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Open AccessArticle

Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR

1
Department of Pharmacology, Hubei University of Science and Technology, Xianning 437100, China
2
Department of Pharmacy, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China
3
Hubei Province Key Laboratory on Cardiovascular, Cerebrovascular, and Metabolic Disorders, Hubei University of Science and Technology, Xianning 437100, China
4
Fisheries College, Huazhong Agricultural University, Wuhan 430070, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Masato Matsuoka
Int. J. Mol. Sci. 2015, 16(12), 28077-28086; https://doi.org/10.3390/ijms161226083
Received: 13 October 2015 / Revised: 16 November 2015 / Accepted: 17 November 2015 / Published: 25 November 2015
(This article belongs to the Special Issue Modulators of Endoplasmic Reticulum Stress)
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. View Full-Text
Keywords: microcystin-LR; endoplasmic reticulum stress; cognitive impairment; tauroursodeoxycholic acid microcystin-LR; endoplasmic reticulum stress; cognitive impairment; tauroursodeoxycholic acid
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MDPI and ACS Style

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.

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