amyloid-beta-peptides and triptolide

Although the exact cause of Alzheimer's disease (AD) remains elusive, mounting evidence continues to support the involvement of neuroinflammation in the development of AD. Triptolide isolated from the herb Tripterygium wilfordii Hook F has anti-inflammatory and immunosuppressive activities. In this study, we observed the effects of triptolide on dendritic spines of hippocampal neurons in model rats with AD. Thirty male SD rats were randomly divided into control group, AD model group and triptolide-treated group. The AD model group was made with bilateral microinjection of aggregated beta-amyloid protein (Aβ)1-40 into hippocampus in rats and the control group rats were injected with normal saline in the same way. The triptolide-treated group rats were administered triptolide intraperitoneally for 30 days after microinjection of aggregated Aβ1-40 into hippocampus. Dendritic morphology of hippocampal neurons in each group was analyzed using Golgi staining and ImageJ software. Our data showed that the total number of intersection points of dendrites and spine density in hippocampal neurons in the AD model group were decreased as compared with the control group. However, the total number of intersection points of dendrites and spine density in hippocampal neurons in the triptolide-treated group were increased as compared with the AD model group. Our results indicate that triptolide can alleviate the degeneration of dendritic spines in hippocampal neurons in model rats with AD.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Dendritic Spines; Disease Models, Animal; Diterpenes; Epoxy Compounds; Hippocampus; Immunosuppressive Agents; Male; Nerve Degeneration; Peptide Fragments; Phenanthrenes; Rats; Rats, Sprague-Dawley

Due to the immunoinflammatory pathology of Alzheimer's disease (AD) brain, recent studies have begun to focus attention on the role of anti-inflammatory drugs or immunomodulators in AD. Triptolide isolated from the herb Tripterygium wilfordii Hook F has anti-inflammatory and immunosuppressive activities. In this study, we observed the effects of triptolide on synaptophysin expression in AD cellular model. AD cellular model was established by action of Aβ-stimulated microglial conditioned medium (MCM) on cultured rat hippocampal neurons (HN). Immunocytochemical staining, western blot and RT-PCR were used to observe the effects of triptolide at different dosages on the synaptophysin expression of hippocampal neurons in AD cellular model at different time points during incubation of cultures. After 24 h of cultivation, the expression level of synaptophysin in MCM/HN model group was decreased as compared with normal HN group and MCM/HN control group, and the expression level of synaptophysin in MCM/HN low-dose triptolide group and MCM/HN high-dose triptolide group was increased as compared with MCM/HN model group. It is concluded that triptolide can promote the synaptophysin expression of hippocampal neurons in the AD cellular model.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents, Non-Steroidal; Base Sequence; Cells, Cultured; Culture Media, Conditioned; Disease Models, Animal; Diterpenes; Epoxy Compounds; Gene Expression; Hippocampus; Immunologic Factors; Microglia; Neurons; Neuroprotective Agents; Peptide Fragments; Phenanthrenes; Protein Multimerization; Rats; RNA, Messenger; Synaptophysin; Vesicular Transport Proteins