Protective effects of isofraxidin against scopolamine-induced cognitive and memory impairments in mice involve modulation of the BDNF-CREB-ERK signaling pathway.
Bingliang LianJingwen GuChen ZhangZhicong ZouMeng YuFanghong LiXiao-Li WuAllan Zijian ZhaoPublished in: Metabolic brain disease (2022)
These results suggested that isofraxidin ameliorated scopolamine-induced cognitive and memory impairments, possibly through regulating AChE activity, suppressing oxidative stress and inflammatory response, and modulating BDNF-CREB-ERK pathways.
Keyphrases
- signaling pathway
- diabetic rats
- pi k akt
- inflammatory response
- oxidative stress
- induced apoptosis
- high glucose
- epithelial mesenchymal transition
- working memory
- cell proliferation
- stress induced
- dna damage
- lipopolysaccharide induced
- metabolic syndrome
- adipose tissue
- type diabetes
- lps induced
- skeletal muscle
- immune response
- toll like receptor