Study on the Mechanism of Resveratrol Regulating MIP-1α to Stabilize the Blood–Brain Barrier in Alzheimer’s Disease Mice Through β-Amyloid Peptide

Background In Alzheimer’s disease (AD), β-amyloid protein and the blood–brain barrier (BBB) are important factors in its pathogenesis. Research has found that resveratrol has a certain therapeutic effect on AD. It inhibits the expression of macrophage inflammatory protein-1α (MIP-1α), thereby reducing the number of white blood cells crossing the BBB and protecting the integrity. Purpose This article will explore the role of resveratrol in AD. Materials and Methods The amyloid precursor protein (APP)/presenilin 1B (PS1) dementia mouse model was successfully constructed. Morris water maze test, total superoxide dismutase (SOD) activity detection, catalase (CAT) activity detection, glutathione reductase activity detection, lipid oxidation detection, Western blot detection of Aβ and CCR5 protein expression, and polymerase chain reaction (PCR) detection of MIP-1α and CCR5. Results The APP/PS1 mouse model successfully mimicked the pathological characteristics of AD patients in terms of amyloid plaque formation and cognitive function decline based on the established APP/PS1 mouse model. After adding various doses of resveratrol and culturing for a period of time, it was detected that resveratrol affected the expression of β-amyloid protein (Aβ) in the APP/PS1 mouse model and reduced Aβ protein deposition, thereby regulating MIP-1α expression and stabilizing blood circulation. Brain barrier, further studies have found that Aβ expression is proportional to the increase in MIP-1α. Still, due to the decrease in the expression of BBB-related proteins, the BBB function will be weakened to a certain extent. By comparing the Aβ and resveratrol groups injected into the hippocampus of normal mice, in the Aβ1-42 group, MIP-α and CCR5 were highly expressed, and occludin and claudin-5 were low in protein expression. Conclusion Aβ can increase the expression of MIP-α, downregulate occludin and claudin-5 proteins, thereby destroying BBB stability.