenic exposure.
科研通智能强力驱动
Strongly Powered by AbleSci AI