Effects of Dianxianqing Granules on Tau protein in a mouse model of Alzheimer' s disease via NLRP3/Caspase-1 pathway
AIM To study the effects of Dianxianqing Granules on Tau protein in a mouse model of Alzheimer's disease (AD).METHODS The mice expressing P301S mutant Tau variant were randomly divided into the model group,the MCC950 group (NLRP3 inhibitor,10 mg/kg),the Dianxianqing Granules group (12.48 g/kg),the MCC950+Dianxianqing Granules group,in contrast to the C57BL/6 mice of the control group.After 5 months of administration,the mice had their learning and memory ability tested by Y maze test and Morris water maze test;their cerebral morphological changes observed by HE staining;their cerebral expressions of Caspase-1 and GSDMD proteins detected by immunohistochemical method;their expression of cerebral Tau protein detected by immunofluorescence;and their cerebral expressions of Tau,p-Tau (ser202),p-Tau (thr205),NLRP3,Caspase-1,IL-1β and IL-18 detected by Western blot.RESULTS Compared with the control group,the model group displayed decreased rate of spontaneous alternate reaction and times of crossing platform (P<0.05,P<0.01);abnormal hippocampal morphology,decreased number of neurons,increased cerebral positive expressions of Caspase-1 and GSDMD (P<0.05);deposition of a large number of brown granules in cytoplasm,and increased protein expressions of Tau,p-Tau (ser202),p-Tau (thr205),NLRP3,Caspase-1,IL-1βand IL-18 in the hippocampus and the cortex (P<0.05,P<0.01).Compared with the model group,the group intervened with Dianxianqing Granules demonstrated both increased rate of spontaneous alternate reaction and times of crossing platform (P<0.05);complete and normal morphology of the brain,a diversity of fine neurons,reduced cerebral positive expressions of Caspase-1 and GSDMD (P<0.05);and decreased protein expressions of Tau,p-Tau (ser202),p-Tau (thr205),NLRP3,Caspase-1,IL-1β and IL-18 in the hippocampus and the cortex (P<0.05,P<0.01).CONCLUSION Dianxianqing Granules may inhibit Tau protein expression in the mouse model of AD via NLRP3/Caspase-1 pathway.
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