未经授权:红参(RG)可缓解精神疾病。发酵红参(fRG)缓解应激诱导的肠道炎症。肠道菌群失调会导致肠道炎症的精神疾病。了解RG和fRG对焦虑/抑郁(AD)的肠道菌群介导的作用机制,我们调查了RG的影响,fRG,人参皂苷Rd,和20(S)-β-D-吡喃葡萄糖基原人参二醇(CK)对小鼠肠道菌群失调诱导的AD和结肠炎的影响。
UNASSIGNED:通过暴露于固定应激(IS)或移植溃疡性结肠炎和抑郁症(UCDF)患者的粪便来制备患有AD和结肠炎的小鼠。在高架迷宫中测量了类似AD的行为,亮/暗过渡,强迫游泳,和尾部悬挂试验。
未经证实:口服灌胃UCDF可增加AD样行为并诱导神经炎症,胃肠道炎症,和小鼠肠道菌群波动。口服fRG或RG治疗减少UCDF诱导的AD样行为,海马和下丘脑IL-6表达,和血液皮质酮水平,而UCDF抑制的海马BDNF+NeuN+细胞群和多巴胺和下丘脑5-羟色胺水平增加。此外,他们的治疗抑制了UCDF诱导的结肠炎症,并部分恢复了UCDF诱导的肠道微生物群波动。口服fRG,RG,Rd,或CK也减少了IS诱导的AD样行为,血IL-6和皮质酮,结肠IL-6和TNF-α水平,和肠道生态失调,而IS抑制的下丘脑多巴胺和5-羟色胺水平升高。
未经批准:口服灌胃UCDF导致AD,神经炎症,和小鼠的胃肠道炎症。fRG通过调节微生物群-肠-脑轴减轻了UCDF暴露小鼠的AD和结肠炎,通过调节下丘脑-垂体-肾上腺轴减轻了IS暴露小鼠的AD和结肠炎。
UNASSIGNED: Red ginseng (RG) alleviates psychiatric disorders. Fermented red ginseng (fRG) alleviates stress-induced gut inflammation. Gut dysbiosis causes psychiatric disorders with gut inflammation. To understand the gut microbiota-mediated action mechanism of RG and fRG against anxiety/depression (AD), we investigated the effects of RG, fRG, ginsenoside Rd, and 20(S)-β-D-glucopyranosyl protopanaxadiol (CK) on gut microbiota dysbiosis-induced AD and colitis in mice.
UNASSIGNED: Mice with AD and colitis were prepared by exposing to immobilization stress (IS) or transplanting the feces of patients with ulcerative colitis and depression (UCDF). AD-like behaviors were measured in the elevated plus maze, light/dark transition, forced swimming, and tail suspension tests.
UNASSIGNED: Oral gavage of UCDF increased AD-like behaviors and induced neuroinflammation, gastrointestinal inflammation, and gut microbiota fluctuation in mice. Oral administration of fRG or RG treatment reduced UCDF-induced AD-like behaviors, hippocampal and hypothalamic IL-6 expression, and blood corticosterone level, whereas UCDF-suppressed hippocampal BDNF+NeuN+ cell population and dopamine and hypothalamic serotonin levels increased. Furthermore, their treatments suppressed UCDF-induced colonic inflammation and partially restored UCDF-induced gut microbiota fluctuation. Oral administration of fRG, RG, Rd, or CK also decreased IS-induced AD-like behaviors, blood IL-6 and corticosterone and colonic IL-6 and TNF-α levels, and gut dysbiosis, while IS-suppressed hypothalamic dopamine and serotonin levels increased.
UNASSIGNED: Oral gavage of UCDF caused AD, neuroinflammation, and gastrointestinal inflammation in mice. fRG mitigated AD and colitis in UCDF-exposed mice by the regulation of the microbiota-gut-brain axis and IS-exposed mice by the regulation of the hypothalamic-pituitary-adrenal axis.