Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage.
Ling Ling ChenDong Rui ZhangJie LiHe Meng WangChun Hua SongXun TangYalin GuanYing ChangWen Fei WangPublished in: Neurochemical research (2021)
Albicanol is a natural terpenoid derived from Dryopteris fragrans. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.
Keyphrases
- oxidative stress
- signaling pathway
- poor prognosis
- pi k akt
- gene expression
- machine learning
- dna damage
- type diabetes
- rheumatoid arthritis
- binding protein
- cell proliferation
- multiple sclerosis
- dna methylation
- blood brain barrier
- endothelial cells
- deep learning
- brain injury
- high glucose
- subarachnoid hemorrhage
- drug induced
- cerebral ischemia
- resting state
- wild type
- electronic health record