Protective effects of trehalose against Mn-induced α-synuclein oligomerization in mice: Involvement of oxidative stress and autophagy.
Meng-Jiao JingKuan LiuChang LiuDong-Ying YanZhuo MaCan WangYu DengWei LiuBin XuPublished in: Environmental toxicology (2019)
Overexposure to manganese (Mn) is widely known to induce alpha-synuclein (α-Syn) oligomerization, which has been attributed to the oxidative damage of α-Syn protein. Trehalose has been shown to induce autophagy and serve as a chemical chaperone, but little information has been reported about its effect on Mn-induced α-Syn oligomerization. In this study, we investigate whether trehalose can effectively interfere with Mn-induced α-Syn oligomerization, using different concentrations of trehalose (2% and 4% (g/vol [mL])) in a mouse model of manganism. After 6 weeks of exposure to Mn, both oxidative stress and autophagy were activated and resulted in α-Syn oligomerization and neuronal cell damage in the mouse brain tissue. Our results also revealed that pretreatment with trehalose significantly reduced the oxidative damage to α-Syn protein and increased autophagy activation. These findings clearly demonstrated that trehalose can relieve Mn-induced α-Syn oligomerization and neuronal cell damage through its anti-oxidative and autophagy-inducing effects.
Keyphrases
- oxidative stress
- diabetic rats
- cell death
- high glucose
- endoplasmic reticulum stress
- signaling pathway
- mouse model
- single cell
- induced apoptosis
- transition metal
- drug induced
- endothelial cells
- type diabetes
- stem cells
- metal organic framework
- mesenchymal stem cells
- healthcare
- adipose tissue
- metabolic syndrome
- amino acid
- blood brain barrier
- subarachnoid hemorrhage