Total Alkaloids of Tripterygium wilfordii Improve Alzheimer's Disease in Mice Through Antioxidation, Anti-Neuronal Apoptosis and Anti-Neuroinflammation

Abstract

Objectives: To explore the effect of total alkaloids of Tripterygium wilfordii (TAPC) on Alzheimer's Disease (AD) in mice through antioxidation, anti-neuronal apoptosis and anti-neuroinflammation. Materials and Methods: The experimental mice were divided into control (group A), model (group B) and total alkaloid treatment (group C) group. AD model was induced by D-galactose/ AICI3. The group A was normal and healthy mice, the group B and A were given 160 mg/kg normal saline, and the AD mice in the group C were given 160 mg/kg total alkaloids. The behavior of mice in each group was compared and the cell morphology was detected by HE staining. The TNF-α, IL-1β, NF-κB and Cox-2 were detected by ELISA, and the expression levels of GSH-PX, CAT and SOD were detected by IHC. The apoptosis-related proteins and Caspase-3 was detected by Western blot. Results: The escape latency time of the group B was increased than group A, the crossing times of the target area and the stay time in the target area decreased, and the escape latency time decreased in the group C. The number of hippocampal nerve cells in the group B was decreased than group A, the arrangement was irregular, the tissue was loose, and a small number of cell bodies shrunk. Nuclear pyknosis and deep staining. The hippocampal neurons in the group C were arranged in an orderly and orderly manner, and the cells were no longer pyknotic, but the local tissue was still loose and tended to improve as a whole. The TNF-α, IL-1β, NF-κB and cox-2 in the group B were increased than group A, these in the group C were decreased than group B, while the e GSH-PX, CAT, SOD and MDA in the group B were reduced than group A, these in the group B were raised than group A. The Bax and Caspase-3 increased and the Bcl-2 decreased in the group B than group A, while these increased in the group C. Conclusion: The total alkaloids of TAPC have the potential to improve AD through the mechanisms of antioxidation, anti-neuronal apoptosis and anti-neuroinflammation.