Silibinin Alleviates the Learning and Memory Defects in Overtrained Rats Accompanying Reduced Neuronal Apoptosis and Senescence.
Bo LiuWeiwei LiuPanwen LiuXiumin LiuXiaoyu SongToshihiko HayashiSatoshi OnoderaTakashi IkejimaPublished in: Neurochemical research (2019)
Excessive physical exercise (overtraining; OT) increases oxidative stress and induces damage in multiple organs including the brain, especially the hippocampus that plays an important role in learning and memory. Silibinin, a natural flavonoid derived from milk thistle of Silybum marianum, has been reported to exert neuroprotective effect. In this study, rats were subjected to overtraining exercise, and the protective effects of silibinin were investigated in these models. Morris water maze and novel object recognition tests showed that silibinin significantly attenuated memory defects in overtrained rats. At the same time, the results of Nissl, TUNEL and SA-β-gal staining showed that silibinin reversed neuronal loss caused by apoptosis, and delayed cell senescence of the hippocampus in the overtrained rats, respectively. In addition, silibinin decreased malondialdehyde (MDA) levels which is associated with reactive oxygen species (ROS) generation. Silibinin prevented impairment of learning and memory caused by excessive physical exercise in rats, accompanied by reduced apoptosis and senescence in hippocampus cells.
Keyphrases
- oxidative stress
- cell cycle arrest
- dna damage
- cerebral ischemia
- cell death
- induced apoptosis
- reactive oxygen species
- endoplasmic reticulum stress
- endothelial cells
- single cell
- working memory
- white matter
- stem cells
- physical activity
- signaling pathway
- cognitive impairment
- high resolution
- body composition
- resting state
- bone marrow
- breast cancer cells
- body mass index