Protective effect of pterostilbene in a streptozotocin‐induced mouse model of Alzheimer's disease by targeting monoamine oxidase B
Qiushi Li, Xidong Li, Buxian Tian, Long Chen
Abstract
Abstract Alzheimer's disease (AD) is a neurodegenerative disease in elderly population. Pterostilbene (PTS) is a resveratrol analog with neuroprotective activity. However, the biological mechanisms of PTS in AD progression are largely uncertain. An animal model of AD was established using streptozotocin (STZ)‐treated C57BL/6J mice. Monoamine oxidase B (MAOB) expression was analyzed by bioinformatics analysis and detected by western blotting assay. The memory impairment was investigated by Morris water maze test. The levels of Tau hyperphosphorylation and death‐related proteins were detected by western blotting analysis. The levels of amyloid β (Aβ) 1–42 accumulation, oxidative stress‐related markers (ROS, MDA, SOD, and GSH), and inflammation‐relative markers (TNF‐α, IL‐1β, IL‐6, and p‐NF‐κB) were measured by ELISA. MAOB expression was increased in hippocampus of AD mice, and it was decreased by PTS. PTS attenuated STZ‐induced body weight loss and memory impairment by regulating MAOB. PTS mitigated Aβ 1–42 accumulation and Tau hyperphosphorylation by regulating MAOB in STZ‐treated mice. PTS attenuated neuronal death by decreasing cleaved caspase‐3 and Bax levels and increasing Bcl2 expression in hippocampus by regulating MAOB in STZ‐treated mice. PTS weakened STZ‐induced oxidative stress in hippocampus by decreasing ROS and MDA levels and increasing SOD and GSH levels by regulating MAOB. PTS protected against STZ‐induced neuroinflammation in hippocampus by inhibiting TNF‐α, IL‐1β, IL‐6, and p‐NF‐κB levels through regulating MAOB. In conclusion, PTS alleviates STZ‐induced memory impairment, Aβ 1–42 accumulation, Tau hyperphosphorylation, neuronal death, oxidative stress, and inflammation by decreasing MAOB in AD mice, proving anti‐AD potential of PTS.