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作 者:Tao Jiang Ruoxi Wang Wen Yin Yuxi Zhou Dexu Kong Saihong Xu Po Gao Weifeng Yu Yingfu Jiao Daxiang Wen
出 处:《Acta Biochimica et Biophysica Sinica》2019年第12期1216-1222,共7页生物化学与生物物理学报(英文版)
基 金:This work was supported by the grants from the National Natural Science Foundation of China(Nos.81771236 and 81501190);Joint Research Project of Pudong New Area Health and Family Planning Commission(No.PW2015D-3).
摘 要:The hypothalamus-pituitary-adrenal(HPA)axis is known to mediate gut-brain interaction,and the pathological inflammatory process in the intestine can induce HPA axis involved'fight or flight response to suppress or facilitate intestinal inflammation.Hypothalamic paraventricular nucleus(PVN)neurons are responsible for controlling the HPA axis activity,but their exact role in modulating intestinal inflammation remains unclear.In this study,we used the dextran sulfate sodium(DSS)-induced mice colitis model,gene editing,and RNA interference to determine the effects of PVN neurons on intestinal inflammation.We found that at the early stage(third day)after DSS treatment,there was a mild inflammation in the colorectal area and an increased neuron activatio n in the PVN but not in the adjace nt area.At the same time,~80% of activated PVN n eurons also expressed novel estrogen GPER1 receptor.The colitis noticeably worsened in GPER1-knockout mice and local PVN GPER1-knockdown mice.These results indicated that PVN GPER1 positive neurons potentially have a protective function during the early stages of DSS-induced colitis,and this may be a mechanism by which the central nervous system attempts to suppress intestinal inflammation to achieve self-protection.
关 键 词:inflammatory BOWEL disease hypothalamus-pituitary-adrenal axis PARAVENTRICULAR nucleus GPER1 receptor gut-brain interaction
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