| First Author | Li Q | Year | 2021 |
| Journal | Neuropsychiatr Dis Treat | Volume | 17 |
| Pages | 261-268 | PubMed ID | 33542629 |
| Mgi Jnum | J:351951 | Mgi Id | MGI:7703853 |
| Doi | 10.2147/NDT.S279147 | Citation | Li Q, et al. (2021) Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer's Disease. Neuropsychiatr Dis Treat 17:261-268 |
| abstractText | BACKGROUND: In recent years, schisandrin (SCH) was proved to improve Alzheimer's Disease (AD). The aim of our study is to explore the effect of SCH on neuronal pyroptosis in the disease. METHODS: A Morris water maze test was performed to evaluate the spatial learning and memory retention of AD mouse. ELISA was fulfilled to examine the concentration of Abeta, IL-1beta, and IL-18. Western blot was performed to detect the expression of apoptosis- and pyroptosis-related proteins. Besides, the neuronal apoptosis rate was examined using TUNEL assay. Immunohistochemistry was utilized to detect the activation of NLRP1 inflammasome. RESULTS: Here, AD mice have serious cognitive impairment. Meantime, Abeta was highly expressed in the brains of AD mice. SCH could effectively rescue the cognitive impairment in AD mice and impede the production of Abeta. Subsequently, we further demonstrated that SCH repressed neuronal apoptosis, pyroptosis-related proteins expression, and the activation of NLRP1 inflammasome in the hippocampus of AD mice. We also proved that Abeta induced neuronal apoptosis and pyroptosis in vitro. However, the effects of Abeta on neuronal apoptosis and pyroptosis were partly reversed by SCH treatment. CONCLUSION: Overall, our data indicated that SCH improved cognitive impairment in AD mice through inhibition of NLRP1 inflammasome-mediated neuronal pyroptosis and neuronal apoptosis. Our works provided new evidence to support SCH acting as a potential treatment method in AD. |
