Alzheimer's disease (AD) is the leading cause of dementia, and no effective treatment has been developed for it thus far. Recently, the use of natural compounds in the treatment of neurodegenerative diseases has garnered significant attention owing to their minimal adverse reactions. Accordingly, the potential therapeutic effect of pterostilbene (PTS) on AD has been demonstrated in multiple in vivo and in vitro experiments. In this study, we systematically reviewed and summarized the results of these studies investigating the use of PTS for treating AD. Analysis of the literature revealed that PTS may play a role in AD treatment through various mechanisms, including anti-oxidative damage, anti-neuroinflammation, anti-apoptosis, cholinesterase activity inhibition, attenuation of β-amyloid deposition, and tau protein hyperphosphorylation. Moreover, PTS interferes with the progression of AD by regulating the activities of peroxisome proliferator-activated receptor alpha (PPAR-α), monoamine oxidase B (MAO-B), silent information regulator sirtuin 1 (SIRT1), and phosphodiesterase 4A (PDE4A). Furthermore, to further elucidate the potential therapeutic mechanisms of PTS in AD, we employed network pharmacology and molecular docking technology to perform molecular docking of related proteins, and the obtained binding energies ranged from -2.83 to -5.14 kJ/mol, indicating that these proteins exhibit good binding ability with PTS. Network pharmacology analysis revealed multiple potential mechanisms of action for PTS in AD. In summary, by systematically collating and summarizing the relevant studies on the role of PTS in treatment of AD, it is anticipated that this will serve as a reference for the precise targeted prevention and treatment of AD, either using PTS or other developed drug interventions.

Objective To study inhibition effect of rosiglitazone on lung injury induced by paraquat. Methods 72 male SD rats were randomly divided into three groups ( n=24 ): model control group, paraquat ( PQ ) was administered intraperitoneally at the dose of 20 mg·kg-1;rosiglitazone group, rosiglitazone (10 mg·kg-1 , ip) was administered 1 h before PQ administration; blank control group, 1 mL 0. 9% sodium chloride solution was administered intraperitoneally. The concentration of TNF-α and IL-1β in serum was measured by ELISA at 4, 8 h and 1, 3 day(s) after PQ exposure. The lung injury scores and nuclear factor-kappa B( NF-κB) positive signal were investigated 3 days after PQ exposure by HE staining and immunohistochemistry, respectively. Protein expression levels of NF-κB and activating protein-1(AP-1) were also determined by using Western blotting. Results The levels of IL-1β and TNF-α in serum of PQ-treated rats were significantly increased as compared with blank control group. Rosiglitazone pretreatment reduced the degree of lung tissue injury, the levels of IL-1β and TNF-α in serum, and the protien expression levels of NF-κB and AP-1 as compared with the model control group. Conclusion Rosiglitazone can inhibit NF-κB and AP-1 protein expression in lung tissue, reduce the levels of IL-1β and TNF-α in serum after PQ exposure, and exert an inhibition effect on inflammation in PQ-induced lung injury of rats.