Catalpol rescues cognitive deficits by attenuating amyloid beta plaques and neuroinflammation

This study sought to investigate the anti-amyloid beta (A beta) and anti-neuroinflammatory effects of catalpol in an Alzheimer's disease (AD) mouse model. Methods: The effects of catalpol on A beta formation were investigated by thioflavin T assay. The effect of catalpol on generating inflammatory cytokines from microglial cells and the cytotoxicity of microglial cells on HT22 hippocampal cells were assessed by real-time quantitative PCR, ELISA, redox reactions, and cell viability. APP(swe)/PS1(Delta E9) mice were treated with catalpol, and their cognitive ability was investigated using the water maze and novel object recognition tests. Immunohistochemistry and immunofluorescence were used to probe for protein markers of microglia and astrocyte, A beta deposits, and NF-.B pathway activity. A beta peptides, neuroinflammation, and nitric oxide production were examined using ELISA and redox reactions. Results: Catalpol potently inhibited A beta fibril and oligomer formation. In microglial cells stimulated by A beta, catalpol alleviated the expression of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and inducible nitric oxide synthase (iNOS) but promoted the expression of the anti-inflammatory cytokine IL-10. Catalpol alleviated the cytotoxic effects of A beta-exposed microglia on HT22 cells. Treatment with catalpol in APP(swe)/PS1(Delta E9) mice downregulated neuroinflammation production, decreased A beta deposits in the brains and alleviated cognitive impairment. Catalpol treatment decreased the number of IBA-positive microglia and GFAPpositive astrocytes and their activities of the NF-kappa B pathway in the hippocampus of APP(swe)/PS1(Delta E9) mice. Conclusion: The administration of catalpol protected neurons by preventing neuroinflammation and A beta deposits in an AD mouse model. Therefore, catalpol may be a promising strategy for treating AD.

Automated summary

The study aimed to investigate the effects of catalpol on anti-amyloid beta (Aβ) and anti-neuroinflammatory effects in an Alzheimer's disease (AD) mouse model. Catalpol inhibited Aβ formation, reduced proinflammatory cytokines and cytotoxicity, downregulated neuroinflammation production, decreased Aβ deposits, and alleviated cognitive impairment. The administration of catalpol may be a promising strategy for treating AD.