The impact of the gut microbiota on Huntington's disease mice

摘要

Lf have neuroprotective effects in vivo and explore their central and peripheral mechanisms, so as to provide experimental basis for finding new prevention target for PD. Immunohistochemistry, Immunofluorescence, Western Blot, HPLC, Prussian blue staining, ELISA, behavior observation, ultravio- let spectroscopy and blood routine examination were used to detect substantia nigra (SN) Lf receptor expression; tyrosine hydroxylase immunoreactivity changes in SN; dopamine and its metabolites content changes in striatum; iron staining positive neurons in SN; the change of the mice body movement coordination; content changes of monoamine oxidase-B in brain and peripheral blood; the expression changes of DMT1 and FPN1 in SN, and the levels of Bcl-2, Bax, Caspase-3, Cu/Zn-SOD, CD86; the changes of iron stain- ing positive neurons in liver and spleen; serum iron, serum ferritin, total iron binding force and the changes of RBC and hemoglobin related indicators. Results indicate that Lf has a neuroprotective effect on MPTP-induced PD model mice, and its mechanism may be related to the reduction of brain iron, anti-oxidative stress, anti- apoptosis and anti-microglia-mediated inflammatory response. Lf does not affect indicators of blood routine test. As a consequence, our research first put forward a hypothesis that spleen weight loss and lower spleen iron levels might be the original source of iron overload in SN. Apo-Lf does not chelate peripheral iron, holo-Lf does not release iron to cause peripheral iron deposition. There- fore, Lf is a safe and reliable neuroprotective agent that can reduce brain iron without affecting peripheral iron.