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• W4280532236 abstract "<b><i>Introduction:</i></b> Isoflurane-associated perioperative neurocognitive disorders (PNDs) is a common complication that occurs commonly in elderly patients characterized by deterioration of hippocampus-dependent cognitive function. Mounting evidence has shown that hippocampal impairment and inflammatory processes are implicated in the pathogenesis of PNDs. Catalpol has been suggested to play a role in the modulation of neuroprotection and neurotransmission. Therefore, we surmised that catalpol may play a similar role during isoflurane-induced PNDs. <b><i>Methods:</i></b> In our current study, aged mice were exposed to isoflurane to develop a mouse model of PNDs and preconditioned with catalpol for 2 weeks before modeling. Three weeks after isoflurane exposure, behavioral, histological, biochemical, electrophysiological, and immunofluorescent assays were performed. <b><i>Results:</i></b> Our results showed that catalpol preadministration significantly alleviated cognitive impairment in the Morris water maze, novel object recognition, and Y-maze behavioral tests. Neuropathological analyses showed that catalpol preadministration reduced the loss of neurons and synapses; in line with this, it is revealed that hippocampal synaptic plasticity was restored. Mechanistically, catalpol preadministration suppressed the activation of microglia and decreased the expression of NLRP3 inflammasome. <b><i>Conclusion:</i></b> Our results indicate that catalpol preadministration could effectively alleviate cognitive impairment and neuropathological damage in isoflurane-exposed aged mice with its neuroprotective effects via modulation of the NLRP3 inflammatory pathway. Furthermore, the NLRP3 inflammatory pathway was revealed to be involved in these effects." @default.
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• W4280532236 date "2022-01-01" @default.
• W4280532236 modified "2023-09-29" @default.
• W4280532236 title "Catalpol Alleviates Isoflurane-Induced Hippocampal Learning and Memory Dysfunction and Neuropathological Changes in Aged Mice" @default.
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• W4280532236 doi "https://doi.org/10.1159/000524236" @default.
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