Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR
AbstractRecent studies showed that cyanobacteria-derived microcystin-leucine-arginine (MCLR) can cause hippocampal pathological damage and trigger cognitive impairment; but the underlying mechanisms have not been well understood. The objective of the present study was to investigate the mechanism of MCLR-induced cognitive deficit; with a focus on endoplasmic reticulum (ER) stress. The Morris water maze test and electrophysiological study demonstrated that MCLR caused spatial memory injury in male Wistar rats; which could be inhibited by ER stress blocker; tauroursodeoxycholic acid (TUDCA). Meanwhile; real-time polymerase chain reaction (real-time PCR) and immunohistochemistry demonstrated that the expression level of the 78-kDa glucose-regulated protein (GRP78); C/EBP homologous protein (CHOP) and caspase 12 were significantly up-regulated. These effects were rescued by co-administration of TUDCA. In agreement with this; we also observed that treatment of rats with TUDCA blocked the alterations in ER ultrastructure and apoptotic cell death in CA1 neurons from rats exposed to MCLR. Taken together; the present results suggested that ER stress plays an important role in potential memory impairments in rats treated with MCLR; and amelioration of ER stress may serve as a novel strategy to alleviate damaged cognitive function triggered by MCLR. View Full-Text
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Cai, F.; Liu, J.; Li, C.; Wang, J. Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR. Int. J. Mol. Sci. 2015, 16, 28077-28086.
Cai F, Liu J, Li C, Wang J. Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR. International Journal of Molecular Sciences. 2015; 16(12):28077-28086.Chicago/Turabian Style
Cai, Fei; Liu, Jue; Li, Cairong; Wang, Jianghua. 2015. "Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR." Int. J. Mol. Sci. 16, no. 12: 28077-28086.