Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 16, Issue 12, Pages 28077-28086Publisher
MDPI
DOI: 10.3390/ijms161226083
Keywords
microcystin-LR; endoplasmic reticulum stress; cognitive impairment; tauroursodeoxycholic acid
Funding
- National Natural Science Foundation of China [31370525]
- Fundamental Research Funds for Central Universities [2014PY027, 2662015PY030]
- Natural Science Foundation of Hubei Province of China [2014CFA031]
- Chenguang plan of Wuhan Municipal Science and Technology Bureau [2014070404010226]
- foundation of Department of Education of Hubei Province [D20142802]
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Recent 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.
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